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Landmark Papers
in Rheumatology
Landmark Papers in… series
Titles in the series:

Landmark Papers in Rheumatology

Edited by Richard A. Watts and David G. I. Scott
Landmark Papers in Cardiovascular Medicine
Edited by Aung Myat, Tony Gershlick
Landmark Papers in General Surgery
Edited by Graham MacKay, Richard Molloy, and Patrick O’Dwyer
Landmark Papers in Allergy
Edited by Aziz Sheikh, Thomas Platts-Mills, and Allison Worth
Advisory Editor Stephen Holgate
Landmark Papers in Nephrology
Edited by John Feehally, Christopher McIntyre, and J. Stewart Cameron
Landmark Papers in Anaesthesia
Edited by Nigel R. Webster and Helen F. Galley
Landmark Papers in Neurosurgery
Second Edition
Edited by Reuben D. Johnson and Alexander L. Green
Landmark Papers
in Rheumatology

Edited by

Dr. Richard A. Watts

Consultant Rheumatologist
Department of Rheumatology
Ipswich Hospital NHS Trust
Ipswich UK;
Honorary Senior Lecturer Norwich Medical School,
University of East Anglia, Norwich UK

Professor David G. I. Scott

Honorary Consultant Rheumatologist,
Norfolk and Norwich University Foundation NHS Trust;
Honorary Professor of Rheumatology Norwich Medical School,
University of East Anglia, Norwich UK

1
1
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 Preface

The rheumatism is a common name for many aches and pains, which have yet got no peculiar ap-
pellation, though owing to very many different causes.

(William Heberden (1710–1801) Commentaries on the History and Cure of Disease, Chapter 79
(1802)).

William Heberden in many respects summarized the state of rheumatic disease nomen-
clature and classification in 1802 with the statement quoted above. At that time, probably
only gout was clearly distinguished from many types of aches and pains. In the commen-
taries he also gives the first description of the bony nodes over the distal interphalangeal
joints—‘What are those little hard knobs, about the size of a small pea, which are frequently
seen upon the fingers, particularly a little below the top, near the joint?’ He does not under-
stand their aetiology but recognizes them not to be linked with psoriasis. During the late
eighteenth and nineteenth centuries, descriptions of disease patterns that we now recog-
nize began to be made. Sir Archibald Garrod in 1859 gave the name ‘rheumatoid arthritis’
to a disease that, although around for many years, had no nomenclature and up until that
stage had been described as ‘rheumatic gout’, ‘chronic rheumatism’, and ‘rheumalgia’. The
first steps in the scientific investigation of arthritis were also made around this time; for ex-
ample, Garrod differentiated gouty arthritis using the presence of serum hyperuricaemia.
This process has continued up to the present day, with differentiation of further types of ar-
thritis, using both traditional methods of clinical pattern recognition combined with im-
proved investigative techniques, for example, the clear differentiation of inflammation due
to synovitis from that due to enthesial inflammation using MRI, and better understanding
of causation, for example, the recognition that a certain form of inflammatory arthritis of
children is due to borrelia infection. As the study of rheumatic disease has become more
scientific simple descriptions of disease patterns have become inadequate for clinical stud-
ies and this has led to the development of validated diagnostic and classification systems
for many of the rheumatic diseases.
Treatment in Heberden’s day was limited and primarily consisted bleeding or purg-
ing, although the antipyretic properties of cinchona bark were recognized. The only
specific therapy for a form of arthritis then was colchicine for gout, which had been
used since the time of Hippocrates. Garrod suggested that hyperuricaemia could be
controlled by limiting dietary intake of purines. The nineteenth century saw the de-
velopment of aspirin and early analgesics. The twentieth century saw the introduction
of corticosteroids—for which Hench won the Nobel prize—immunosuppressive drugs,
and most recently the products of the biotechnology revolution, monoclonal antibodies
and fusion proteins.
vi PREFACE

The aim of this book is to provide both practising and trainee rheumatologists with an
overview of the history of their specialty by presenting some of the key papers, together
with brief commentary as to why the paper is important. The authors were asked to select
up to ten papers in their field covering in their opinion key developments. The papers
range from initial descriptions of disease up to very recent innovations in our scientific
understanding of aetiopathogenesis and therapy.
Richard A. Watts
David G. I. Scott
 Acknowledgements

