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100% found this document useful (21 votes)
106 views87 pages

Pediatric Gynecology An Illustrated Guide For Surgeons 1st Edition by Ahmed Al Salem 3030499839 9783030499839

The document provides information about various medical ebooks available for download at ebookball.com, including titles such as 'Pediatric Gynecology An Illustrated Guide for Surgeons' by Ahmed Al Salem. It highlights the focus on pediatric gynecology, covering conditions and treatments relevant to the female reproductive system in children. The document also lists additional medical titles and their respective links for instant download.

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Pediatric
Gynecology
An Illustrated Guide
for Surgeons
Ahmed H. Al-Salem

123
Pediatric Gynecology
Ahmed H. Al-Salem

Pediatric Gynecology
An Illustrated Guide for Surgeons
Ahmed H. Al-Salem
Pediatric Surgery
Alsadiq Hospital
Saihat, Saudi Arabia

ISBN 978-3-030-49983-9    ISBN 978-3-030-49984-6 (eBook)


https://doi.org/10.1007/978-3-030-49984-6

© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature
Switzerland AG 2020
This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether
the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and
transmission or information storage and retrieval, electronic adaptation, computer software, or by similar
or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication
does not imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
editors give a warranty, express or implied, with respect to the material contained herein or for any errors
or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims
in published maps and institutional affiliations.

This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Preface

The word “gynecology” comes from the Greek γυνή (gyne), “woman,” and -logia,
“study.”
Pediatric gynecology is the medical specialty dealing with the medical and surgi-
cal abnormalities of the vulva, vagina, uterus, and ovaries of infants, children, and
adolescents. This includes a number of pediatric gynecologic conditions that include
both benign and malignant conditions. Disorders of the breast, disorders of sexual
development, and precocious puberty are also included.
The specialty of pediatric gynecology is evolving rapidly and has witnessed sev-
eral advancements during the last 20 years including minimal invasive surgery. This
book is written in a simple and easy-to-read way. It covers most areas in the field of
pediatric gynecology with an emphasis on the most important areas relevant to the
patient’s presentation, diagnosis, and management. This book is well illustrated and
includes clinical, operative, pathological, radiological, and hand-drawn illustra-
tions. This book should prove valuable to all involved in the care of these patients.
This book will be useful to consultant pediatric surgeons, specialists, fellows, and
residents. The book should be also useful to general surgeons, accident and emer-
gency doctors, pediatricians, neonatologists, pediatric endocrinologist, gynecolo-
gists, general practitioners, trainees, medical students, and nurses.

Saihat, Saudi Arabia Ahmed H. Al-Salem

v
Acknowledgments

I would like to express special thanks of gratitude to my family who supported me


and made this project possible. I would also like to thank all my patients and their
families and my colleagues and friends who supported and encouraged me.

vii
Contents

1 Development of the Female Reproductive System��������������������������������    1


Ahmed H. Al-Salem
1.1 Introduction��������������������������������������������������������������������������������������    1
1.2 Gonadal and Internal Genital System Development������������������������    3
1.3 Development of the External Genitalia��������������������������������������������    7
Further Reading ����������������������������������������������������������������������������������������    8
2 Delayed Puberty in Girls ������������������������������������������������������������������������   11
Ahmed H. Al-Salem
2.1 Introduction��������������������������������������������������������������������������������������   11
2.2 Tanner Stages������������������������������������������������������������������������������������   12
2.3 Normal Puberty and Causes of Delayed Puberty������������������������������   13
2.4 Management��������������������������������������������������������������������������������������   18
Further Reading ����������������������������������������������������������������������������������������   20
3 Precocious Puberty����������������������������������������������������������������������������������   23
Ahmed H. Al-Salem
3.1 Introduction��������������������������������������������������������������������������������������   23
3.2 Regulation of Normal Puberty����������������������������������������������������������   26
3.3 Epidemiology������������������������������������������������������������������������������������   29
3.4 Classification and Etiology ��������������������������������������������������������������   29
3.5 Pathophysiology��������������������������������������������������������������������������������   31
3.6 Clinical Features, Morbidity and Mortality��������������������������������������   32
3.7 Investigations and Diagnosis������������������������������������������������������������   34
3.8 Treatment������������������������������������������������������������������������������������������   37
Further Reading ����������������������������������������������������������������������������������������   40
4 Breast Disorders in Female Children and Adolescents������������������������   43
Ahmed H. Al-Salem
4.1 Introduction��������������������������������������������������������������������������������������   43
4.2 Normal Breast Development������������������������������������������������������������   45
4.3 Congenital Breast Abnormalities������������������������������������������������������   49

ix
x Contents

4.4 Non-neoplastic Breast Lesions ��������������������������������������������������������   57


4.5 Fibrocystic Disease ��������������������������������������������������������������������������   60
4.6 Breast Hematoma������������������������������������������������������������������������������   61
4.7 Galactocele����������������������������������������������������������������������������������������   61
4.8 Benign Premature Thelarche������������������������������������������������������������   62
4.9 Precocious Puberty����������������������������������������������������������������������������   63
4.10 Mammary Duct Ectasia��������������������������������������������������������������������   64
4.11 Trauma����������������������������������������������������������������������������������������������   65
4.12 Fibrocystic Changes��������������������������������������������������������������������������   65
4.13 Benign and Malignant Breast Tumors in Children
and Adolescents��������������������������������������������������������������������������������   66
4.14 Fibroadenoma ����������������������������������������������������������������������������������   66
4.15 Pseudoangiomatous Stromal Hyperplasia (PASH) ��������������������������   69
4.16 Breast Hamartoma����������������������������������������������������������������������������   69
4.17 Intraductal Papilloma (Solitary Central Papilloma)��������������������������   70
4.18 Juvenile Papillomatosis (Multiple Peripheral Papillomas) ��������������   71
4.19 Fibrous Nodule����������������������������������������������������������������������������������   72
4.20 Phyllodes Tumor (Cystosarcoma Phyllodes)������������������������������������   72
4.21 Metastatic Breast Tumors ����������������������������������������������������������������   74
4.22 Primary Breast Carcinoma����������������������������������������������������������������   76
4.23 Genetics��������������������������������������������������������������������������������������������   80
4.24 Screening������������������������������������������������������������������������������������������   82
4.25 Chest Wall Malignancies������������������������������������������������������������������   82
Further Reading ����������������������������������������������������������������������������������������   83
5 Fused Labia (Labial Adhesions) ������������������������������������������������������������   87
Ahmed H. Al-Salem
5.1 Introduction��������������������������������������������������������������������������������������   87
5.2 Incidence ������������������������������������������������������������������������������������������   88
5.3 Etiology��������������������������������������������������������������������������������������������   89
5.4 Clinical Features ������������������������������������������������������������������������������   89
5.5 Treatment������������������������������������������������������������������������������������������   90
Further Reading ����������������������������������������������������������������������������������������   93
6 Imperforate Hymen ��������������������������������������������������������������������������������   95
Ahmed H. Al-Salem
6.1 Introduction��������������������������������������������������������������������������������������   95
6.2 Embryology��������������������������������������������������������������������������������������   98
6.3 Incidence ������������������������������������������������������������������������������������������   99
6.4 Pathophysiology�������������������������������������������������������������������������������� 100
6.5 Clinical Features ������������������������������������������������������������������������������ 101
6.6 Diagnosis and Management�������������������������������������������������������������� 104
Further Reading ���������������������������������������������������������������������������������������� 105
7 Labial and Inter-Labial Masses�������������������������������������������������������������� 107
Ahmed H. Al-Salem
7.1 Introduction�������������������������������������������������������������������������������������� 107
7.2 Normal Genital Anatomy������������������������������������������������������������������ 108
Contents xi

7.3 Vulvar Abnormalities and Labial Adhesions������������������������������������ 110


7.4 Genital Bleeding ������������������������������������������������������������������������������ 112
7.5 Congenital Paraurethral Cysts���������������������������������������������������������� 114
7.6 Inguinal Hernia �������������������������������������������������������������������������������� 117
7.7 Urethral Polyps �������������������������������������������������������������������������������� 117
7.8 Imperforate Hymen�������������������������������������������������������������������������� 118
7.9 Ureterocele���������������������������������������������������������������������������������������� 119
7.10 Vulvar Abscess���������������������������������������������������������������������������������� 122
7.11 Sarcoma Botryoides�������������������������������������������������������������������������� 126
Further Reading ���������������������������������������������������������������������������������������� 128
8 Pediatric Vulvovaginal Disorders and Vulvovaginitis �������������������������� 129
Ahmed H. Al-Salem
8.1 Introduction�������������������������������������������������������������������������������������� 129
8.2 Anatomy of the Pediatric Vulva�������������������������������������������������������� 130
8.3 Lichen Sclerosus ������������������������������������������������������������������������������ 132
8.4 Lichen Planus������������������������������������������������������������������������������������ 134
8.5 Labial Adhesions (Labial Fusion)���������������������������������������������������� 134
8.6 Genital Ulcers ���������������������������������������������������������������������������������� 137
8.7 Urethral Prolapse������������������������������������������������������������������������������ 140
8.8 Atopic Dermatitis������������������������������������������������������������������������������ 141
8.9 Seborrheic Dermatitis ���������������������������������������������������������������������� 142
8.10 Lichen Simplex �������������������������������������������������������������������������������� 143
8.11 Psoriasis�������������������������������������������������������������������������������������������� 143
8.12 Straddle Injury���������������������������������������������������������������������������������� 145
8.13 Pediatric Vulvovaginitis�������������������������������������������������������������������� 146
8.14 Etiology�������������������������������������������������������������������������������������������� 147
8.15 Diagnosis������������������������������������������������������������������������������������������ 148
8.16 Noninfectious Vulvovaginitis������������������������������������������������������������ 150
8.17 Infectious Vulvovaginitis, Nonsexually Transmitted������������������������ 151
8.18 Infectious Vulvovaginitis, Sexually Transmitted������������������������������ 153
Further Reading ���������������������������������������������������������������������������������������� 154
9 Inguinal and Femoral Hernias in Girls�������������������������������������������������� 157
Ahmed H. Al-Salem and Osama Bawazir
9.1 Introduction�������������������������������������������������������������������������������������� 157
9.2 Inguinal Hernia �������������������������������������������������������������������������������� 158
9.3 Etiology�������������������������������������������������������������������������������������������� 160
9.4 Clinical Features ������������������������������������������������������������������������������ 162
9.5 Complications of Inguinal Hernias �������������������������������������������������� 163
9.6 Treatment������������������������������������������������������������������������������������������ 164
9.7 Hydrocele of the Canal of Nuck ������������������������������������������������������ 165
9.8 Femoral Hernia �������������������������������������������������������������������������������� 166
9.9 Etiology�������������������������������������������������������������������������������������������� 167
9.10 Diagnosis������������������������������������������������������������������������������������������ 168
9.11 Treatment������������������������������������������������������������������������������������������ 169
Further Reading ���������������������������������������������������������������������������������������� 169
xii Contents

10 Persistent Mullerian Duct Syndrome���������������������������������������������������� 171


Ahmed H. Al-Salem and Moustafa Hamchou
10.1 Introduction������������������������������������������������������������������������������������ 171
10.2 Embryology and Etiology �������������������������������������������������������������� 172
10.3 Clinical Features ���������������������������������������������������������������������������� 174
10.4 Diagnosis and Surgical Management���������������������������������������������� 175
Further Reading ���������������������������������������������������������������������������������������� 179
11 Vaginal Atresia, Agenesis and Vaginal Septum ������������������������������������ 181
Ahmed H. Al-Salem
11.1 Introduction������������������������������������������������������������������������������������ 181
11.2 Embryology������������������������������������������������������������������������������������ 182
11.3 Classification���������������������������������������������������������������������������������� 190
11.4 Associated Anomalies�������������������������������������������������������������������� 194
11.5 Clinical Features ���������������������������������������������������������������������������� 196
11.6 Investigations���������������������������������������������������������������������������������� 200
11.7 Treatment���������������������������������������������������������������������������������������� 203
11.8 Complications �������������������������������������������������������������������������������� 215
Further Reading ���������������������������������������������������������������������������������������� 215
12 Cloacal Anomalies������������������������������������������������������������������������������������ 217
Ahmed H. Al-Salem and Munther J. Haddad
12.1 Introduction������������������������������������������������������������������������������������ 217
12.2 Associated Anomalies�������������������������������������������������������������������� 219
12.3 Classification���������������������������������������������������������������������������������� 220
12.4 Clinical Features ���������������������������������������������������������������������������� 221
12.5 Investigations���������������������������������������������������������������������������������� 222
12.6 Management������������������������������������������������������������������������������������ 225
Further Reading ���������������������������������������������������������������������������������������� 229
13 Menstruation Disorders in Adolescents ������������������������������������������������ 231
Ahmed H. Al-Salem and Salah Radwan
13.1 Introduction������������������������������������������������������������������������������������ 231
13.2 Pathophysiology������������������������������������������������������������������������������ 235
13.3 Etiology and Classification ������������������������������������������������������������ 236
13.4 Primary Amenorrhea���������������������������������������������������������������������� 236
13.5 Abnormal Uterine Bleeding������������������������������������������������������������ 240
13.6 Polycystic Ovary Syndrome (PCOS)���������������������������������������������� 242
13.7 Heavy Menstrual Bleeding������������������������������������������������������������� 243
13.8 Intermenstrual Bleeding������������������������������������������������������������������ 244
13.9 Dysmenorrhea �������������������������������������������������������������������������������� 245
13.10 Treatment Options�������������������������������������������������������������������������� 246
13.11 Management of Primary Amenorrhea�������������������������������������������� 248
13.12 Treatment of Heavy Menstrual Bleeding���������������������������������������� 249
Further Reading ���������������������������������������������������������������������������������������� 250
Contents xiii

14 Polycystic Ovarian Syndrome���������������������������������������������������������������� 253


Ahmed H. Al-Salem
14.1 Introduction������������������������������������������������������������������������������������ 253
14.2 Epidemiology���������������������������������������������������������������������������������� 255
14.3 Definition of Polycystic Ovarian Syndrome ���������������������������������� 256
14.4 Pathogenesis of Polycystic Ovarian Syndrome������������������������������ 258
14.5 Etiology������������������������������������������������������������������������������������������ 263
14.6 Clinical Features ���������������������������������������������������������������������������� 265
14.7 Diagnosis and Diagnostic Criteria�������������������������������������������������� 267
14.8 Treatment and Outcome������������������������������������������������������������������ 269
14.9 Prognosis���������������������������������������������������������������������������������������� 273
Further Reading ���������������������������������������������������������������������������������������� 273
15 Endometriosis in Adolescent Girls �������������������������������������������������������� 275
Ahmed H. Al-Salem
15.1 Introduction������������������������������������������������������������������������������������ 275
15.2 Etiology������������������������������������������������������������������������������������������ 276
15.3 Incidence ���������������������������������������������������������������������������������������� 277
15.4 Clinical Features ���������������������������������������������������������������������������� 277
15.5 Staging of Endometriosis���������������������������������������������������������������� 279
15.6 Investigations and Diagnosis���������������������������������������������������������� 281
15.7 Approach and Management Considerations ���������������������������������� 282
15.8 Surgical Management �������������������������������������������������������������������� 287
Further Reading ���������������������������������������������������������������������������������������� 289
16 Amenorrhea in Adolescents�������������������������������������������������������������������� 295
Ahmed H. Al-Salem and Salah Radwan
16.1 Introduction������������������������������������������������������������������������������������ 295
16.2 Pathophysiology������������������������������������������������������������������������������ 298
16.3 Polycystic Ovary Syndrome (PCOS)���������������������������������������������� 299
16.4 Causes of Amenorrhea in Adolescents�������������������������������������������� 299
16.5 Primary Hypogonadism������������������������������������������������������������������ 301
16.6 Hypothalamic Causes of Amenorrhea�������������������������������������������� 301
16.7 Functional Hypothalamic Amenorrhea ������������������������������������������ 301
16.8 Kallman Syndrome ������������������������������������������������������������������������ 302
16.9 Pituitary Causes of Amenorrhea ���������������������������������������������������� 302
16.10 Multifactorial Causes of Amenorrhea�������������������������������������������� 304
16.11 Laboratory Investigation ���������������������������������������������������������������� 305
16.12 Amenorrhea in Female Athletes������������������������������������������������������ 308
16.13 Management������������������������������������������������������������������������������������ 309
Further Reading ���������������������������������������������������������������������������������������� 313
17 Ovarian Cysts and Tumors��������������������������������������������������������������������� 317
Ahmed H. Al-Salem, Munther J. Haddad, and Moustafa Hamchou
17.1 Introduction������������������������������������������������������������������������������������ 317
17.2 Incidence ���������������������������������������������������������������������������������������� 322
xiv Contents