We are grateful to Eloise Moir-Ford and James Oates of Oxford University Press for all
their unstinting help and enthusiasm during the production of this book. Without them,
it would never have happened.
Our families, particularly Lesley and Dee, have been very supportive during the editing
process and we are indebted to them.
Richard A. Watts
David G. I. Scott
 Contents

Contributors xv
1 Epidemiology and genetics 1
James Bluett, Suzanne Verstappen, and Deborah Symmons
Introduction 1
Paper 1.1: Radiological assessment of osteoarthritis—the Kellgren and Lawrence
score 4
Paper 1.2: The association between rheumatoid arthritis and lymphoma 7
Paper 1.3: The American Rheumatism Association 1987 revised criteria for the
classification of rheumatoid arthritis 10
Paper 1.4: The global burden of disease 15
Paper 1.5: The shared epitope hypothesis 19
Paper 1.6: The association between protein tyrosine phosphatase 22 and rheumatoid
arthritis 23
Paper 1.7: The Wellcome Trust genome-wide association study of rheumatoid
arthritis 25
Paper 1.8: Five amino acids in three proteins encoded by MHC genes explain most
of the association between the MHC locus and seropositive rheumatoid
arthritis 27
Paper 1.9: High-density genetic mapping identifies new susceptibility loci for
rheumatoid arthritis 30
Paper 1.10: Gene–environment interaction in the aetiology of rheumatoid arthritis 32

2 Rheumatoid arthritis 37
Elena Nikiphorou and Adam Young
Introduction 37
Landmark paper selection 38
Paper 2.1: Rheumatoid arthritis in a population sample 39
Paper 2.2: Judging disease activity in clinical practice in rheumatoid arthritis: first
steps in the development of a disease activity score 42
Paper 2.3: Measurement of patient outcome in rheumatoid arthritis 48
Paper 2.4: Effects of cortisone acetate and pituitary adrenocorticotropic hormone on
rheumatoid arthritis, rheumatic fever, and certain other conditions 53
Paper 2.5: Efficacy of low-dose methotrexate in rheumatoid arthritis 56
Paper 2.6: Infliximab (chimeric anti-tumour necrosis factor alpha monoclonal
antibody) versus placebo in rheumatoid arthritis patients receiving
concomitant methotrexate: a randomized phase III trial 59
Paper 2.7: Taking mortality in rheumatoid arthritis seriously—predictive markers,
socio-economic status, and co-morbidity 62
x CONTENTS

Paper 2.8: Rheumatoid arthritis: treatment which controls the C-reactive protein
and erythrocyte sedimentation rate reduces radiological progression 65
Paper 2.9: Effect of a treatment strategy of tight control for rheumatoid arthritis
(the TICORA study): a single-blind randomized controlled trial 68
Paper 2.10: Clinical and radiographic outcomes of four different treatment strategies
in patients with early rheumatoid arthritis (the BeSt study): a randomized,
controlled trial 73
3 Spondyloarthropathies 77
Carmel Stober and Hill Gaston
Introduction 77
Paper 3.1: Recognition of psoriatic arthritis 79
Paper 3.2: Associations between ankylosing spondylitis, psoriatic arthritis, Reiter’s
disease, the intestinal arthropathies, and Behçet’s syndrome 83
Paper 3.3: The discovery of the association between ankylosing spondylitis and
HLA-B27 88
Paper 3.4: A syndrome of seronegative enthesopathy and arthropathy in children 91
Paper 3.5: Yersinia antigens in synovial-fluid cells from patients with reactive
arthritis 95
Paper 3.6: Transgenic expression of HLA-B27 in rats induces various inflammatory
disorders with clear links to spondyloarthritis 98
Paper 3.7: The evolution of spondyloarthropathies in relation to gut histology 103
Paper 3.8: A hypothesis that enthesitis is the primary pathological process occurring
in spondylarthropathy 108
Paper 3.9: First, and dramatic, indication of the effectiveness of tumour necrosis
factor α blockade in ankylosing spondylitis 113
Paper 3.10: Additional genes which influence susceptibility to ankylosing spondylitis,
including ERAP1, which affects HLA-B27 assembly 117
4 Systemic lupus erythematosus 121
Benjamin Parker and Ian N. Bruce
Introduction 121
Paper 4.1: Common overlapping pathological features of systemic autoimmune
rheumatic diseases 122
Paper 4.2: The LE cell phenomenon 125
Paper 4.3: Complement deposition demonstrated in systemic lupus erythematosus
tissue 128
Paper 4.4: Premature cardiovascular disease in systemic lupus erythematosus
patients 131
Paper 4.5: Long-term trials demonstrate the efficacy of immunosuppression for lupus
nephritis 135
Paper 4.6: Development of classification criteria for systemic lupus erythematosus 139
Paper 4.7: Interferon implicated in immunopathogenesis of systemic lupus
erythematosus 142
Paper 4.8: Successful clinical trials of belimumab in systemic lupus erythematosus 144
 CONTENTS xi