17.3 Classification���������������������������������������������������������������������������������� 322


17.4 Ovarian Cysts in the Fetus�������������������������������������������������������������� 324
17.5 Diagnosis���������������������������������������������������������������������������������������� 325
17.6 Management and Outcome ������������������������������������������������������������ 327
17.7 Ovarian Cysts in Neonates�������������������������������������������������������������� 328
17.8 Management������������������������������������������������������������������������������������ 329
17.9 Ovarian Cysts in Infants and Prepubertal Girls������������������������������ 330
17.10 Investigations���������������������������������������������������������������������������������� 331
17.11 Management and Outcome ������������������������������������������������������������ 332
17.12 Ovarian Cysts in Adolescents �������������������������������������������������������� 333
17.13 Management and Outcome ������������������������������������������������������������ 335
17.14 Ovarian Tumors������������������������������������������������������������������������������ 338
17.15 Introduction������������������������������������������������������������������������������������ 338
17.16 Fibromas ���������������������������������������������������������������������������������������� 342
17.17 Thecoma������������������������������������������������������������������������������������������ 342
17.18 Ovarian Cystadenoma �������������������������������������������������������������������� 343
17.19 Germ Cell Tumors�������������������������������������������������������������������������� 343
17.20 Ovarian Teratoma���������������������������������������������������������������������������� 344
17.21 Immature Teratoma ������������������������������������������������������������������������ 347
17.22 Yolk Sac (Endodermal Sinus) Tumors�������������������������������������������� 352
17.23 Primary Choriocarcinoma�������������������������������������������������������������� 352
17.24 Mixed Germ Cell Tumors �������������������������������������������������������������� 353
17.25 Sex-Cord Stromal Cell Tumors������������������������������������������������������ 353
17.26 Epithelial Ovarian Tumors�������������������������������������������������������������� 355
17.27 Dysgerminoma�������������������������������������������������������������������������������� 357
17.28 Clinical Manifestations of Ovarian Tumors������������������������������������ 359
17.29 Investigations���������������������������������������������������������������������������������� 360
17.30 Staging�������������������������������������������������������������������������������������������� 365
17.31 Treatment���������������������������������������������������������������������������������������� 366
17.32 Prognosis���������������������������������������������������������������������������������������� 369
Further Reading ���������������������������������������������������������������������������������������� 369
18 Rhabdomyosarcoma of Female Children Genital Tract���������������������� 373
Ahmed H. Al-Salem
18.1 Introduction������������������������������������������������������������������������������������ 373
18.2 Histology���������������������������������������������������������������������������������������� 377
18.3 Botryoid Embryonal Rhabdomyosarcoma�������������������������������������� 381
18.4 Introduction������������������������������������������������������������������������������������ 381
18.5 Clinical Features ���������������������������������������������������������������������������� 383
18.6 Investigations and Diagnosis���������������������������������������������������������� 384
18.7 Staging�������������������������������������������������������������������������������������������� 385
18.8 Treatment and Outcome������������������������������������������������������������������ 389
Further Reading ���������������������������������������������������������������������������������������� 391
Contents xv

19 Disorders of Sexual Development���������������������������������������������������������� 393


Ahmed H. Al-Salem
19.1 Introduction������������������������������������������������������������������������������������ 393
19.2 Embryology and Physiology of Sex Development ������������������������ 397
19.3 Classification���������������������������������������������������������������������������������� 401
19.4 Sex Chromosome DSDs ���������������������������������������������������������������� 402
19.5 Classification of Disorders of Sexual Development ���������������������� 409
19.6 Evaluation of a Newborn with DSD ���������������������������������������������� 410
19.7 Sex Assignment������������������������������������������������������������������������������ 411
19.8 Diagnosis and Investigations���������������������������������������������������������� 414
19.9 Management of Patients with DSD������������������������������������������������ 416
Further Reading ���������������������������������������������������������������������������������������� 419
20 Congenital Adrenal Hyperplasia (CAH)������������������������������������������������ 421
Ahmed H. Al-Salem
20.1 Introduction������������������������������������������������������������������������������������ 421
20.2 Diagnosis���������������������������������������������������������������������������������������� 428
20.3 Management������������������������������������������������������������������������������������ 429
Further Reading ���������������������������������������������������������������������������������������� 431
21 Androgen Insensitivity Syndrome (Testicular Feminization
Syndrome)������������������������������������������������������������������������������������������������ 433
Ahmed H. Al-Salem
21.1 Introduction������������������������������������������������������������������������������������ 433
21.2 Etiology������������������������������������������������������������������������������������������ 436
21.3 Clinical Features ���������������������������������������������������������������������������� 437
21.4 Treatment���������������������������������������������������������������������������������������� 438
Further Reading ���������������������������������������������������������������������������������������� 442
22 Deficient Testosterone Biosynthesis�������������������������������������������������������� 445
Ahmed H. Al-Salem
22.1 Introduction������������������������������������������������������������������������������������ 445
22.2 Pathophysiology������������������������������������������������������������������������������ 449
22.3 Clinical Features ���������������������������������������������������������������������������� 456
22.4 Diagnosis���������������������������������������������������������������������������������������� 459
22.5 Management������������������������������������������������������������������������������������ 459
Further Reading ���������������������������������������������������������������������������������������� 459
23 Gonadal Dysgenesis �������������������������������������������������������������������������������� 461
Ahmed H. Al-Salem
23.1 Introduction������������������������������������������������������������������������������������ 461
23.2 Partial Gonadal Dysgenesis������������������������������������������������������������ 463
23.3 A Dysgenetic Testis������������������������������������������������������������������������ 463
23.4 Pure Gonadal Dysgenesis �������������������������������������������������������������� 464
23.5 Mixed Gonadal Dysgenesis (MGD) ���������������������������������������������� 466
23.6 Management������������������������������������������������������������������������������������ 467
Further Reading ���������������������������������������������������������������������������������������� 467
xvi Contents

24 Ovotestis Disorders of Sexual Development������������������������������������������ 469


Ahmed H. Al-Salem
24.1 Introduction������������������������������������������������������������������������������������ 469
24.2 Etiology������������������������������������������������������������������������������������������ 469
24.3 Pathophysiology������������������������������������������������������������������������������ 472
24.4 Clinical Features ���������������������������������������������������������������������������� 474
24.5 Investigations���������������������������������������������������������������������������������� 474
24.6 Management������������������������������������������������������������������������������������ 476
Further Reading ���������������������������������������������������������������������������������������� 477
List of Contributors

Osama A. Bawazir Pediatric Surgery, KFSHRC, Jeddah, Saudi Arabia


Department of Surgery, Collage of Medicine, Umm Al-Qura University, Makkah,
Saudi Arabia
Munther J. Haddad Chelsea and Westminster Hospital NHS Foundation Trust,
London, UK
St. Mary’s Hospital, Imperial College School of Medicine, London, UK
Moustafa Hamchou Pediatric Surgery-Medical Affairs, Tawam Hospital, Al Ain,
United Arab Emirates
Salah Radwan Al Sadiq Hospital, Saihat, Saudi Arabia

xvii
Chapter 1
Development of the Female Reproductive
System

Ahmed H. Al-Salem

1.1 Introduction

• The male and female reproductive systems develop initially embryonically


“indifferent”. This is known as the indifferent stage.
• In this stage of gonadal development, it is impossible to distinguish between the
male and female gonad.
• It is the product of the Y chromosome SRY gene that makes the “difference” and
directs the development of the indifferent gonad into a male gonad (Testes) or
female gonad (Ovaries).
• The presence of the Y chromosome SRY gene directs the gonad to develop
into testes.
• The development of the indifferent gonads begin as a pair of longitudinal genital
ridges which are derived from intermediate mesoderm and overlying epithelium.
• They initially do not contain any germ cells.
• The germ cells develop subsequently around the fourth week of intrauterine life.
• They begin to migrate from the endoderm lining of the yolk sac to the genital
ridges, via the dorsal mesentery of the hindgut.
• The germ cells reach the genital ridges around the sixth week of intrauterine
development.
• The epithelium of the genital ridges proliferates and penetrates the intermediate
mesoderm to form the primitive sex cords.
• The indifferent gonads are composed of germ cells and primitive sex cords.

A. H. Al-Salem (*)
Pediatric Surgery, Alsadiq Hospital, Saihat, Saudi Arabia

© The Editor(s) (if applicable) and The Author(s), under exclusive license 1
to Springer Nature Switzerland AG 2020
A. H. Al-Salem, Pediatric Gynecology,
https://doi.org/10.1007/978-3-030-49984-6_1
2 A. H. Al-Salem

• The indifferent gonads subsequently develop into the testes or ovaries.


• In a female embryo (46, XX chromosomes):
–– The absence of Y chromosome SRY gene influence degeneration of the primi-
tive sex cords and do not form the testis cords.
–– The epithelium of the gonad continues to proliferate, producing cortical cords.
–– These cortical cords break up into clusters, surrounding each germ cell with a
layer of epithelial follicular cells, forming a primordial follicle.
• The ovaries initially develop on the posterior abdominal wall and migrate cau-
dally in a similar fashion to the testes reaching their final position just within the
true pelvis.
• The gubernaculum becomes the ovarian ligament and round ligament of the uterus.
• In the first weeks of urogenital development, each embryo has two pairs of ducts,
both ending at the cloaca.
–– The Mesonephric (Wolffian) ducts
–– The Paramesonephric (Mullerian) ducts
• In a female embryo (46, XX chromosomes):
–– The absence of Leydig cells which produce testosterone leads to degeneration of
the mesonephric ducts leaving behind a vestigial remnant called Gartner’s duct.
–– The absence of anti-Mullerian hormone which is normally secreted by Sertoli
cells of testes allows for development of the paramesonephric ducts.
–– The Mullerian ducts develop into:
The Fallopian tubes
The uterus and cervix
The upper 2/3 of the vagina
–– The lower 1/3 of the vagina is formed by sinovaginal bulbs (derived from the
pelvic part of the urogenital sinus).
• The development of the external genitalia begins in the third week of intrauter-
ine life.
• In females, this is under the influence of estrogens.
–– Mesenchymal cells from the primitive streak migrate to the cloacal membrane
to form a pair of cloacal folds.
–– Cranially, these folds fuse to form the genital tubercle.
–– Caudally, they divide into the urethral folds (anterior) and anal folds
(posterior).
–– Genital swellings develop on either side of the urethral folds.
–– The genital tubercle elongates slightly to form the clitoris.
–– The urethral folds and genital swellings do not fuse, but instead form the labia
minora and labia majora respectively.
–– The urogenital groove remains open, forming the vestibule into which the
urethra and vagina open.
1 Development of the Female Reproductive System 3

1.2 Gonadal and Internal Genital System Development

• In females the reproductive system or genital organs comprise of:


–– Two gonads (ovaries)
–– The reproductive organs (Uterus and Fallopian tubes)
–– The external genitalia (labia mjora, labia minora, clitoris and vagina)
• The genotype and chromosomal sex of a fetus is determined at the time of
conception.
• The phenotype of the fetus depends on the presence of sex chromosomes and the
prevailing biochemical and hormonal milieu.
• A male fetus will develop in the presence of:
–– A Y-chromosome which encodes the SRY protein.
–– The SRY protein enables differentiation of the indifferent gonads into a testis.
–– Testicular differentiation of the indifferent gonad will result in the production
of androgens including testosterone.
–– In addition to the SRY protein and androgens, testicular differentiation of the
indifferent gonad produces a third factor, anti-Müllerian hormone (AMH).
–– AMH prevents female genital ductal differentiation as it leads to regression of
the Mullerian ducts.
• Gonadal development begins in the fifth week of intrauterine life.
• The gonads develop on the posterior abdominal wall on either side of the spine.
• Until the seventh week of intrauterine life, the gonads are similar in both male
and female fetuses.
• These are called indifferent gonads and initially, they develop as urogenital
(gonadal) ridges from the mesothelium medial to the mesonephros (the develop-
ing kidney).
• The primitive or primordial germ cells develop around the fourth week of intra-
uterine life and migrate from the yolk sac of the embryo along the dorsal mesen-
tery of the hindgut to the mesenchyme of the gonadal ridges by the sixth week
and incorporate into the primary sex cords.
• The primary sex cords are not well developed in the female embryo and they
regress by the eighth week of intrauterine life.
• The presence of two X-chromosomes in a female fetus and absence of the Y
chromosome leads to the development of a female fetus.
–– The undifferentiated gonads will develop into ovaries.
–– The absence of AMH which is secreted by the Sertoli cells of testes will result
in further development and maturation of the Mullerian ducts.
–– The Mullerian ducts will develop into the uterus, Fallopian tubes and upper
two thirds of the vagina.
–– Further development and maturation of the female external genitalia is under
the influence of estrogen secreted by the ovary.
4 A. H. Al-Salem

• Gonadal differentiation takes place in the second month of intrauterine life.


• The first step is primitive germ cells differentiation.
–– This is under the influence of placental gonadotropins.
–– The germ cells migrating from the endoderm lining of the yolk sac to the
genital ridge.
–– The germ cells undergo successive mitotic divisions differentiating into sev-
eral million oogonia.
• The primitive follicles organize within the fetal ovarian cortex and by 5–6 months
of intrauterine life the ovaries contain 6–7 million primordial follicles.
• These primordial follicles subsequently become enveloped by a layer of epithe-
lial cells, and are referred to as primary oocytes.
• The vast majority of oocytes eventually degenerate over time.
• The remaining oogonia enter a dormant state referred to as meiotic arrest (first
phase of meiosis).
• First phase meiosis will not complete until the onset of ovulation.
• Ovulatory follicles complete meiotic differentiation.
• It is estimated that at birth, between 2 and 4 million follicles remain and around
400,000 follicles are present at menarche.
• Ovarian follicles undergo varying rates of maturation and involution.
• The vast majority remains quiescent and eventually involutes by apoptosis, but
can remain dormant for decades.
• The maturing ovaries descend into the pelvis at around the third month of intra-
uterine life.
• This descend of the ovary into the pelvis is guided by the gubernaculum and
facilitated by the marked growth of the upper abdomen relative to the pelvis.

46, XY 46, XX

Y CHROMOSOME NO Y CHROMOSOME
SRY PROTEIN NO SRY PROTEIN

INDIFFERENT
GONAD

TESTIS OVARY
1 Development of the Female Reproductive System 5

• The gubernaculum is a peritoneal fold which attaches the caudal aspect of the
ovary to the uterus.
• The gubernaculum eventually forms the uteroovarian ligment and round uterine
ligaments.
• Embryologically, there are two paramesonephric (Müllerian) ducts which arise
from the mesoderm lateral to the mesonephric ducts.
• The Müllerian ducts in females and in the absence of AMH which is secreted by
the Sertoli cells of testes mature and differentiate and give rise to:
–– The uterus
–– The fallopian tubes
–– The cervix
–– The upper 2/3 of the vagina.
• The paramesonephric ducts fuse to form a confluence.
• This occurs between the seventh and ninth weeks when the lower segments of the
paramesonephric ducts fuse.
• The cranial end of the fused paramesonephric ducts yields the future uterus
which contains mesoderm that will form the uterine endometrium and myome-
trium. At this stage, a midline septum is present in the uterine cavity; this usually
regresses and disappears at around 20 weeks of intrauterine life.
• The unfused cranial ends of the paramesonephric ducts assume a funnel shaped
configuration and remain open to the future peritoneal cavity as the fimbrial por-
tions of the fallopian tubes (Figs. 1.1 and 1.2a–c).
• The caudal end of the fused ducts will form the upper two-thirds of the vagina.
• The lower third of the vagina is formed as the sinovaginal node (bulb) canalizes.
• The sinovaginal node inserts into the urogenital sinus at Müller’s tubercle.
• The development of the lower abdominal wall is important to the development of
the lower urogenital system.
• The lower abdominal wall is formed from the cloacal membrane and the prolif-
erating adjacent mesenchyme.

Fig. 1.1 An illustration showing the development of the uterus and vagina. Note that the upper
two-thirds of the vagina are formed from the caudal end of the fused paramesonephric ducts. The
lower third of the vagina is formed from canalization of the sinovaginal node
6 A. H. Al-Salem

a b
GONAD
MULLERIAN OVARY
DUCT
FALLOPIAN
TUBE

UTERUS
FUSED
MULLERIAN BLADDER
DUCTS BLADDER

VAGINA

c
TESTIS

VAS

BLADDER
SEMINAL
VESICLE

PROSTATE

Fig. 1.2 (a–c) Illustrated diagrams showing the development of the female and male geni-
tal system

• The cloacal folds fuse anteriorly to give rise to the genital tubercle.
• During the seventh week of intrauterine life, the urorectal septum fuses to the
inner surface of the cloacal membrane dividing it into two parts:
–– The anterior (ventral) urogenital membrane
–– The posterior anal membrane
• This will divide the rectum proper from the urogenital tract.
• The urogenital membrane subsequently perforates creating free communication
between the amniotic cavity and the primary urogenital sinus.
• The folds surrounding the urogenital membrane are now referred to as the ure-
thral folds and those around the anus the anal folds.
• The primary urogenital sinus develops into the definitive urogenital sinus (UGS).
–– The UGS consists of a caudal phallic portion and a pelvic portion.
–– The urethral groove and phallic (distal) portion of the UGS enlarge to form
the vaginal introitus (vestibule).
–– This is closed off externally by the urogenital membrane which perforates in
the seventh week.
–– The narrow pelvic (proximal) segment of the definitive urogenital sinus con-
tributes to the short distal female urethra and lower third of the vagina.
1 Development of the Female Reproductive System 7

1.3 Development of the External Genitalia

• The external genitalia remain sexually undifferentiated until around the seventh
week of intrauterine life.
• Complete differentiation of the female external genitalia occurs around the
twelfth week of intrauterine life.
• The genital tubercle develops around the fourth week of intrauterine life from
mesenchymal proliferation.
• A protophallus develops ventral to the cloacal membrane.
• During the sixth week, the urethral groove and anal pit form resulting in focal
depressions along the cloacal membrane.
• The primary urethral (urogenital) folds surround the primary urethral groove.

46, XX

NO Y CHROMOSOME
NO SRY PROTEIN

INDIFFERENT
GONAD

OVARY

NO
MULLERIAN
MULLERIAN MULLERIAN
INHIBITING
DUCT DUCT
FACTOR

FUSE TOGETHER AND GIVE RISE TO

FALLOPIAN TUBES

UPPER 2/3 OF VAGINA


UTERUS
8 A. H. Al-Salem

• The genital or labioscrotal swellings form lateral to the urethral folds.


• In the seventh week, the cloacal membrane involutes and the primary urethral
groove becomes continuous with the definitive urogenital sinus.
• The secondary urethral groove forms as a result of deepening and widening the
primary urethral groove in the eighth week.
• The external genitalia begin display sexual differentiation during the tenth week.
• In developing females:
–– The unfused parts of the labioscrotal (genital) swellings give rise to the
labia majora.
–– These folds fuse anteriorly to form the mons pubis and anterior labial com-
missure, and posteriorly the posterior labial commissure.
–– The urethral folds fuse posteriorly to form the frenulum of the labia minora.
–– The unfused urethral (urogenital) folds give rise to the labia minora.
–– The unfused genital swellings enable the urogenital sinus to open into the
anterior (urethral) part of the vagina and the vaginal vestibule.
–– The genital tubercle becomes the clitoris.
• The accessory urethral glands including the paraurethral glands (Skene) and ure-
thral glands arise from the urogenital sinus from endodermal (epithelial) buds
growing into the urethral mesenchyme.
• The paired greater vestibular glands (Bartholin) form in the 12th week and empty
into the vaginal vestibule.
• The mesonephric (Wollfian) ducts regress in a female, but remnants of the meso-
nephric duct typically persist.
–– The Gartner’s ducts are paired remnants of the mesonephric duct that may
give rise to Gartner’s duct cysts and are typically located in the broad ligament.
• The canal of Nuck is a virtual space and is the female analogue of the processus
vaginalis in the male; if patent it is abnormal and forms a pouch of peritoneum in
the labia majora.
• The epoophoron is the most cranial part of the mesonephric duct remnant. It is
situated in the lateral portion of the broad ligament and may communicate with
the Gartner’s ducts more inferiorly in the broad ligament.
• It is homologous to the epididymis in males.
• The paraoophoron is also a mesonephric remnant analogous to the paradidymis
in males. It is usually positioned medially in each broad ligament.

Further Reading

1. Moore KL, Persaud TVN. The urogenital system. In: Moore KL, Persaud TVN, editors. The
developing human. Clinically oriented embryology. 6th ed. Philadelphia: WB Saunders; 1998.
p. 303–47.
2. Nakhuda GS. The role of mullerian inhibiting substance in female reproduction. Curr Opin
Obstet Gynecol. 2008;20:257–64.
1 Development of the Female Reproductive System 9

3. Massé J, Watrin T, Laurent A, Deschamps S, Guerrier D, Pellerin I. The developing female


genital tract: from genetics to epigenetics. Int J Dev Biol. 2009;53(2–3):411–24.
4. Rendi MH, Muehlenbachs A, Garcia RL, Boyd KL. In: Treuting PM, Dintzis S, Liggitt D,
Freve CW, editors. Female reproductive system. Comparative anatomy and histology; 2011.
p. 253–84.
5. Beckman DA, Feuston M. Landmarks in the development of the female reproductive system.
Birth Defects Res B Dev Reprod Toxicol. 2003 Apr;68(2):137–43.
6. Kim HH, Laufer MR. Developmental abnormalities of the female reproductive tract. Curr Opin
Obstet Gynecol. 1994 Dec;6(6):518–25.
7. Yamada G, Satoh Y, Baskin LS, Cunha GR. Cellular and molecular mechanisms of develop-
ment of the external genitalia. Differentiation. 2003 Oct;71(8):445–60.
Chapter 2
Delayed Puberty in Girls

Ahmed H. Al-Salem

2.1 Introduction

• Puberty changes occur when the body starts making sex hormones. These
changes normally begin to appear in girls between ages 8–14 years old.
• Puberty refers to the phase of development between childhood and adulthood in
which complete functional maturation of the reproductive glands and external
genitalia occurs.
• The other processes that characterize this transitional phase are the development
of secondary sex characteristics, growth spurts, and psychosocial changes.
• Delayed puberty is defined clinically as the absence of the first signs of pubertal
development beyond the normal range for the population.
• However, there are clear racial and ethnic variations in the timing of puberty,
such as earlier onset of puberty in African American girls compared with
Caucasian counterparts.
• In the United States, delayed puberty means the absence of breast development
by age 12 years in girls.
• Delayed pubertal development with the absence of breast development by age 13
is strongly associated with impaired reproductive potential and should prompt an
assessment to rule out ovarian failure with abnormal karyotype or other poten-
tially irreversible problems.
• The stages of development during puberty are classified according to the Tanner stages.
• Although there is considerable variation between individuals, on average puberty
begins at the age of 11 in girls and 13 in boys.

A. H. Al-Salem (*)
Pediatric Surgery, Alsadiq Hospital, Saihat, Saudi Arabia

© The Editor(s) (if applicable) and The Author(s), under exclusive license 11
to Springer Nature Switzerland AG 2020
A. H. Al-Salem, Pediatric Gynecology,
https://doi.org/10.1007/978-3-030-49984-6_2
12 A. H. Al-Salem

• Puberty that begins abnormally early is referred to as precocious puberty and can
be due to a peripheral cause (peripheral precocious puberty) or a central cause
involving the hypothalamo-hypophyseal axis (central precocious puberty, or CPP).
• Traditionally, precocious puberty has been defined as any pubertal development
occurring before age 8. Other authors define precocious puberty as pubertal
development before age 7 in whites and age 6 in African Americans.
• At the other end of the spectrum, puberty may be delayed or absent. This delay can
be constitutional, secondary to underlying conditions, or due to hypogonadism.
• Delayed puberty in girls occurs when breasts don’t develop by age 13 or men-
strual periods do not begin by age 16.
• Delayed puberty is more common in boys than in girls.
• The most common cause of delayed puberty is a functional defect in production
of gonadotropin-releasing hormone (GnRH) from the hypothalamus.
• This may be due to physiologic individual variation, known as constitutional
delay of growth and puberty, or other functional defects, such as undernutrition
or chronic illness.
• The GnRH deficiency leads to defective secretion of gonadotropins (luteinizing
hormone [LH] and follicle-stimulating hormone [FSH]) from the anterior pitu-
itary, which results in inadequate steroid secretion by the ovaries.
• Other causes of delayed puberty include a variety of hypothalamic, pituitary, and
gonadal disorders.

2.2 Tanner Stages

• Tanner stage 1:
–– Tanner stage 1 represents the girl’s appearance before any physical signs of
puberty appear. There are no noticeable physical changes for girls at this stage.
–– Toward the end of stage 1, the brain starts to send signals to prepare the body
for changes.
–– The hypothalamus begins to release gonadotropin-releasing hormone (GnRH).
–– GnRH stimulates the pituitary gland to release two other hormones: luteiniz-
ing hormone (LH) and follicle-stimulating hormone (FSH).
–– These early signals typically start after a girl’s eighth birthday.
• Tanner stage 2:
–– Stage 2 marks the beginning of physical development.
–– Puberty usually starts between ages 9 and 11 years.
–– The first signs of breasts development is called “buds”.
–– This starts to form under the nipple. They may be itchy or tender, which is normal.
–– It is also common for breasts to differ in size and growth rate.
–– It is normal if one bud appears larger than the other.
–– The areola of the breast will also expand.
–– The uterus begins to get larger, and small amounts of pubic hair start growing.
• Tanner stage 3:
2 Delayed Puberty in Girls 13

–– The physical changes become more obvious at this stage.


–– Physical changes in girls usually start after age 12.
–– Breasts “buds” continue to grow and expand.
–– Pubic hair gets thicker and curlier.
–– Hair starts forming under the armpits.
–– The first signs of acne may appear on the face and back.
–– The highest growth rate for height begins (around 3.2 inches per year).
–– Hips and thighs start to build up fat.
• Tanner stage 4:
–– Puberty is in full swing during stage 4.
–– In girls, stage 4 usually starts around age 13.
–– Breasts take on a fuller shape, passing the bud stage.
–– Many girls get their first period, typically between ages of 12 and 14, but it
can happen earlier.
–– Height growth will slow down to about 2–3 inches per year.
–– Pubic hair gets thicker.
• Tanner stage 5:
–– This final phase marks the end of the child’s physical maturation.
–– In girls, stage 5 usually happens around age 15.
–– Breasts reach approximate adult size and shape, though breasts can continue
to change through age 18.
–– Periods become regular after 6 months to 2 years.
–– Girls reach adult height 1–2 years after their first period.
–– Pubic hair fills out to reach the inner thighs.
–– Reproductive organs and genitals are fully developed.
–– Hips, thighs, and buttocks fill out in shape.

Tanner
stages Age at the start Changes
Stage 1 After the eighth None
birthday
Stage 2 From age 9 to 11 Breast “buds” start to form; pubic hair starts to form
Stage 3 After age 12 Acne first appears; armpit hair forms; height increases at
its fastest rate
Stage 4 Around age 13 First period arrives
Stage 5 Around age 15 Reproductive organs and genitals are fully developed

2.3 Normal Puberty and Causes of Delayed Puberty

• Normal puberty is a phase of development between childhood and adulthood


which manifest as complete, functional maturation of the reproductive glands
and external genitalia.
14 A. H. Al-Salem

• The start of sexual maturation (puberty) takes place when the hypothalamus
gland begins to secrete gonadotropin-releasing hormone.
• The pituitary gland responds to this by releasing gonadotropins (FSH and LH)
which stimulate the growth of the ovaries.
• The ovaries secrete the sex hormone (estrogen). These hormones cause the
development of secondary sex characteristics, including breasts developments in
girls, and pubic and underarm hair and sexual desire (libido).
• Some adolescents do not start their sexual development at the usual age (Fig. 2.1).

TANNER STAGE I

TANNER STAGE II

TANNER STAGE III

TANNER STAGE IV

TANNER STAGE V

Fig. 2.1 Diagrammatic representation of Tanner stages


2 Delayed Puberty in Girls 15

• In girls, delayed puberty is defined as:


–– No breast development by age 13 years.
–– A time lapse of more than 5 years from the beginning of breast growth to the
first menstrual period.
–– No menstruation (amenorrhea) by age 16.

Hypothalamus

Gonadotropin-releasing hormone

Pituitary gland

Gonadotropins (FSH and LH)

Ovaries

Sex hormone (Estrogen)

Secondary sexual characteristics

• There are several phases of normal pubertal changes:


–– Gonadarche: The activation of reproductive glands by the pituitary hormones
follicular stimulating hormone and lutenizing hormone (FSH and LH).
–– Adrenarche: The activation of production and secretion of adrenal androgens.
–– Thelarche: The onset of breast development (age of onset 8–11 years).
–– Pubarche: The onset of pubic hair growth (mean age of onset 12 years).
16 A. H. Al-Salem

–– Menarche: The onset of menstrual bleeding (age of onset 10–16 years; mean
age: 13 years).
–– Anovulatory cycle: The menstrual cycle may be irregular in adolescents dur-
ing the first few months/years after menarche. This is not pathological.
• Puberty starts when the pituitary gland begins to produce two hormones, lutein-
izing hormone (LH) and follicle-stimulating hormone (FSH).
• These hormones cause the ovaries to enlarge and begin producing estrogens.
• The growth spurt starts shortly after breasts begin to develop.
• The first menstrual cycle begins about 2–3 years later.
• A girl who has not started to have breast development by the age of 13 is consid-
ered to be delayed.
• There are also several factors that influence puberty:
–– General health including nutritional state and body weight
–– Genetics factors
–– Social environment (e.g. family stress)
• Delayed puberty is defined as lack of secondary sexual characteristics from the
age of 13 years in females.
• CNS abnormalities result in hypogonadotrophic hypogonadism.
• Gonadal failure causes hypergonadotrophic hypogonadism.
• There are many possible causes of delayed puberty, some of which affect both
genders and some of which are gender-specific.
• The causes of delayed puberty are divided into two broad categories:
–– Central causes
–– Peripheral causes
• Central causes may affect both genders and stem from the hypothalamic-­pituitary
axis or other areas of the body that are not specific to a gender.
• Peripheral causes, on the other hand, are gender specific and linked to the sexual
organs of the individual.
• The most common cause of delayed puberty in both boys and girls is constitu-
tional delay. However, a diagnosis of constitutional delay can only be made when
other possible causes have been excluded.
• Central Causes of delayed puberty:
–– These are similar in males and females.
–– Many central causes are related to impaired structure or function of the
hypothalamic-­pituitary axis.
–– The causes for this include:
A tumor near the hypothalamic-pituitary axis:
• Astrocytoma
• Craniopharyngioma
• Germinomas
• Optic glioma
• Pituitary tumor
2 Delayed Puberty in Girls 17

Physical trauma to the head secondary to head injury or surgery.


Radiation therapy directed towards the hypothalamic-pituitary axis.
Congenital abnormality of the hypothalamic-pituitary axis.
Abnormal hormone levels (e.g. low gonadotropin and sex steroid
concentration).
–– There are also several central causes that are not associated with abnormal
structure and function of the hypothalamic-pituitary axis. These include:
Health conditions:
• Kidney disease
• Crohn’s disease
• Cystic fibrosis
• Hypothyroidism
Medications (e.g. steroid therapy)
Malnutrition:
• Coeliac disease
• Anorexia nervosa
Excessive physical exertion (e.g. professional athletes and gymnasts)
Psychosocial deprivation
• Peripheral Causes of delayed puberty
–– These are gender specific and linked to the sexual organs of the individual.
–– Peripheral causes that may lead to delayed puberty in girls include:
Health conditions:
• Turner syndrome
• Prader-Willi syndrome
• Bardet-Biedl syndrome
• Swyer syndrome
• Polycystic ovary syndrome
Medications (e.g. cyclophosphamide, busulfan).
Radiation therapy directed to the abdominal and pelvic region.
Sexual disorders:
• Androgen insensitivity syndrome
• Congenital adrenal hyperplasia
Thalassaemia secondary to iron overload.
• It is important to establish the cause of delayed puberty, as it provides valuable
information about the most appropriate therapy options.
• It is also important to establish a detailed patient’s and family history including:
–– Growth pattern
–– General health
–– History of other medical conditions
18 A. H. Al-Salem

–– Family history of similar symptoms


–– Psychosocial symptoms
• The diagnosis of delayed puberty is usually made based on the medical and fam-
ily history of the individual and a physical examination to assess changes
expected according to the age of the individual.
• The physical examination should include signs of growth, such as height and
weight, and development of sexual characteristics, such as breast and the growth
of pubic hair. It is also helpful to test for an abnormal sense of smell, which is a
characteristic symptom of Kallmann’s syndrome.

2.4 Management

• The initial evaluation of delayed puberty should consist of a complete history


and physical examination to evaluate pubertal development, nutritional status,
and growth.
• Take x-rays of one or more bones to see the level of bone maturity (a bone
age x-ray).
• Some girls with delayed puberty are simply late to mature, but once they start,
puberty will progress normally.
• This is called constitutional delayed puberty and is more common in boys than
girls. These adolescents have a normal growth rate and are otherwise healthy.
Although the growth spurt and puberty are delayed, they eventually proceed
normally.
• Constitutional delayed puberty is often familial inherited from the parents, so it
is more likely to occur if the mother started her periods after age 14.
• In girls with constitutional delayed puberty, breast development will eventually
start on its own.
• The treatment for delayed puberty depends on its cause. When an underlying
disorder is the cause of delayed puberty, puberty usually proceeds once the dis-
order has been treated.
• In many individuals with delayed puberty, medical treatment is not required and
patients should be reassured that the body will have the expected sexual changes
in time.
• However, short courses of sex hormones (estrogen) may be used to allow indi-
viduals to catch up with their peers and prevent psychological and emotional
sequelae.
• This can be useful to prevent psychological and emotional consequences associ-
ated with a delay.
• Some authors advocate giving estrogens for 4–6 months hoping this will help get
things started sooner.
• It is important to identify and treat any cause of delayed puberty.
• It is also important for these patients to have a counselor or psychological sup-
port. Counselling with respect to sexual function and fertility as appropriate.
2 Delayed Puberty in Girls 19

• Pubertal induction followed by ongoing hormone replacement. Subsequent estro-


gen production may be adequate and ongoing hormone treatment unnecessary.
• Treat the underlying cause if possible; induction of puberty and hormone treat-
ment may be required.
• In those with severe congenital hypogonadism, early gonadotrophins in the neo-
natal period or infancy may be indicated.
• Estrogen replacement should be gradual to avoid premature fusion of the epiphy-
ses and prevent overdevelopment of the areolae of the breasts.
• Induction of puberty usually starts around age 10. Gradually increased doses of
oral ethinylestradiol or transdermal estradiol are used, with cyclical progesterone
therapy once adequate estrogen levels have been achieved or if breakthrough
bleeding occurs. If growth hormone is also needed, estrogen therapy is usually
delayed until age 12 years.
• Transdermal estradiol is thought to be more effective and have a better safety
profile.
• A low-dose combined oral contraceptive pill can then be used.
• Decreased body fat is a major cause of pubertal delay in girls.
–– It can be seen in girls who are very athletic, particularly in gymnasts, ballet
dancers, and competitive swimmers.
–– It can also be seen in girls with anorexia nervosa, who fear becoming too fat
even when they are abnormally thin.
–– It can be seen in a number of chronic illnesses in which body fat is often
decreased.
• For girls with delayed puberty secondary to decreased body fat, dietary manipu-
lations and gaining weight will help get puberty started.
• Other causes of delayed puberty include:
–– Primary ovarian insufficiency
–– Turner syndrome
–– The major acquired cause of ovarian insufficiency is damage to the ovaries as
a result of radiation therapy, usually to treat leukemia.
• For girls with primary ovarian insufficiency or a permanent deficiency of
gonadotropins:
–– Long-term estrogen replacement is needed and can be given either in the form
of a daily tablet of estradiol or as a patch that needs to be applied to the skin
twice a week.
–– Some authors advocate starting these patients on a low dose and often increase
the dose about every 6 months.
–– After 12–18 months, a progestin (for example, Provera) is to be added. This
will, after a few months, result in a period, usually within a day or two of stop-
ping the progestin.
• Various disorders, such as diabetes mellitus, inflammatory bowel disease, kidney
disease, cystic fibrosis, and anemia, can delay or prevent sexual development.
These should be identified and treated accordingly.
20 A. H. Al-Salem

• Development may be delayed or absent in adolescents receiving radiation ther-


apy or cancer chemotherapy.
• Puberty may also be delayed by autoimmune disorders such as Hashimoto thy-
roiditis, Addison disease (primary adrenocortical insufficiency), and some disor-
ders that directly affect the ovaries).
• A tumor that damages the pituitary gland or the hypothalamus can lower the
levels of gonadotropins or stop production of the hormones altogether.
• Genetic disorders cannot be cured, but hormone therapy may help sex character-
istics develop.

Further Reading

1. Herman-Giddens ME, Slora EJ, Wasserman RC, et al. Secondary sexual characteristics and
menses in young girls seen in office practice: a study from the pediatric research in office set-
tings network. Pediatrics. 1997;99:505–12.
2. Argente J. Diagnosis of late puberty. Horm Res. 1999;51(Suppl 3):95.
3. Sedlmeyer IL, Palmert MR. Delayed puberty: analysis of a large case series from an academic
center. J Clin Endocrinol Metab. 2002;87:1613–20.
4. Raivio T, Falardeau J, Dwyer A, et al. Reversal of idiopathic hypogonadotropic hypogonad-
ism. N Engl J Med. 2007;357:863–73.
5. Waldstreicher J, Seminara SB, Jameson JL, et al. The genetic and clinical heterogene-
ity of gonadotropin-releasing hormone deficiency in the human. J Clin Endocrinol Metab.
1996;81:4388.
6. Zhu J, Choa RE, Guo MH, et al. A shared genetic basis for self-limited delayed puberty and
idiopathic hypogonadotropic hypogonadism. J Clin Endocrinol Metab. 2015;100:E646.
7. Rosenfield RL. Clinical review 6: diagnosis and management of delayed puberty. J Clin
Endocrinol Metab. 1990;70:559–62.
8. Kaplowitz PB. Delayed puberty. Pediatr Rev. 2010;31:189–95.
9. Boepple PA. Precocious and delayed puberty. Curr Opin Endocrinol Diabetes Obes.
1995;2:111–8.
10. Pugliese MT, Lifshitz F, Grad G, et al. Fear of obesity: a cause of short stature and delayed
puberty. N Engl J Med. 1983;309:513.
11. Sedlmeyer IL, Hirschhorn JN, Palmert MR. Pedigree analysis of constitutional delay of
growth and maturation: determination of familial aggregation and inheritance patterns. J Clin
Endocrinol Metab. 2002;87:5581–6.
12. Balasubramanian R, Dwyer A, Seminara SB, et al. Human GnRH deficiency: a unique disease
model to unravel the ontogeny of GnRH neurons. Neuroendocrinology. 2010;92:81–99.
13. Mitchell AL, Dwyer A, Pitteloud N, Quinton R. Genetic basis and variable phenotypic
expression of Kallmann syndrome: towards a unifying theory. Trends Endocrinol Metab.
2011;22:249.
14. Balasubramanian R, Crowley WF Jr. Isolated GnRH deficiency: a disease model serving as a
unique prism into the systems biology of the GnRH neuronal network. Mol Cell Endocrinol.
2011;346:4–12.
15. Tanner JM, Whitehouse RH. Clinical longitudinal standards for height, weight, height veloc-
ity, weight velocity, and stages of puberty. Arch Dis Child. 1976;51:170–9.
16. Marshall JC, Kelch RP. Low dose pulsatile gonadotropin-releasing hormone in anorexia ner-
vosa: a model of human pubertal development. J Clin Endocrinol Metab. 1979;49:712–8.
2 Delayed Puberty in Girls 21

17. Kelch RP, Hopwood NJ, Marshall JC. Diagnosis of gonadotropin deficiency in adolescents:
limited usefulness of a standard gonadotropin-releasing hormone test in obese boys. J Pediatr.
1980;97:820–4.
18. Savage MO, Preece MA, Cameron N, et al. Gonadotrophin response to LH-RH in boys with
delayed growth and adolescence. Arch Dis Child. 1981;56:552–6.
19. Harman SM, Tsitouras PD, Costa PT, et al. Evaluation of pituitary gonadotropic function in
men: value of luteinizing hormone-releasing hormone response versus basal luteinizing hor-
mone level for discrimination of diagnosis. J Clin Endocrinol Metab. 1982;54:196–200.
20. Wilson DA, Hofman PL, Miles HL, et al. Evaluation of the buserelin stimulation test in diag-
nosing gonadotropin deficiency in males with delayed puberty. J Pediatr. 2006;148:89–94.
21. Ghai K, Cara JF, Rosenfield RL. Gonadotropin releasing hormone agonist (nafarelin) test to
differentiate gonadotropin deficiency from constitutionally delayed puberty in teen-age boys-
-a clinical research center study. J Clin Endocrinol Metab. 1995;80:2980.
22. Coutant R, Biette-Demeneix E, Bouvattier C, et al. Baseline inhibin B and anti-Mullerian
hormone measurements for diagnosis of hypogonadotropic hypogonadism (HH) in boys with
delayed puberty. J Clin Endocrinol Metab. 2010;95:5225–32.
23. Brook CG. Management of delayed puberty. Br Med J (Clin Res Ed). 1985;290:657.
24. Richman RA, Kirsch LR. Testosterone treatment in adolescent boys with constitutional delay
in growth and development. N Engl J Med. 1988;319:1563–7.
25. Soliman AT, Khadir MM, Asfour M. Testosterone treatment in adolescent boys with constitu-
tional delay of growth and development. Metabolism. 1995;44:1013–5.
26. Wilson DM, Kei J, Hintz RL, Rosenfeld RG. Effects of testosterone therapy for pubertal delay.
Am J Dis Child. 1988;142:96.
27. Butler GE, Sellar RE, Walker RF, et al. Oral testosterone undecanoate in the management of
delayed puberty in boys: pharmacokinetics and effects on sexual maturation and growth. J Clin
Endocrinol Metab. 1992;75:37.
28. Adan L, Souberbielle JC, Brauner R. Management of the short stature due to pubertal delay in
boys. J Clin Endocrinol Metab. 1994;78:478.
29. Albanese A, Kewley GD, Long A, et al. Oral treatment for constitutional delay of growth and
puberty in boys: a randomised trial of an anabolic steroid or testosterone undecanoate. Arch
Dis Child. 1994;71:315–7.
30. Büyükgebiz A. Treatment of constitutional delayed puberty with a combination of testosterone
esters. Horm Res. 1995;44(Suppl 3):32.
31. Bergadá I, Bergadá C. Long term treatment with low dose testosterone in constitutional delay
of growth and puberty: effect on bone age maturation and pubertal progression. J Pediatr
Endocrinol Metab. 1995;8:117.
32. Albanese A, Stanhope R. Predictive factors in the determination of final height in boys with
constitutional delay of growth and puberty. J Pediatr. 1995;126:545–50.
33. Arrigo T, Cisternino M, Luca De F, et al. Final height outcome in both untreated and
testosterone-­treated boys with constitutional delay of growth and puberty. J Pediatr Endocrinol
Metab. 1996;9:511.
34. Raivio T, Dunkel L, Wickman S, Jänne OA. Serum androgen bioactivity in adolescence: a
longitudinal study of boys with constitutional delay of puberty. J Clin Endocrinol Metab.
2004;89:1188–92.
Chapter 3
Precocious Puberty

Ahmed H. Al-Salem

3.1 Introduction

• Premature thelarche is the development of breast tissue in young girls in the


absence of other signs of precocious puberty.
• Premature thelarche is also characterized by the lack of thickening and pigmen-
tation of the nipples and the areola which is commonly seen in girls with preco-
cious puberty.
• Premature thelarche is typically seen in girls aged 3 years or younger.
• In some of these cases, small ovarian cysts can be found and these transiently
produce estrogens which may be responsible for premature thelarche.
• Premature pubarche on the other hand refers to the early appearance of pubic
hair, axillary hair, or both in children without other signs of puberty. These
patients will have adult-type axillary body odor.
• Premature pubarche refers to appearance of pubic hair and or axillary hair with-
out other signs of puberty in girls younger than 7–8 years.
• Premature pubarche and premature thelarche are 2 common, benign, normal
variant conditions that can resemble precocious puberty but are nonprogressive
or very slowly progressive.
• Precocious puberty can be classified based upon the underlying pathologic
process.
–– Central precocious puberty
Central precocious puberty is also known as gonadotropin-dependent pre-
cocious puberty or true precocious puberty.
It is caused by early maturation of the hypothalamic-pituitary-gonadal axis.

A. H. Al-Salem (*)
Pediatric Surgery, Alsadiq Hospital, Saihat, Saudi Arabia

© The Editor(s) (if applicable) and The Author(s), under exclusive license 23
to Springer Nature Switzerland AG 2020
A. H. Al-Salem, Pediatric Gynecology,
https://doi.org/10.1007/978-3-030-49984-6_3
24 A. H. Al-Salem

It is characterized by sequential maturation of breasts and pubic hair


in girls.
The sexual characteristics are appropriate for the child’s gender (isosexual).
Central precocious puberty is idiopathic in 80–90% of cases in girls.
–– Peripheral precocity
Peripheral precocious puberty is also known as gonadotropin-independent
precocious puberty or peripheral precocious puberty.
Some authors use term peripheral precocity instead of peripheral puberty
because puberty implies activation of the hypothalamic-pituitary-gonadal
axis, as occurs in central precocious puberty.
Precocity refers only to the secondary sexual characteristics.
Peripheral precocity is most commonly either isosexual (concordant with
the child’s gender), or contrasexual (with virilization of girls and feminiza-
tion of boys), but can also present with both virilizing and feminizing fea-
tures in rare cases.
It is caused by:
• Excess secretion of sex hormones (estrogens or androgens) derived
either from the gonads or adrenal glands.
• Exogenous sources of sex steroids.
• Ectopic production of gonadotropins from a germ cell tumor (e.g.,
human chorionic gonadotropin, hCG).
• Severe androgen excess should prompt further investigation to exclude a rare
virilizing tumor or a variant form of congenital adrenal hyperplasia. This will
manifest as:
–– Clitoral enlargement
–– Growth acceleration
–– Severe acne
• The etiology of premature pubarche is an earlier-than-usual increase in the secre-
tion of weak androgens by the adrenal glands.
• This is also called premature adrenarche.
• Puberty can be normal, precocious or delayed.
• Precocious puberty is defines as puberty occurring at an unusually early age.
• Precocious puberty is considered when normal puberty occurs before 8 years of
age in girls.
• This is opposite to delayed puberty.
• This comes from the Latin term Pubertas praecox which was used by physicians
in the nineteenth century.
• For many years, puberty was considered precocious when it occurs in girls
younger than 8 years; however, recent studies indicate that signs of early puberty
are often present in girls aged 6–8 years.
• Physiologically, precocious puberty represents a variation of normal develop-
ment that occurred at unusually early age.
3 Precocious Puberty 25

• Precocious puberty (early pubic hair appearance, breast development, or genital


development) may result from natural early maturation or from several other
conditions.
• Rarely, precious puberty is triggered by a disease such as a tumor or injury of
the brain.
• Precocious puberty is known to be associated with adverse effects on social
behavior and psychological development.
• Precocious puberty is broadly classified into central and peripheral.
• Central precocious puberty is gonadotropin-dependent and represents the early
maturation of the entire hypothalamic-pituitary-gonadal (HPG) axis.
• Precocious pseudopuberty is much less common and results from increased pro-
duction of sex steroids and it is gonadotropin-independent.
• It is important to differentiate the two and correct diagnosis of the etiology of
precocious puberty is important, because evaluation and treatment of patients
with precocious pseudopuberty is quite different than that for patients with cen-
tral precocious puberty.
• Central precocious puberty can be treated by suppressing the pituitary hormones
that induce sex steroid production.
• Secondary sexual development induced by sex steroids from other abnormal
sources is referred to as peripheral precocious puberty or precocious pseudopuberty.
• Symptoms in these children are usually secondary to adrenal insufficiency.
–– This results from 21-hydroxylase deficiency or 11-beta hydroxylase
deficiency.
–– This will result in:
Hypertension
Hypotension
Electrolyte abnormalities
Ambiguous genitalia in females
Signs of virilization in females
Blood tests will typically reveal high level of androgens with low levels of
cortisol.
• Precocious puberty is associated with advancement in bone age, which leads to
early fusion of epiphyses, thus resulting in reduced final height and short
stature.
• One of the sequels of precocious puberty is that a child can be fertile.
• The youngest mother was Lina Medina, who gave birth at the age of 5 years,
7 months and 17 days, in one report and at 6 years 5 months in another.
• Precocious puberty can cause several problems.
–– The early growth spurt initially can cause tall stature, but rapid bone matura-
tion can cause linear growth to cease too early and can result in short adult
stature.
–– The early appearance of breasts or menses in girls and increased libido in can
cause emotional distress for some children.
26 A. H. Al-Salem

3.2 Regulation of Normal Puberty

• For many years there were a lot of controversies over the issues of the timing and
mechanism of normal puberty.
• Normally, the average age at thelarche was commonly believed to be 10.5 years.
• Eight years was the traditionally accepted lower limit of normal for thelarche and
pubarche in girls.
• Currently, these figures are not accurate and several factors must be taken in
consideration. These include:
–– The socioeconomic status
–– The color
–– The race
–– The dietary habits
• Recently, it was found that breast development was present in 15% of African
American girls and 5% of white girls at age 7 years.
• The average age at thelarche was 10 years for white girls and 8.9 years for
African American girls (Fig. 3.1a–e).
• It was also found that:
–– Between their seventh and eighth birthdays, 10% of white girls, 23% of
African American girls, and 15% of Hispanic girls had breast development of
at least Tanner stage 2.
–– An average age at breast Tanner stage 2 of 9.9 years for white girls and
9.1 years for African American girls.
• With a larger number of female children entering puberty at an earlier age, it is
important to distinguish the early-normal maturing patient from the one with
pathologically precocious puberty.
• This calls for a thorough history and clinical evaluation, assessment of the rate of
maturation, and hormonal measurements.
• The mechanism of normal puberty was not fully understood.
• Over the last 10 years, there was a lot of advancement and understanding of the
regulation of normal puberty.
• One important contributing factor is the discovery of kisspeptin and its receptor.
• Kisspeptin which is produced by hypothalamic neurons promotes GnRH
secretion.
• Kisspeptin-producing hypothalamic neurons are located in the arcuate nucleus
(ARC) and anteroventral periventricular area.
• These neurons also coproduce neurokinin B and dynorphin.
• Neurokinin B has local stimulatory effect on kisspeptin release.
• Dynorphin on the other hand has a repressive action on kisspeptin release.
• These neurons are also known as KNDy (Kisspeptin, Neurokinin B, Dynorphin)
neurons.
3 Precocious Puberty 27

TANER STAGE I

TANER STAGE II

TANER STAGE III

TANNER STAGE IV

TANNER STAGE V

Fig. 3.1 (a–e) Diagramatic representations of Tanner stages of development


28 A. H. Al-Salem

• This overlapping autocrine feedback allows for fine control of kisspeptin


secretion.
• Additionally, KNDy neurons may be a site of action for the negative feedback
effects of estradiol, and decreases in the intensity of this negative feedback occur
as puberty begins.
• In reproductively mature females, regulation of hypothalamic reproductive
capacity is influenced by the energy status of the organism, with peripheral
energy stores being signaled to the brain by leptin and ghrelin.
• Leptin:
–– This is produced in adipose tissue and directly related to stored energy.
–– It acts through its receptor to stimulate kisspeptin secretion in the ARC.
• Ghrelin:
–– Ghrelin appears to suppress kisspeptin secretion in the ARC and anteroventral
periventricular area.
–– Ghrelin secretion varies over the short term with food intake but also is influ-
enced in the long term by energy stores.
• Additional signals of energy balance that may influence kisspeptin secretion
include neuropeptide Y and proopiomelanocortin.
• These mechanisms are important for maintenance of ovarian function, but their
role in the initiation of puberty is not known.
• Activating mutations of the genes for kisspeptin and its receptor have been found
in girls with precocious puberty.
• It was also found that the regulation of puberty and reproductive function is also
influenced by hypothalamic astrocytes and other neuroglial cells.
–– Neuroglial cells influence GnRH neurons in at least 2 ways.
–– Hypothalamic astrocytes secrete a host of growth factors, such as TGF-β,
basic fibroblast growth factor, and epidermal growth factor-like peptides.
–– These growth factors act via specific receptors on GnRH neurons to increase
neuronal growth and function.
–– Additionally, glial cells are directly opposed to GnRH neurons in a dynamic
fashion.
–– Increases in levels of apposition are associated with greater GnRH secretion.
–– The apposition is negatively influenced by estradiol, and this may be a mecha-
nism by which negative feedback occurs.
• Collections of neuroglial cells forming hypothalamic hamartomas are commonly
associated with precocious puberty.
• Although this form of precocious puberty has been attributed to an ectopic source
of GnRH pulsatility within the hamartoma, there is evidence that neuroglial
effects on hypothalamic GnRH neurons may play a role.
3 Precocious Puberty 29

3.3 Epidemiology

• The average age of thelarche was found to be around 11 years.


• Precocious puberty in girls is diagnosed when it starts before age 8 years.
• It was estimated that approximately 8% of white and 25% of black girls in the
United States exhibited evidence of sexual precocity.
• Others considered precocious puberty only when breast development or pubic
hair appear before age 7 years in white girls and age 6 years in black girls.
• It is important to note that in certain parts of the world, a decline in the age of
puberty in girls has been noted.
• It was also found that black girls in the United States have onset of precocious
puberty about 1 year earlier than white girls.

3.4 Classification and Etiology

• Precocious puberty is classified into central and peripheral.


• Central precocious puberty is also called complete or true precocious puberty.
• Central precocious puberty is considered if its cause can be traced to the hypo-
thalamus or pituitary.
• The causes of central precocious puberty include:
–– Idiopathic or constitutional when no cause can be identified.
–– Damage to the inhibitory system of the brain. This can be secondary to:
Infection
Trauma
Irradiation
–– Hypothalamic hamartoma: This can produce pulsatile gonadotropin-releasing
hormone (GnRH)
–– Langerhans cell histiocytosis
–– McCune–Albright syndrome
–– Intracranial neoplasm
–– Infection of the central nervous system most commonly tuberculosis
–– Trauma
–– Hydrocephalus
–– Angelman syndrome
–– Suprasellar arachnoid cysts
–– Slipped capital femoral epiphysis occurs in patients with central preco-
cious puberty because of rapid growth and changes of growth hormone
secretion.
30 A. H. Al-Salem

• The causes of peripheral precocious puberty include:


–– Endogenous sources
gonadal tumors (such as arrhenoblastoma)
Adrenal tumors
Germ cell tumor
Congenital adrenal hyperplasia
McCune–Albright syndrome
–– Exogenous hormones
Environmental exogenous hormones
Secondary to treatment for another condition
• Isosexual precocious puberty
–– This is seen in patients with precocious puberty who develop phenotypically
appropriate secondary sexual characteristics.
• Heterosexual precocious puberty
–– This is also called heterosexual precocious puberty.
–– This is seen in patients with precocious puberty who develop phenotypically
inappropriate secondary sexual characteristics.
–– A female may develop a deepened voice and facial hair.
–– This is a very rare condition.
–– It can be seen in children with a very rare genetic condition called aromatase
excess syndrome in which exceptionally high circulating levels of estrogen
are present.
–– Patients with this syndrome are hyperfeminized.
• Girls who have a high-fat diet and are not physically active or are obese are more
likely to physically mature earlier.
• Exposure to chemicals that mimic estrogen (known as xenoestrogens) is a pos-
sible cause of early puberty in girls.
• Bisphenol A, a xenoestrogen found in hard plastics, has been shown to affect
sexual development.
• Genetic and/or environmental factors.
• There is a higher prevalence of early puberty in black versus white girls.
• A pineal gland tumor (a chorionic gonadotropin secreting pineal tumor) with
high levels of beta-hCG in serum and cerebrospinal fluid.
• Elevated melatonin could be responsible for some cases of precocious puberty.
• Familial cases of idiopathic central precocious puberty.
• Mutations in genes such as LIN28, and LEP and LEPR, which encode leptin and
the leptin receptor, have been associated with precocious puberty.
• Mutations in the kisspeptin (KISS1) and its receptor, KISS1R (also known as
GPR54), involved in GnRH secretion and puberty onset.
3 Precocious Puberty 31

• The gene MKRN3 (Zinc finger protein 127) which is located on human chro-
mosome 15 on the long arm in the Prader-Willi syndrome critical region2 was
identified as a cause of premature sexual development with early breast and
testes development, increased bone aging and elevated hormone levels of
GnRH and LH.

3.5 Pathophysiology

• Normally, the onset of puberty is caused by the secretion of high-amplitude


pulses of gonadotropin-releasing hormone (GnRH) by the hypothalamus.
• High-amplitude pulses of GnRH causes pulsatile increases in the pituitary
gonadotropin-luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
• Increased LH levels stimulate production of sex steroids by ovarian granu-
losa cells.
• Most girls suspected of having central precocious puberty, are otherwise healthy
children whose pubertal maturation begins at an earlier age (6–8 years old).
• Pubertal levels of androgens or estrogens cause the physical changes of puberty,
including breast development in girls.
• These levels also mediate the pubertal growth spurt.
• Increased FSH levels cause enlargement of the gonads and eventually promote
follicular maturation in girls.
• The timing of puberty has a genetic component.
–– Precocious puberty was found to be familial in one fourth of cases.
–– The mode of inheritance was autosomal dominant.
• An increased body mass index (BMI) has been associated with early puberty.
–– This association is stronger in white girls than in black girls.
–– Body weight and fat mass are among the factors that may influence puberty
onset in girls.
–– Increased BMI at age 3 years and the rate of increase in BMI from age
3–6 years were both positively associated with an earlier onset of puberty.
• These girls are otherwise healthy with no CNS structural abnormalities.
• CNS abnormalities associated are found in a small number of these children with
precocious puberty and include the following:
–– Tumors of the CNS:
Astrocytomas
Gliomas
Germ cell tumors secreting human chorionic gonadotropin (HCG).
–– Hypothalamic hamartomas
32 A. H. Al-Salem

–– Acquired CNS injury caused by:


Inflammation
Surgery
Trauma
Radiotherapy
Brain abscess
–– Congenital anomalies including:
Hydrocephalus
Arachnoid cysts
Suprasellar cysts

3.6 Clinical Features, Morbidity and Mortality

• Breast enlargement is the first and most obvious sign of early precocious puberty
in girls.
• Breast enlargement may initially be unilateral.
• The most reliable sign of precocious puberty as a result of increased estrogen
production is breast enlargement.
• Initially, breast budding may be unilateral or asymmetric.
• Gradually, the breast diameter increases, the areola darkens and thickens, and the
nipple becomes more prominent.
• This differentiates precocious puberty from premature thelarche where there is
lack of thickening and pigmentation of the nipples and the areola.
• It is also important to distinguish enlargement of glandular breast tissue from fat
as this can mimic true breast tissue.
• Pubic and axillary hair may appear before, at about the same time, or well after
breast enlargement.
• These patients have axillary odor similar to adults and this usually starts about
the same time as the appearance of pubic hair.
• Menarche occurs late usually 2–3 years after onset of breast enlargement.
• The pubertal growth spurt occurs early in females.
• Genital examination may or may not reveal pubic hair.
• Enlargement of the clitoris indicate significant androgen excess and this must be
promptly evaluated.
• The vaginal mucosa has normally a deep-red color in prepubertal girls but in
girls with precocious puberty it takes on a moist pastel-pink appearance as estro-
gen exposure increases.
• Mild acne may be normal in early puberty, but rapid onset of severe acne should
increase suspicion of an androgen-excess disorder.
• Exposure to exogenous sex hormones is an occasional cause of early precocious
puberty.
3 Precocious Puberty 33

–– This can result from inadvertent exposure to androgens through contact with
adult males who use topical androgens such as Androgel.
• Isolated sexual precocity of unknown etiology carries no increased risk of
mortality.
• Children with a CNS, adrenal, or ovarian tumor may be at risk for tumor-related
complications.
• Some studies have found an association between early puberty in girls and a
higher risk of developing breast cancer as adults.
• Children with precocious puberty may be stressed because of physical and hor-
monal changes which may not be easy for them to cope with. These young girls
will need support in order to understand.
–– They may be teased by their peers because of their physical difference.
–– Girls who reach menarche before age 9–10 may become withdrawn.
–– They may have difficulty adjusting to their environment.
–– They may have difficulties wearing and changing pads.
–– Girls with precocious puberty may have behavioral problems and are less
socially competent than age-matched peers.
–– These emotional problems may persist into adulthood.
–– Girls with precocious puberty are at higher risk of sexual abuse because they
have developed secondary sex characteristics.
–– Girls with precocious puberty are at a higher risk for socio-psychological
problems.
• To overcome the distress associated with precocious puberty and early menses,
parents should be encouraged to prepare their daughters for this event when they
reach stage III–IV of breast development.
• Girls with precocious puberty may have increases in libido leading to increased
masturbation or inappropriate sexual behaviors at a young age.
• Girls with precocious puberty have a slightly earlier age of initiation of sexual
activity.
• Precocious puberty accelerates growth of the child.
–– These children may initially be considerably taller than their peers.
–– Because bone maturation is also accelerated, growth may be completed at an
unusually early age.
–– This may result in short stature at the end.
–– This short stature is more likely if precocious puberty starts very early, before
age 6 years than if it begins around 6–8 years.
–– There are several studies which showed that most untreated girls with idio-
pathic central precocious puberty reach an adult height within the refer-
ence range.
–– Determination of bone age can be used to predict adult height and to select
patients with high risk for short stature if left untreated.
–– Most girls with precocious puberty who are aged 6–8 years at the onset of
puberty achieve an adult height within the reference range.
34 A. H. Al-Salem

–– Treatment with GnRH analogues such as Lupron is usually associated with


only a modest gain in final height in this age group.
• Several authors advocate that treatment should be considered following an initial
evaluation for girls who have predicted heights less than 4 ft 11 in or who are
well below their target height.
–– Average of parents’ heights, less 2.5 in.
–– Or when the patient also has very advanced bone age, a height below the 25th
percentile, or both.
• The benefit of treatment which aims at increasing adult height is the greatest in
patients who are diagnosed with central precocious puberty and started on GnRH
analogues at younger ages.
• Normal adult height can be achieved in most cases if treatment is started before
bone maturation is too advanced (>12 year in girls) and if good gonadal suppres-
sion is maintained for several years.
• Treatment allows growth to continue while dramatically slowing the rate of bone
maturation.
• Girls with central precocious puberty are at increased risk for psychosocial prob-
lems and also significant behavior problems such as;
–– Poor self-esteem
–– Higher anxiety
–– Irritability
–– Withdrawal

3.7 Investigations and Diagnosis

• There is no defined age that separates normal from abnormal puberty development.
• The followings are indicative for evaluation:
–– The development of pubic hair (pubarche) before 8 years.
–– Breast development (thelarche) in girls with onset before 7 years.
–– The appearance of menstruation (menarche) in girls before 10 years of age.
• Early precocious puberty warrants evaluation for the following reasons:
–– Precocious puberty induce early bone maturation and reduce eventual
adult height.
–– Precocious puberty may indicate the presence of a tumor or other serious
medical problem.
–– Precocious puberty may help recognize the few children with serious
conditions.
–– Precocious puberty cause a girl to become an object of adult sexual interest.
–– Precocious puberty cause social and psychological problems for both the
child and parents.
3 Precocious Puberty 35

• For girls, estradiol measurements are less reliable indicators of the stage of
puberty.
–– Estradiol levels that exceed 20 pg/mL usually indicate puberty, but some girls
who are clearly pubertal may have levels of less than 20 pg/mL.
–– In addition, estradiol levels may fluctuate from week to week.
–– Girls who have ovarian tumors or ovarian cysts often have estradiol levels that
exceed 100 pg/mL.
• Levels of adrenal androgens (e.g., dehydroepiandrosterone [DHEA], dehydro-
epiandrosterone sulfate [DHEAS]) are usually elevated in girls with premature
pubarche.
–– DHEA-S, the storage form of DHEA, is the preferred steroid to measure
because its levels are much higher and vary much less during the day.
–– In most children with premature pubarche, DHEA-S levels are 20–100 mcg/
dL, whereas in rare patients with virilizing adrenal tumors, levels may exceed
500 mcg/dL.
–– A 17-OH progesterone serum level should be done if mild or nonclassic con-
genital adrenal hyperplasia is suspected.
–– If a basal serum level of 17-OH is below 200 ng/dL, the diagnosis of nonclas-
sic congenital adrenal hyperplasia can be excluded.
–– If the random 17-OH progesterone serum level is elevated, a corticotropin
(i.e., Cortrosyn)–stimulation test should be done.
–– This is more valuable and provides the greatest diagnostic accuracy.
–– A post corticotropin 17-hydroxyprogesterone greater than 1000 ng/dL is
diagnostic.
• The random LH serum level is now the best screening test for central precocious
puberty (CPP).
–– The immunochemiluminometric (ICMA) method for LH is more specific
than the immunofluorometric (IFMA) method.
–– An LH level of less than 0.1 IU/L is generally prepubertal.
–– Random follicle-stimulating hormone (FSH) levels do not discriminate
between prepubertal and pubertal children.
–– Suppressed levels of LH and FSH accompanied by highly elevated testoster-
one or estradiol levels suggest precocious pseudopuberty rather than central
precocious puberty.
–– A definitive diagnosis of central precocious puberty may be confirmed by
measuring LH and FSH levels 30–60 min after stimulation with gonadotropin-­
releasing hormone (GnRH) at 100 mcg or with a GnRH analogue.
–– Most centers are using the analogue leuprolide (aqueous form) at a dose of
20 mcg/kg, up to a maximum of 500 mcg because native GnRH is no longer
available.
–– An increase in FSH levels much greater than the increase in LH levels sug-
gests that the child is prepubertal.
36 A. H. Al-Salem

–– Some studies suggest that an increase in LH levels to more than 8 IU/L is


diagnostic of central precocious puberty, but this depends on the specific LH
assay used.
It was found that a peak LH level measured by ICMA that defined CPP
was found to be 3.3 IU/L in girls.
It was found that when the baseline LH level is prepubertal, an increase in
LH level to 5 IU/L or more after leuprolide correlates well with progres-
sion of pubertal signs during a 6-month period of observation.
It was found that no increase in LH and FSH levels after the infusion of
GnRH suggests precocious pseudopuberty.
• It was also found that serum anti-Müllerian hormone and inhibin B offer markers
for differentiating progressive central precocious puberty from slowly progres-
sive central precocious puberty.
–– It was found that anti-Müllerian hormone levels are lower and inhibin B
levels are higher in girls with the progressive form of central precocious
puberty.
• Radiography of the hand and wrist is used to determine bone age.
–– If bone age is within 1 year of chronological age, puberty has not started.
A 2-year-old girl with premature thelarche.
Or the duration of the pubertal process has been relatively brief.
–– If bone age is advanced by 2 years or more, puberty likely has been present
for a year or more or is progressing more rapidly.
• Head MRI:
–– MRI is indicated for those suspected to have a tumor or a hamartoma after
hormonal studies indicate a diagnosis of central precocious puberty.
–– A high-resolution study that focuses on the hypothalamic-pituitary area is
important.
–– For healthy girls aged 6–8 years with no signs or symptoms of CNS disease,
the likelihood of finding a tumor or hamartoma is only about 2%.
–– The younger the child with central precocious puberty, the greater the chance
of finding CNS pathology.
• Pelvic ultrasonography:
–– Ultrasonography is unnecessary for girls with a definite diagnosis of central
precocious puberty.
–– In girls with central precocious puberty, ultrasonography usually reveals
bilaterally enlarged ovaries, often with multiple small follicular cysts, and an
enlarged uterus with an endometrial stripe.
–– Pelvic ultrasonography is essential when precocious pseudopuberty is sus-
pected in girls because an ovarian tumor or cyst may be detected.
3 Precocious Puberty 37

• If central precocious puberty is caused by a tumor in the hypothalamic-pituitary


area, the histology of the tumor is important to the patient’s prognosis.
–– Gliomas tend to grow more rapidly than astrocytomas.
–– Hamartomas are benign.
–– Treatment of precocious puberty associated with a hamartoma suppresses
gonadotropin production by the pituitary without effect on the hamar-
toma itself.

3.8 Treatment

• Precocious puberty is a common problem affecting up to 29 per 100,000 girls


per year.
• Precocious puberty is traditionally defined as the onset of secondary sexual
development before the age of 8 years in girls.
• Because of trends towards earlier pubertal development, some healthy girls will
have breast or pubic hair development before this age, and extensive evaluation
and treatment may not be required.
• If the clinical evaluation and investigations leads to a diagnosis of progressive
precocious puberty, treatment should be considered.
• The reasons for treatment include:
–– Preservation of adult height potential.
This is especially so for girls under 6 years old.
These girls have the greatest potential to achieve adult height with
treatment.
–– Psychosocial difficulties with early puberty and menarche.
• Non-continuous usage of GnRH agonists stimulates the pituitary gland to release
follicle stimulating hormone (FSH) and luteinizing hormone (LH).
• However, when used regularly, GnRH agonists cause a decreased release of
FSH and LH.
• Continuous administration of LHRH and GnRH agonists provides negative feed-
back and results in decreased levels of LH and FSH 2–4 weeks after initiating
treatment.
• The mainstay of treatment for central precocious puberty is GnRH analogs
(GnRHa).
• These drugs provide constant serum levels of GnRH activity and thus override
the pulsatility of endogenous GnRH.
• In the past, the 1-month formulation of leuprolide, called Lupron-Depot, was the
mainstay of therapy.
• In 2011, 3-month formulations of Lupron-Depot 11.25 mg and 30 mg, were
approved for children with precocious puberty.
Another Random Scribd Document
with Unrelated Content
numbers were daily augmented, until they became a vast flock
which no man could easily number—thousands upon thousands,
tens of thousands, and myriads—so great, indeed, that the spectator
would almost have concluded that the whole of the swallow race
were there collected in one huge host. It was their manner, while
there, to rise from the willows in the morning, a little before six
o’clock, when their thick columns literally darkened the sky. Their
divisions were formed into four, five, and sometimes six grand wings,
each of these filing off and taking a different route—one east,
another west, another south, and so on; as if not only to be equally
dispersed throughout the country, to provide food for their numerous
troops; but also to collect with them whatever of their fellows, or
straggling parties, might be still left behind. Just before the
respective columns arose, a few birds might be observed first in
motion at different points, darting through their massy ranks—these
appeared like officers giving the word of command. In the evening,
about five o’clock, they began to return to their station, and
continued coming in, from all quarters, until nearly dark. It was here
that you might see them go through their various aerial evolutions,
in many a sportive ring and airy gambol—strengthening their pinions
in these playful feats for their long etherial journey; while
contentment and cheerfulness reigned in every breast, and was
expressed in their evening song by a thousand pleasing twitters from
their little throats, as they cut the air and frolicked in the last beams
of the setting sun, or lightly skimmed the surface of the glassy pool.
The notes of those that had already gained the willows sounded like
the murmur of a distant waterfall, or the dying roar of the retreating
billow on the sea beach.
“‘The verdant enamel of summer had already given place to the
warm and mellow tints of autumn, and the leaves were now fast
falling from their branches, while the naked tops of many of the
trees appeared—the golden sheaves were safely lodged in the barns,
and the reapers had, for this year, shouted their harvest home—
frosty and misty mornings now succeeded, the certain presages of
the approach of winter. These omens were understood by the
swallows as the route for their march; accordingly, on the morning
of the 7th of October, their mighty army broke up their encampment
debouched from their retreat, and, rising, covered the heavens with
their legions; thence, directed by an unerring guide, they took their
trackless way. On the morning of their going, when they ascended
from their temporary abode, they did not, as they had been wont to
do, divide into different columns, and take each a different route,
but went off in one vast body, bearing to the south. It is said that
they would have gone sooner, but for a contrary wind which had
some time prevailed; that on the day before they took their
departure, the wind got round, and the favourable breeze was
immediately embraced by them. On the day of their flight, they left
behind them about a hundred of their companions; whether they
were slumberers in the camp, and so had missed the going of their
troops, or whether they were left as the rear-guard, it is not easy to
ascertain; they remained, however, till the next morning, when the
greater part of them mounted on their pinions, to follow, as it should
seem, the celestial route of their departed legions. After these a few
stragglers only remained; these might be too sick or too young to
attempt so great an expedition; whether this was the fact or not,
they did not remain after the next day. If they did not follow their
army, yet the dreary appearance of their depopulated camp and
their affection for their kindred, might influence them to attempt it,
or to explore a warmer and safer retreat.’”

NATURALISTS’ CALENDAR.
Mean Temperature 50·00.

[367] Gentleman’s Magazine.


[368] Mirror of the Months.
[369] Sheffield Mercury.

October 4.
Chronology.
On the 4th of October, 1749,[370] died at Paris, John Baptist Du
Halde, a jesuit, who was secretary to father Le Tellier, confessor to
Louis XIV. Du Halde is celebrated for having compiled an elaborate
history and geography of China from the accounts of the Romish
missionaries in that empire; he was likewise editor of the “Lettres
edifiantes et curieuses,” from the ninth to the twenty-sixth collection,
and the author of several Latin poems and miscellaneous pieces. He
was born in the city wherein he died, in 1674, remarkable for piety,
mildness, and patient industry.[371]

NATURALISTS’ CALENDAR.
Mean Temperature 54·92.

[370] Gentleman’s Magazine.


[371] A General Biographical Dictionary, (Hunt and Clarke,) vol. ii.

October 5.
NATURALISTS’ CALENDAR.
Mean Temperature 55·12.

October 6.
St. Faith.
Of this saint in the church of England calendar, there is an
account in vol. i. col. 1362.

Somnambulism.
On Sunday evening, the 6th of October, 1823, a lad named
George Davis, sixteen and a half years of age, in the service of Mr.
Hewson, butcher, of Bridge-road, Lambeth, at about twenty minutes
after nine o’clock, bent forward in his chair, and rested his forehead
on his hands. In ten minutes he started up, fetched his whip, put on
his one spur, and went thence to the stable; not finding his own
saddle in the proper place, he returned to the house, and asked for
it. Being asked what he wanted with it, he replied, to go his rounds.
He returned to the stable, got on the horse without the saddle, and
was proceeding to leave the stable; it was with much difficulty and
force that Mr. Hewson junior, assisted by the other lad, could remove
him from the horse; his strength was great, and it was with difficulty
he was brought in doors. Mr. Hewson senior, coming home at this
time, sent for Mr. Benjamin Ridge, an eminent practitioner, in Bridge-
road, who stood by him for a quarter of an hour, during which time
the lad considered himself stopped at the turnpike gate, and took
sixpence out of his pocket to be changed; and holding out his hand
for the change, the sixpence was returned to him. He immediately
observed, “None of your nonsense—that is the sixpence again, give
me my change.” When threepence halfpenny was given to him, he
counted it over, and said, “None of your gammon; that is not right, I
want a penny more;” making the fourpence halfpenny, which was his
proper change. He then said, “give me my castor,” (meaning his
hat,) which slang terms he had been in the habit of using, and then
began to whip and spur to get his horse on; his pulse at this time
was one hundred and thirty-six, full and hard; no change of
countenance could be observed, nor any spasmodic affection of the
muscles, the eyes remaining close the whole of the time. His coat
was taken off his arm, his shirt sleeve stripped up, and Mr. Ridge
bled him to thirty-two ounces; no alteration had taken place in him
during the first part of the time the blood was flowing; at about
twenty-four ounces, the pulse began to decrease; and when the full
quantity named above had been taken, it was at eighty, with a slight
perspiration on the forehead. During the time of bleeding Mr.
Hewson related the circumstance of a Mr. Harris, optician in Holborn,
whose son some years before walked out on the parapet of the
house in his sleep. The boy joined the conversation, and observed
he lived at the corner of Brownlow-street. After the arm was tied up,
he unlaced one boot, and said he would go to bed. In three minutes
from this time he awoke, got up, and asked what was the matter,
(having then been one hour in the trance,) not having the slightest
recollection of any thing that had passed, and wondered at his arm
being tied up, and at the blood, &c. A strong aperient medicine was
then administered, he went to bed, slept sound, and the next day
appeared perfectly well, excepting debility from the bleeding and
operation of the medicine, and had no recollection whatever of what
had taken place. None of his family or himself were ever affected in
this way before.[372]

Remarkable Storm.
The following remarkable letter in the “Gentleman’s Magazine,”
relates to the present day seventy years ago.
Mr. Urban, Wigton, Oct. 23, 1756.

O na the 6th inst. at night, happened a most violent hurricane; such


one perhaps as has not happened in these parts, in the
memory of man. It lasted full 4 hours from about 11 till 3. The
damage it has done over the whole county is very deplorable. The
corn has suffered prodigiously.—Houses were not only unroofed, but
in several places overturned by its fury.—Stacks of hay and corn
were entirely swept away.—Trees without number torn up by the
roots. Others, snapt off in the middle, and scattered in fragments
over the neighbouring fields. Some were twisted almost round; bent,
or split to the roots, and left in so shattered a condition as cannot be
described.
The change in the herbage was also very surprising; its leaves
withered shrivelled up, and turned black. The leaves upon the trees,
especially on the weather side, fared in the same manner. The
Evergreens alone seem to have escaped, and the grass recovered in
a day or two.
I agreed, at first, with the general opinion, that this mischief was
the effect of Lightning; but, when I recollected that, in some places,
very little had been taken notice of; in others none at all; and that
the effect was general, I begun to think of accounting for it from
some other cause. I immediately examined the dew or rain which
had been left on the grass, windows, &c. in hopes of being enabled,
by its taste, to form some better judgment of the particles with
which the air had been impregnated, and I found it as salt as any
sea water I had ever tasted. The several vegetables also were all
saltish more or less, and continued so for 5 or 6 days, the saline
particles not being then washed off; and when the moisture was
exhaled from the windows, the saline chrystal sparkled on the
outside, when the sun shined, and appeared very brilliant.
This salt water, I conceive, has done the principal damage, for I
find upon experiment, that common salt dissolved in fresh water
affected some fresh vegetables, when sprinkled upon them, in the
very same manner, except that it did not turn them quite so black,—
but particles of a sulphurous, or other quality,[373] may have been
mixed with it.
I should be glad to see the opinions of some of your ingenious
correspondents on this wonderful phenomenon;—whether they think
this salt water was brought from the sea,[374] and in what manner.
Yours, A. B.

NATURALISTS’ CALENDAR.
Mean Temperature 54·55.

[372] The Times, October, 1823.


[373] In an adjoining bleach-yard, some cloth which had lain out all night
was turned almost yellow.—Other pieces also which were spread out the
next morning, contracted the same colour, which was not without great
difficulty washed out.
[374] The wind was westerly, and consequently in its passage swept the
Irish sea.

October 7.
Conjugal Indifference.
On the 7 of of October, 1736, a man and his wife, at Rushal, in
Norfolk, “having some words,” the man went out and hanged
himself. The coroner’s inquest found it “self-murder,” and ordered
him to be buried in the cross-ways; but his wife sent for a surgeon,
and sold the body for half a guinea. The surgeon feeling about the
body, the wife said, “He is fit for your purpose, he is as fat as butter.”
The deceased was thereupon put into a sack with his legs hanging
out, and being thrown upon a cart, conveyed to the surgeon’s.[375]

Old Times and New Times.


In a journal of 1826,[376] we have the following pleasant account
of a similar publication ninety years ago.
A curious document, for we may well term it so, has come to our
hands—a copy of a London newspaper, dated Thursday, March 24,
1736-7. Its title is, “The Old Whig, or the Consistent Protestant.” It
seems to have been a weekly paper, and, at the above date, to have
been in existence for about two years. How long it lived after, we
have not, at present, any means of ascertaining. The paper is similar
in size to the French journals of the present day, and consists of four
pages and three columns in each. The show of advertisements is
very fair. They fill the whole of the back page, and nearly a column
of the third. They are all book advertisements. One of these is a
comedy called “The Universal Passion,” by the author of “The Man of
Taste,” no doubt, at that time, an amply sufficient description of the
ingenious playwright. The “Old Whig” was published by “J. Roberts,
at the Oxford Arms, in Warwick-lane,” as likewise by “H. Whitridge,
bookseller, the corner of Castle-alley, near the Royal-exchange, in
Cornhill, price two-pence!” It has a leading article in its way, in the
shape of a discourse on the liberty of the press, which it lustily
defends, from what, we believe, it was as little exposed to, in 1786-
7, as it is in 1826—a censorship. The editor apologises for omitting
the news in his last, on account of “Mr. Foster’s reply to Dr.
Stebbing!” What would be said of a similar excuse now-a-days?
The following epigram is somewhat hacknied, but there is a
pleasure in extracting it from the print, where it probably first
appeared:—
“As we were obliged to omit the News in last week’s paper, by
inserting Mr. Foster’s answer to the Rev. Dr. Stebbing, we shall in this
give the few articles that are any way material.”
“Cries Celia to a reverend dean,
What reason can be given,
Since marriage is a holy thing,
That there is none in Heaven?”
“There are no Women,” he replied;
She quick returns the jest;
“Women there are, but I’m afraid,
They cannot find a priest!”
The miscellaneous part is of nearly the same character as at
present, but disposed in rather a less regular form. We have houses
on fire, and people burnt in them, exactly as we had last week; but
what is wonderful, as it shows the great improvement in these
worthy gentlemen in the course of a century, the “Old Whig” adds to
its account—“The watch, it seems, though at a small distance, knew
nothing of the matter!”
There is a considerable number of deaths, for people died even
in those good old times, and one drowning; whether intentional or
not we cannot inform our readers, as the “Old Whig” went to press
before the inquest was holden before Mr. Coroner and a most
respectable jury.
We still tipple a little after dinner, but our fathers were prudent
men; they took time by the forelock, and began their convivialities
with their dejeune. The following is a short notice of the exploits of a
few of these true men. It is with a deep feeling of the transitory
nature of all sublunary things, that we introduce this notice, by
announcing to our readers at a distance, that the merry Boar’s Head
is merry no more, and that he who goes thither in the hope of
quaffing port, where plump Jack quaffed sack and sugar, will return
disappointed. The sign remains, but the hostel is gone.
“On Saturday last, the right hon. the Lord Mayor held a wardmote at St. Mary
Abchurch, for the election of a common councilman, in the room of Mr. Deputy
Davis. His lordship went sooner than was expected by Mr. Clay’s friends, and
arriving at the church, ordered proclamation to be made, when Mr. Edward Yeates
was put up by every person present; then the question being asked, whether any
other was offered to the ward, and there being no person named, his lordship
declared Mr. Yeates duly elected, and ordered him to be sworn in, which was
accordingly done; and just at the words ‘So help you God,’ Mr. Clay’s friends (who
were numerous, and had been at breakfast at the Boar’s Head Tavern, in
Eastcheap) came into the church, but it was too late, for the election was over.
This has created a great deal of mirth in the ward, which is likely to continue for
some time. The Boar’s Head is said to be the tavern so often mentioned by
Shakspeare, in his play of Henry the Fourth, which occasioned a gentleman, who
heard the circumstances of the election, to repeat the following lines from that
play:—
“‘Falst. Now Hall, what a time of day is it, lad?’
“‘P. Hen.——What a devil has thou to do with the time of the day? unless hours
were cups of sack, and minutes capons,’” &c.

The above account gives a specimen of the sobriety of our


fathers; another of their virtues is exemplified in the following:—
“By a letter from Penzance, in Cornwall, we have the following account, viz.:
—‘That on the 12th instant at night, was lost near Portlevan (and all the men
drowned, as is supposed), the queen Caroline, of Topsham, Thomas Wills, master,
from Oporto, there being some pieces of letters found on the sands, directed for
Edward Mann, of Exon, one for James La Roche, Esq. of Bristol, and another for
Robert Smyth, Esq. and Company, Bristol. Some casks of wine came on shore,
which were immediately secured by the country people; but on a composition with
the collector, to pay them eight guineas for each pipe they brought on shore, they
delivered to him twenty-five pipes; and he paid so many times eight guineas, else
they would have staved them, or carried them off.’”

The order maintained in England at that time was nothing


compared to the strictness of discipline observed on the continent.
“They write from Rome, that count Trevelii, a Neapolitan, had been beheaded
there, for being the author of some satirical writings against the Pope: that Father
Jacobini, who was sentenced to be beheaded on the same account, had obtained
the favour of being sent to the gallies, through the intercession of cardinal
Guadagni, the pope’s nephew, who was most maltreated by the priest and the
count.”

These were times, as Dame Quickly would say, when honourable


men were not to be insulted with impunity.
We sometimes hear of a terrible species of mammalia, called
West India Planters, and there is an individual specimen named
Hogan, or something like it, whose wonderful fierceness has been
sounded in our ears for some ten or twelve years. But what will the
abolitionists say to the extract of a letter from Antigua? Compared
with these dreadful doings, Mr. Hogan’s delinquencies were mere
fleabites.
“Extract of a letter from Antigua, January 15, 1736-7:—‘We are in a great deal
of trouble in this island, the burning of negroes, hanging them on gibbets alive,
racking them on the wheel, &c. takes up almost all our time; that from the 20th of
October to this day, there has been destroyed sixty-five sensible negro men, most
of them tradesmen, as carpenters, masons, and coopers. I am almost dead with
watching and warding, as are many more. They were going to destroy all the
white inhabitants on the island. Court, the king of the negroes, who was to head
the insurrection; Tomboy, their general, and Hercules their lieutenant-general,
were all racked upon the wheel, and died with amazing obstinacy. Mr. Archibald
Hamilton’s Harry, after he was condemned, stuck himself with a knife in eighteen
places, four whereof were mortal, which killed him. Colonel Martin’s Jemmy, who
was hung up alive from noon to eleven at night, was then taken down to give
information. Colonel Morgan’s Ned, who, after he had been hung up seven days
and seven nights, that his hands grew too small for his hand-cuffs, he got them
out and raised himself up, and fell down from a gibbet fifteen feet high, without
any harm; he was revived with cordials and broth, in hopes to bring him to a
confession, but he would not confess, and was hung up again, and in a day and
night after expired. Mr. Yeoman’s Quashy Coomah jumped out of the fire half
burnt, but was thrown in again. And Mr. Lyon’s Tim jumped out of the fire, and
promised to declare all, but it took no effect. In short, our island is in a poor,
miserable condition, that I wish I could get any sort of employ in England.’”

The following notice is of a more pleasing character:—


“In a few days, a fine monument to the memory of John Gay, Esq., author of
the Beggar’s Opera, and several other admired pieces, will be erected in
Westminster-abbey, at the expense of his grace the duke of Queensberry and
Dover, with an elegant inscription thereon, composed by the deceased’s intimate
and affectionate friend, Mr. Alexander Pope.”

There are two more observations which we have to make; 1st.


“the Old Whig,” as was meet, was a strong Orangeman; and 2d. the
parliament was sitting when the number before us was published,
and yet it does not contain one line of debate!

NATURALISTS’ CALENDAR.
Mean Temperature 53·77.
[375] Gentleman’s Magazine.
[376] New Times, September 7.

October 8.
Ancient Manners.
Elias Ashmole, the antiquary, enters thus in the diary of his life:
—“1657, October 8. The cause between me and my wife was heard,
when Mr. Serjeant Maynard observed to the court, that there were
800 sheets of depositions on my wife’s part, and not one word
proved against me of using her ill, nor ever giving her a bad or
provoking word.” The decision was against the lady; the court,
refusing her alimony, delivered her to her husband; “whereupon,”
says Ashmole, “I carried her to Mr. Lilly’s, and there took lodgings for
us both.” He and Lilly dabbled in astrology; and he tells no more of
his spouse till he enters “1668, April 1. 2 Hor. ante merid. the lady
Mainwaring my wife died.” Subsequently he writes—“November 3. I
married Mrs. Elizabeth Dugdale, daughter to William Dugdale, Esq.
Norroy, king of arms at Lincoln’s-inn chapel. Dr. William Floyd
married us, and her father gave her. The wedding was finished at 10
hor. post merid.”
Ashmole’s diary minutely records particulars of all sorts:
—“September 5, I took pills; 6, I took a sweat; 7, I took leeches; all
wrought very well.—December 19, Dr. Chamberlain proposed to me
to bring Dr. Lister to my wife, that he might undertake her. 22. They
both came to my house, and Dr. Lister did undertake her.” Though
Dr. Lister was her undertaker on that occasion, yet Ashmole records
—“1687, April 16, my wife took Mr. Bigg’s vomit, which wrought very
well.—19. She took pulvis sanctis; in the afternoon she took cold.”
Death took Ashmole in 1695. He was superstitious and punctilious,
and was perhaps a better antiquary than a friend; he seems to have
possessed himself of Tradescant’s museum at South Lambeth in a
manner which rather showed his love of antiquities than poor old
Tradescant.
It is to be regretted that Ashmole’s life, “drawn up by himself by
way of diary,” was not printed with the Life of Lilly in the
“Autobiography.” Lilly’s Life is published in that pleasant work by
itself. “Tom Davies” deemed them fit companions.

NATURALISTS’ CALENDAR.
Mean Temperature 53·80.

October 9.
St. Denys.
This name in the church of England calendar is properly noticed
in vol. i. col. 1370.

On the celebration of this saint’s festival in catholic countries he


is represented walking with his head in his hands, as we are assured
he did, after his martyrdom. A late traveller in France relates, that on
the 9th of October, the day of St. Denis, the patron saint of France, a
procession was made to the village of St. Denis, about a league from
Lyons. This was commonly a very disorderly and tumultuous
assembly, and was the occasion some years ago of a scene of
terrible confusion and slaughter. The porter who kept the gate of the
city which leads to this village, in order to exact a contribution from
the people as they returned, shut the gate at an earlier hour than
usual. The people, incensed at the extortion, assembled in a crowd
round the gate to force it, and in the conflict numbers were stifled,
squeezed to death, or thrown into the Rhone, on the side of which
the gate stood. Two hundred persons were computed to have lost
their lives on this occasion. The porter paid his avarice with his life:
he was condemned and executed as the author of the tumult, and of
the consequences by which it was attended.[377]

NATURALISTS’ CALENDAR.
Mean Temperature 52·62.
[377] Miss Plumptre.

October 10.
1826. Oxford and Cambridge Terms begin.
Chronology.
On Sunday, October 10, 1742, during the time of worship, the
roof of the church of Fearn, in Ross-shire, Scotland, fell suddenly in,
and sixty people were killed, besides the wounded. The gentry
whose seats were in the niches, and the preacher by falling under
the sounding-board were preserved.[378]

Pack Monday Fair, at Sherborne, Dorsetshire


To the Editor of the Every-Day Book.
Sherborne, September, 1826.
Sir,—Having promised to furnish an account of our fair, I now
take the liberty of handing it to you for insertion in your very
entertaining work.
This fair is annually held on the first Monday after the 10th of
October, and is a mart for the sale of horses, cows, fat and lean
oxen, sheep, lambs, and pigs; cloth, earthenware, onions, wall and
hazle nuts, apples, fruit trees, and the usual nick nacks for children,
toys, gingerbread, sweetmeats, sugar plums, &c. &c. with drapery,
hats, bonnets, caps, ribands, &c. for the country belles, of whom,
when the weather is favourable, a great number is drawn together
from the neighbouring villages.
Tradition relates that this fair originated at the termination of the
building of the church, when the people who had been employed
about it packed up their tools, and held a fair or wake, in the
churchyard, blowing cows’ horns in their rejoicing, which at that time
was perhaps the most common music in use.[379] The date at which
the church was built is uncertain, but it may be conjectured in the
sixth century, for in the year 704, king John fixed an episcopal see
at, and Aldhelm was consecrated the first bishop of, Sherborne, in
705, and enjoyed the bishopric four years. Aldhelm died in 709, is
said to be the first who introduced poetry into England, to have
obtained a proficiency in music, and the first Englishman who ever
wrote in Latin.
To the present time Pack Monday fair, is annually announced
three or four weeks previous by all the little urchins who can procure
and blow a cow’s horn, parading the streets in the evenings, and
sending forth the different tones of their horny bugles, sometimes
beating an old saucepan for a drum, to render the sweet sound
more delicious, and not unfrequently a whistle-pipe or a fife is added
to the band. The clock’s striking twelve on the Sunday night
previous, is the summons for ushering in the fair, when the boys
assemble with their horns, and parade the town with a noisy shout,
and prepare to forage for fuel to light a bonfire, generally of straw,
obtained from some of the neighbouring farmyards, which are sure
to be plundered, without respect to the owners, if they have not
been fortunate enough to secure the material in some safe part of
their premises. In this way the youths enjoy themselves in
boisterous triumph, to the annoyance of the sleeping part of the
inhabitants, many of whom deplore, whilst others, who entertain
respect for old customs, delight in the deafening mirth. At four
o’clock the great bell is rang for a quarter of an hour. From this time,
the bustle commences by the preparations for the coming scene:
stalls erecting, windows cleaning and decorating, shepherds and
drovers going forth for their flocks and herds, which are depastured
for the night in the neighbouring fields, and every individual seems
on the alert. The business in the sheep and cattle fairs (which are
held in different fields, nearly in the centre of the town, and well
attended by the gentlemen farmers, of Dorset, Somerset, and
Devon) takes precedence, and is generally concluded by twelve
o’clock, when what is called the in-fair begins to wear the
appearance of business-like activity, and from this time till three or
four o’clock more business is transacted in the shop, counting-house,
parlour, hall, and kitchen, than at any other time of the day, it being
a custom of the tradespeople to have their yearly accounts settled
about this time, and scarcely a draper, grocer, hatter, ironmonger,
bookseller, or other respectable tradesman, but is provided with an
ample store of beef and home-brewed October, for the welcome of
their numerous customers, few of whom depart without taking
quantum suff. of the old English fare placed before them.
Now, (according to an old saying,) is the town alive. John takes
Joan to see the shows,—there he finds the giant—here the learned
pig—the giantess and dwarf—the menagerie of wild beasts—the
conjuror—and Mr. Merry Andrew cracking his jokes with his quondam
master. Here it is—“Walk up, walk up, ladies and gentlemen, we are
now going to begin, be in time, the price is only twopence.” Here is
Mr. Warr’s merry round-about, with “a horse or a coach for a
halfpenny.”—Here is Rebecca Swain[380] with her black and red cock,
and lucky-bag, who bawls out, “Come, my little lucky rogues, and try
your fortune for a halfpenny, all prizes and no blanks, a faint heart
never wins a fair lady.”—Here is pricking in the garter.—Raffling for
gingerbread, with the cry of “one in; who makes two, the more the
merrier.”—Here is the Sheffield hardwareman, sporting a worn-out
wig and huge pair of spectacles, offering, in lots, a box of razors,
knives, scissors, &c., each lot of which he modestly says, “is worth
seven shillings, but he’ll not be too hard on the gaping crowd, he’ll
not take seven, nor six, nor five, nor four, nor three, nor two, but
one shilling for the lot,—going at one shilling—sold again and the
money paid.”—Here are two earthenware-men bawling their shilling’s
worth one against the other, and quaffing beer to each other’s luck
from that necessary and convenient chamber utensil that has
modestly usurped the name of the great river Po. Here is poor Will,
with a basket of gingerbread, crying “toss or buy.” There is a
smirking little lad pinning two girls together by their gowns, whilst
his companion cracks a Waterloo bang-up in their faces. Here stands
John with his mouth wide open, and Joan with her sloe-black ogles
stretched to their extremity at a fine painted shawl, which Cheap
John is offering for next to nothing; and here is a hundred other
contrivances to draw the “browns” from the pockets of the unwary,
and tickle the fancies of the curious; and sometimes the rogue of a
pickpocket extracting farmer Anybody’s watch or money from his
pockets.
This is Pack Monday fair, till evening throws on her dark veil,
when the visiters in taking their farewell, stroll through the rows of
gingerbread stalls, where the spruce Mrs. or Miss Sugarplum pops
the cover of her nut-cannister forth, with “buy some nice nuts, do
taste, sir, (or ma’me,) and treat your companion with a paper of
nuts.” By this time the country folks are for jogging home, and
vehicles and horses of every description on the move, and the bustle
nearly over, with the exception of what is to be met with at the inns,
where the lads and lasses so disposed, on the light fantastic toe,
assisted by the merry scraping of the fiddler, finish the fun, frolic,
and pastime of Pack Monday Fair.
I am, &c. R. T.

Sonnet.
For the Every-Day Book.
Me, men’s gay haunts delight not, nor the glow
Of lights that glitter in the crowded room;
But nature’s paths where silver waters flow,
Making sweet music as along they go,
And shadowy groves where birds their light wings plume,
Or the brown heath where waves the yellow broom,
Or by the stream where bending willows grow,
And silence reigns, congenial with my gloom.
For there no hollow hearts, no envious eyes,
No flatt’ring tongues, no treacherous hands are found,
No jealous feuds, no gold-born enmities,
Nor cold deceits with which men’s walks abound,
But quietness and health, which are more meet,
Than glaring halls where riot holds her seat.
S. R. J.

The New River at Hornsey.


The New River at Hornsey.
————The stream is pure in solitude,
But passing on amid the haunts of men
It finds pollution there, and rolls from thence
A tainted tide.
Southey.
My memory does not help me to a dozen passages from the
whole range of authors, in verse and prose, put together; it only
assists me to ideas of what I have read, and to recollect where they
are expressed, but not to their words. As the “Minor Poems” are not
at hand, I can only hope I have quoted the preceding lines
accurately. Their import impressed me in my boyhood, and one fine
summer’s afternoon, a year or two ago, I involuntarily repeated
them while musing beside that part of the “New River” represented
in the engraving. I had strolled to “the Compasses,” when “the
garden,” as the landlord calls it, was free from the nuisance of
“company;” and thither I afterwards deluded an artist, who
continues to “use the house,” and supplies me with the drawing of
this sequestered nook.
This “gentle river” meanders through countless spots of
surprising beauty and variety within ten miles of town. When I was a
boy I thought “Sadler’s Well’s arch,” opposite the “Sir Hugh
Myddelton,” (a house immortalized by Hogarth,) the prime part of
the river; for there, by the aid of a penny line, and a ha’porth of
gentles and blood-worms, “mixed,” bought of old Turpin, who kept
the little fishing-tackle shop, the last house by the river’s side, at the
end next St. John’s-street-road, I essayed to gudgeon gudgeons. But
the “prime” gudgeon-fishing, then, was at “the Coffin,” through
which the stream flows after burying itself at the Thatched-house,
under Islington road, to Colebrooke-row, within half a stone’s throw
of a cottage, endeared to me, in later years, by its being the abode
of “as much virtue as can live.” Past the Thatched-house, towards
Canonbury, there was the “Horse-shoe,” now no more, and the
enchanting rear—since despoiled—of the gardens to the retreats of
Canonbury-place; and all along the river to the pleasant village of
Hornsey, there were delightful retirements on its banks, so “far from
the busy haunts of men,” that only a few solitary wanderers seemed
to know them. Since then, I have gone “over the hills and far away,”
to see it sweetly flowing at Enfield Chase, near many a “cottage of
content,” as I have conceived the lowly dwellings to be, which there
skirt it, with their little gardens, not too trim, whence the inmates
cross the neat iron bridges of the “New River Company,” which,
thinking of “auld lang syne,” I could almost wish were of wood.
Further on, the river gracefully recedes into the pleasant grounds of
the late Mr. Gough the antiquary, who, if he chiefly wrote on the
manners and remains of old times, had an especial love and kind
feeling for the amiable and picturesque of our own. Pursuing the
river thence to Theobalds, it presents to the “contemplative man’s
recreation,” temptations that old Walton himself might have coveted
to fall in his way: and why may we not “suppose that the vicinity of
the New River, to the place of his habitation, might sometimes tempt
him out, whose loss he so pathetically mentions, to spend an
afternoon there.” He tells “the honest angler,” that the writing of his
book was the “recreation of a recreation,” and familiarly says, “the
whole discourse is, or rather was, a picture of my own disposition,
especially in such days and times as I have laid aside business, and
gone a fishing with honest Nat. and R. Roe; but they are gone, and
with them most of my pleasant hours,—even as a shadow that
passeth away and returns not.”

I dare not say that I am, and yet I cannot say that I never was,
an angler; for I well remember where, though I cannot tell when,
within a year, I was enticed to “go a fishing,” as the saying is, which
I have sometimes imagined was derived from Walton’s motto on the
title of his book:—“Simon Peter said, I go a fishing: and they said,
we also will go with thee.—John xxi. 3.” This passage is not in all the
editions of the “Complete Angler,” but it was engraven on the title-
page of the first edition, printed in 1653. Allow me to refer to one of
“captain Wharton’s almanacs,” as old Lilly calls them in his “Life and
Times,” and point out what was, perhaps, the earliest advertisement
of Walton’s work: it is on the back of the dedication leaf to
“Hemeroscopeion: Anni Æræ Christianæ 1654.” The almanac was
published of course in the preceding year, which was the year
wherein Walton’s work was printed.

Advertisement of Walton’s Angler, 1653.


“There is published a Booke of Eighteen-pence
price, called The Compleat Angler, Or, The
Contemplative man’s Recreation: being a Discourse of
Fish and Fishing. Not unworthy the perusall. Sold by
Richard Marriot in S. Dunstan’s Church-yard
Fleetstreet.”
This advertisement I deem a bibliomaniacal curiosity. Only think
of the first edition of Walton as a “booke of eighteen-pence price!”
and imagine the good old man on the day of publication, walking
from his house “on the north side of Fleet-street, two doors west of
the end of Chancery-lane,” to his publisher and neighbour just by,
“Richard Marriot, in S. Dunstan’s Churchyard,” for the purpose of
inquiring “how” the book “went off.” There is, or lately was, a large
fish in effigy, at a fishing-tackle-maker’s in Fleet-street, near Bell-
yard, which, whenever I saw it, after I first read Walton’s work,
many years ago, reminded me of him, and his pleasant book, and its
delightful ditties, and brought him before me, sitting on “a primrose
bank” turning his “present thoughts into verse”
The Angler’s Wish.
I in these flowery meads would be:
These crystal streams should solace me;
To whose harmonious bubbling noise
I with my angle would rejoice:
Sit here, and see the turtle-dove
Court his chaste mate to acts of love:
Or, on that bank, feel the west wind
Breathe health and plenty: please my mind,
To see sweet dew-drops kiss these flowers,
And then washed off by April showers;
Here, hear my Kenna sing a song;
There, see a blackbird feed her young,
Or a leverock build her nest:
Here, give my weary spirits rest,
And raise my low-pitch’d thoughts above
Earth, or what poor mortals love:
Thus, free from law-suits and the noise
Of princes’ courts, I would rejoice:
Or, with my Bryan, and a book,
Loiter long days near Shawford-brook;
There sit by him, and eat my meat,
There see the sun both rise and set;
There bid good morning to next day;
There meditate my time away;
And angle on; and beg to have
A quiet passage to a welcome grave.

NATURALISTS’ CALENDAR.
Mean Temperature 52·05.

[378] Gentleman’s Magazine.


[379] Hutchins, in his “History of Dorset,” says, this “Fair is held in the
churchyard,[381] on the first Monday after the feast of St. Michael, (O. S.)
and is a great holyday for the inhabitants of the town and neighbourhood.
It is ushered in by the ringing of the great bell, at a very early hour in the
morning, and by the boys and young men perambulating the street with
cows’ horns, to the no small annoyance of their less wakeful neighbours.
It has been an immemorial custom in Sherborne, for the boys to blow
horns in the evenings in the streets, for some weeks before the fair.”
[380] A tall and portly dame, six feet full, with a particular screw of the
mouth, and whom the writer recollects when he was a mere child, thirty
years ago; none who have seen and heard her once, but will recollect her
as long as they live.
[381] The fair has been removed from the churchyard about six or seven
years, and is now held on a spacious parade, in a street not far from the
church.

October 11.
This is “Old Michaelmas Day.”

“Duncan’s Victory.”
On the 11th of October, 1797, admiral Duncan obtained a
splendid victory over the Dutch fleet off Camperdown, near the isle
of Texel, on the coast of Holland. For this memorable achievement
he was created a viscount, with a pension of two thousand pounds
per annum. His lordship died on the 4th of August, 1804; he was
born at Dundee, in Scotland, on the 1st of July, 1731. After the
battle of Camperdown was decided, he called his crew together in
the presence of the captured Dutch admiral, who was greatly
affected by the scene, and Duncan kneeling on the deck, with every
man under his command, “solemnly and pathetically offered up
praise and thanksgiving to the God of battles;—strongly proving the
truth of the assertion, that piety and courage should be inseparably
allied, and that the latter without the former loses its principal
virtue.”[382]

NATURALISTS’ CALENDAR.
Mean Temperature 51·82.

[382] Butler’s Chronological Exercises.

October 12.
Chronology.
On the 12th of October, 1748, was born at St. John’s near
Worcester, Mr. William Butler, the author of “Chronological,
Biographical, Historical, and Miscellaneous Exercises,” an excellent
work, for young persons especially, a useful compendium in every
library, and one to which the editor of the Every-Day Book has been
indebted as a ready guide to many interesting and important events.
In the seventh edition of Mr. Butler’s work just mentioned, we are
informed by his son, Mr. John Olding Butler, that his father was
educated in the city of Worcester. Having acquired considerable
knowledge, and especially an excellent style of penmanship, he in
1765 repaired to the metropolis, and commenced his career as a
teacher of writing and geography. In these branches of education he
attained the highest repute on account of the improvements which
were introduced by him in his mode of instruction. His copies were
derived from the sources of geography, history, and biographical
memoirs. A yet more extensive and permanent benefit was
conferred upon young persons by the many useful and ingenious
works which he published, a list of which is subjoined. They contain
a mass of information, both instructive and entertaining, rarely
collected in one form, and are admirably adapted to promote the
great design of their author—the moral, intellectual, and religious
improvement of the rising generation; to this he consecrated all his
faculties, the stores of his memory, and the treasures of his
knowledge.
As a practical teacher Mr. Butler had few superiors, and his
success in life was commensurate with his merit: he was the most
popular instructor in his line.
A strict probity, an inviolable regard to truth, an honourable
independence of mind, and a diffusive benevolence, adorned his
moral character; and to these eminent virtues must be added, that
of a rigid economy and improvement of time, for which he was most
remarkable. How much he endeavoured to inculcate that which he
deemed the foundation of every virtue, the principle of religion, may
be seen in his “Chronological, &c., Exercises:” to impress this
principle on the youthful heart and mind was considered by him as
the highest duty. Mr. Butler’s professional labours were commenced
at the early age of seventeen, and were continued with indefatigable
ardour to the last year of his life, a period of fifty-seven years. In
estimating the value of such a man, we should combine his moral
principle with his literary employments; these were formed by him
into duties, which he most conscientiously discharged: and he will be
long remembered as one who communicated to a large and
respectable circle of pupils solid information, examples of virtue, and
the means of happiness; and who, in an age fruitful of knowledge,
by his writings instructed, and will long continue to instruct the rising
generation, and benefit mankind. His virtues will live and have a
force beyond the grave.
Mr. Butler died at Hackney, August 1, 1822, after a painful illness,
borne with exemplary patience and resignation. He was one of the
oldest inhabitants of that parish, and was interred there, by his own
desire, in the burying-ground attached to the meeting-house of his
friend, the late Rev. Samuel Palmer.

A list of Mr. Butler’s books for the use of young persons.


1. Chronological Exercises, already mentioned. Price 6s. bound.
2. An engraved Introduction to Arithmetic, designed to facilitate
young beginners, and to diminish the labour of the tutor. 4s. 6d.
bound.
3. Arithmetical Questions, on a new plan; intended to answer the
double purpose of arithmetical instruction and miscellaneous
information. 6s. bound.
4. Geographical and Biographical Exercises, on a new plan. 4s.
5. Exercises on the Globes, interspersed with historical,
biographical, chronological, mythological, and miscellaneous
information, on a new plan. The ninth edition. 6s. bound.
6. A numerous collection of Arithmetical Tables. 8d.
7. Geographical Exercises in the New Testament; with maps, and a
brief account of the principal religious sects. 5s. 6d. bound.
8. Miscellaneous Questions, relating principally to English history
and biography. Second edition, enlarged. 4s.
Mr. Bourn, son-in-law of Mr. Butler, and his associate in his
profession upwards of thirty years, purchased the copyright of the
greater part of Mr. Butler’s works. They have passed through a
number of editions, and if the Every-Day Book extend a knowledge
of their value, it will be to the certain benefit of those for whose use
they were designed. The envious and suspicious may deny that
there is such a quality as “disinterestedness in human actions,” yet
the editor has neither friendship nor intimacy with any one whom
this notice may appear to favour. He only knows Mr. Butler’s books,
and therefore recommends them as excellent aids to parents and
teachers.

NATURALISTS’ CALENDAR.
Mean Temperature 50·10.

October 13.
Translation K. Edward. Conf.
This notice of the day in the church of England calendar and
almanacs, denotes it as the festival of the translation of king Edward
the Confessor.[383]
Edward the Confessor died on the 5th of January, 1066, and was
buried in the abbey church of St. Peter, Westminster. “His queen,
Edgitha, survived the saint many years;” she was buried beside him,
and her coffin was covered with plates of silver and gold. According
to his biographers, in 1102, the body of St. Edward was found
entire, the limbs flexible, and the clothes fresh. The bishop of
Rochester “out of a devout affection, endeavoured to pluck onely
one hayre from his head, but it stuck so firmly that he was defeated
of his desire.” This was at the saint’s first translation. Upon miracles
“duly proved, the saint was canonized by Alexander III., in 1161.” It
appears that “there are commemorated severall translations of his
sacred body.” In 1163, “it was again translated by S. Thomas à
Becket, archbishop of Canterbury, in the presence of king Henry II.
This translation seems to have been made on the 13th of October;
for on that day “he is commemorated in our martyrologe, whereas in
the Roman he is celebrated on the 5th of January.” It further
appears that, “about a hundred years after, in the presence of king
Henry III., it was again translated, and reposed in a golden shrine,
prepared for it by the same king.[384]

The see of Rome is indebted to Edward the Confessor for a grant


to the pope of what was then called Rome-scot, but is now better
known by the name of “Peterpenny.” The recollection of this tribute
is maintained by the common saying “no penny, no paternoster;” of
which there is mention in the following poem from the
“Hesperides:”—
Fresh strewings allow
To my sepulcher now,
To make my lodging the sweeter;
A staffe or a wand
Put then in my hand,
With a penny to pay S. Peter.
Who has not a crosse,
Must sit with the losse,
And no whit further must venture;
Since the porter he
Will paid have his fee,
Or els not one there must enter.
Who at a dead lift,
Can’t send for a gift,
A pig to the priest for a roster
Shall heare his clarke say,
By yea and by nay,
No penny no pater noster.
Herrick.

NATURALISTS’ CALENDAR.
Mean Temperature 50·62.

[383] See vol. 1. 1376.


[384] Butler. Cresys.

October 14.
A Lucky Day.
“Some Memorable Remarques upon the Fourteenth of October,
being the Auspicious Birth-Day of His Present Majesty The
Most Serene King James II. Luc. xix. 42 In Hoc Die Tuo. In This
Thy Day. London, Printed by A. R. And are to be sold by
Randal Taylor, near Stationers-Hall 1687.” Folio.
In this curious tract, the author purports to set forth “how lucky
the Fourteenth of October hath been to the princes of England,” and
because he discovers “out of Wharton’s Gesta Britannorum, and the
collections of others, that his late royal highness, our magnanimous
magnificent sovereign, (James II.,) was also born upon that augural
day,” he observes—“It made more than ordinary impression upon
me, so that I never saw him, but, I thought, in his very face there
were extraordinary instances and tokens of regality.”
There were some, it seems, who, after “his late royal highness”
the dukes “recess into Holland,” “exceedingly tryumphed, wishing he
might never return; nay, that he durst not, nor would be permitted
so to do; using, moreover, opprobrious terms.” These persons, he
tells us, he “prophetically characteris’d” in his “Introductio ad
Latinam Blasoniam;” hence, he says, “Indignation made me print my
ensuing sentiments,” which “found good acceptance among the
better and more loyal sort;” and hence, he further says, “things by
me forethought, and publickly hinted, being come to pass, my Day
Fatality began to be remembred; and one whom I wish very well,
desiring I would give him leave to reprint that, and two other of my
small pieces together, I assented to his request.” These form the
present treatise, from whence we gather that the Fourteenth of
October
—————“gave the Norman duke
That vict’ry whence he England’s scepter took,”
and was remarkable for the safe landing of Edward III., after being
endangered by a tempest at sea on his returning victorious from
France. Wherefore, says our author, in Latin first, and then in these
English lines—
“Great duke rejoice in this your day of birth,
And may such omens still increase your mirth.”
Afterwards he relates, from Matthew Paris, that when “Lewis king of
France had set footing here, and took some eminent places, he
besieged Calais from 22 of July, to the Fourteenth of October
following, about which time the siege was raised, and England
thereby relieved.” Likewise “a memorable peace, (foretold by
Nostradamus) much conducing to the saving of christian blood, was
made upon the Fourteenth of October, 1557, between pope Paul the
IV., Henry the II. of France, and Philip the II. of Spain.” Whereon,
exclaims our exultant author, “A lucky day this, not only to the
princes of England, but auspicious to the welfare of Europe.” He
concludes by declaring “that it may be so to his royal highness, as
well as it was to the most great queen his mother, are the hearty
prayers of Blew-Mantle.”
From the conclusion of the last sentence, and the previous
reference to his “Blasoniam,” we find this writer to have been John
Gibbon, the author of “An Easie Introduction to Latine Blason, being
both Latine and English”—an octavo volume, now only remembered
by the few collectors of every thing written on “coat-armour.”

Gibbon speaks of one of his pamphlets “whose title should have


been Dux Bonis Omnibus Appellens, or The Swans’ Welcome;” or
rather, as he afterwards set it out at large, “Some Remarks upon the
Note-worthy Passage, mentioned in the True Domestick Intelligence
dated October the Fourteenth 1679, concerning a company of Swans
more than ordinary gathered together at his royal highness’s
landing.” Instead, however, of its having such a title, he tells us
“there was a strange mistake, not only in that, but in other material
circumstances; so that many suppose, the printer could never have
done it himself, but borrowed the assistance of the evil spirit to
render it ridiculous, and not only so, but the very Duke himself and
the Loyal Artillery!”, wherefore “the printer smothered the far
greatest number of them,” yet, as he adds it to the tract on the
Fourteenth of October, we have the advantage to be told “what
authors say of the candid Swan,” that all esteem him for a “bird
royal,” that “oftentimes in coats and crests we meet him either
crown’d or coronally collar’d,” that “he is a bird of great beauty and
strength also,” that “shipmen take it for good luck if in peril of
shipwreck they meet swans,” that “he uses not his strength to prey
or tyrannize over any other fowl, but only to be revenged of such as
offer him wrong,” and so forth. Ergo—according to “Blew-mantle,”
we should believe that, “the most serene king James II.” was
greeted by these honourable birds, “in allegory assembled,” to
signify his kindred virtues. If Gibbon lived from 1687, where he
published his “Remarques, on the Fourteenth of October” as the
auspicious birth-day of James II. until the landing of William III. in
the following year—did he follow the swan-like monarch to the court
of France, or remain “Blew-mantle” in the Herald’s college, to do
honour to the court of “the deliverer?”
Gibbon, in his “Remarques,” on the “auspicious” Fourteenth of
October, prints the following epistle, to himself, which may be
regarded as a curiosity on account of the superstition of its writer.
A letter from Sir Winston Churchil, Knight; Father to the Right
Honourable, John Lord Churchil.
Thank you for your kind Present, the Observation of the Fatality of
I Days. I have made great Experience of the Truth of it; and have
set down Fryday, as my own Lucky Day; the Day on which I was
Born, Christen’d, Married, and, I believe, will be the Day of my
Death: The Day whereon I have had sundry Deliverances, (too long
to relate) from Perils by Sea and Land, Perils by False Brethren,
Perils of Law Suits, &c. I was Knighted (by chance, unexpected by
my self) on the same Day; and have several good Accidents
happened to me, on that Day: And am so superstitious in the Belief
of its good Omen, That I chuse to begin any Considerable Action
(that concerns me) on the same Day. I hope HE, whom it most
concerns, will live to own your Respect, and Good Wishes, expressed
in That Essay of yours: Which discovering a more than common
Affection to the DUKE, and being as valuable for the Singularity of
the Subject, as the Ingenuity of your Fancy, I sent into Flanders, as
soon as I had it; That They on the Other Side the Water may see,
’Tis not all sowre Wine, that runs from our English Press.

“The Right Honourable, John Lord Churchil,” mentioned at the


head of this ominous letter, became celebrated as “the great duke of
Marlborough.” Sir Winston Churchill was the author of “Divi
Britannici, a history of the lives of the English kings” in folio; but his
name is chiefly remembered in connection with his son’s, and from
his having also been father to Arabella Churchill, who became
mistress to the most serene king of Blew-Mantle Gibbon, and from
that connection was mother of the duke of Berwick, who turned his
arms against the country of her birth.
Sir Winston was a cavalier, knighted at the restoration of Charles
II., for exertions in the royal cause, by which his estates became
forfeited. He recovered them under Charles, obtained a seat in the
house of commons, became a fellow of the royal society, had a seat
at the board of green cloth, and died in 1688. He was born in 1620,
at Wootton Glanville, in Dorsetshire.[385] His letter on “Fryday” is
quite as important as his “Divi Britannici.”

Taking Honey without Killing the Bees.


On the 14th day of October, 1766, Mr. Wildman, of Plymouth,
who had made himself famous throughout the west of England for
his command over bees, was sent for to wait on lord Spencer, at his
seat at Wimbledon, in Surrey; and he attended accordingly. Several
of the nobility and persons of fashion were assembled, and the
countess had provided three stocks of bees. The first of his
performances was with one hive of bees hanging on his hat, which
he carried in his hand, and the hive they came out of in the other
hand; this was to show that he could take honey and wax without
destroying the bees. Then he returned into the room, and came out
again with them hanging on his chin, with a very venerable beard.
After showing them to the company, he took them out upon the
grass walk facing the windows, where a table and table cloth being
provided, he set the hive upon the table, and made the bees hive
therein. Then he made them come out again, and swarm in the air,
the ladies and nobility standing amongst them, and no person stung
by them. He made them go on the table and took them up by
handfuls, and tossed them up and down like so many peas; he then
made them go into their hive at the word of command. At five
o’clock in the afternoon he exhibited again with the three swarms of
bees, one on his head, one on his breast, and the other on his arm,
and waited on lord Spencer in his room, who had been too much
indisposed to see the former experiments; the hives which the bees
had been taken from, were carried by one of the servants. After this
exhibition he withdrew, but returned once more to the room with the
bees all over his head, face, and eyes, and was led blind before his
lordship’s window. One of his lordship’s horses being brought out in
his body clothes, Mr. Wildman mounted the horse, with the bees all
over his head and face, (except his eyes;) they likewise covered his
breast and left arm; he held a whip in his right hand, and a groom
led the horse backwards and forwards before his lordship’s window
for some time. Mr. Wildman afterwards took the reins in his hand,
and rode round the house; he then dismounted, and made the bees
march upon a table, and at his word of command retire to their hive.
The performance surprised and gratified the earl and countess and
all the spectators who had assembled to witness this great bee-
master’s extraordinary exhibition.[386]

Can the honey be taken without destroying the bees? There are
accounts to this effect in several books, but some of the methods
described are known to have failed. The editor is desirous of
ascertaining, whether there is a convenient mode of preserving the
bees from the cruel death to which they are generally doomed, after
they have been despoiled of their sweets.

NATURALISTS’ CALENDAR.
Mean Temperature 50·85.

[385] General Biographical Dictionary, (Hunt and Clarke,) vol. i.


[386] Annual Register, 1766.

October 15.
Exhumation.
It appears from a printed half sheet, of which the following is a
copy, that the will of a person who had been resident at Stevenage,
was proved on this day in the year 1724, whereby he desired his
remains to be kept unburied. It is a curious document, and further
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