Paper 4.9: The first description of the association between the lupus anticoagulant
and thrombosis in systemic lupus erythematosus 147
Paper 4.10: The impact of withdrawal of hydroxychloroquine in stable systemic lupus
erythematosus 150
5 Vasculitis 153
Haroon Khan, David G. I. Scott, and Richard A. Watts
Introduction 153
Paper 5.1: Earliest description of systemic vasculitis 155
Paper 5.2: Pathology of giant cell arteritis 157
Paper 5.3: Original description of Kawasaki disease 160
Paper 5.4: Relationship between infection with hepatitis B virus and polyarteritis
nodosa 164
Paper 5.5: The discovery of anti-neutrophil cytoplasmic antibodies as a marker
of Wegener’s granulomatosis 167
Paper 5.6: Definitions and nomenclature of vasculitis—the Chapel Hill Consensus
Conferences, 1994 and 2012 170
Paper 5.7: Development of assessment tools for systemic vasculitis 176
Paper 5.8: Cyclophosphamide as treatment for systemic vasculitis 179
Paper 5.9: Maintenance therapy for systemic vasculitis 181
Paper 5.10: Biologic therapy for systemic vasculitis 184

6 Osteoarthritis 189
Iain Goff and Fraser Birrell
Introduction 189
Paper 6.1: The first description of nodal osteoarthritis 191
Paper 6.2: Arthroplasty of the hip 193
Paper 6.3: Prevalence of symptoms and structural changes of osteoarthritis in the
population 197
Paper 6.4: Effect of age on the prevalence of osteoarthritis 201
Paper 6.5: Predicting progression of osteoarthritis using imaging 205
Paper 6.6: Aerobic exercise and resistance exercise versus an education programme
in knee osteoarthritis 207
Paper 6.7: Glucosamine sulphate for symptoms and progression of knee
osteoarthritis 210
Paper 6.8: Arthroscopy versus sham arthroscopy in knee osteoarthritis 214
Paper 6.9: Association of pain and radiographic change 216
Paper 6.10: Efficacy and toxicity of paracetamol 219

7 Gout and crystal arthropathies 223

Lorna Clarson and Edward Roddy
Introduction 223
Paper 7.1: Identification of urate crystals in gouty synovial fluid 227
Paper 7.2: Molecular identification of a renal urate anion exchanger that regulates
blood urate levels 230
xii CONTENTS

Paper 7.3: Gout-associated uric acid crystals activate the NALP3 inflammasome 234
Paper 7.4: Dietary risk factors for gout 237
Paper 7.5: Gout and coronary heart disease: the Framingham Study 242
Paper 7.6: Allopurinol therapy for gout 246
Paper 7.7: Febuxostat compared with allopurinol in patients with hyperuricemia
and gout 251
Paper 7.8: Can acute attacks of gout be prevented by optimum suppression
of urate? 255
Paper 7.9: Mutations in ANKH cause chondrocalcinosis 258
Paper 7.10: Clinical and radiographic features of pyrophosphate arthropathy 263

8 Paediatric rheumatology 269

Nicola Ambrose, Despina Eleftheriou, and John Ioannou
Introduction 269
Paper 8.1: Comparison of cortisone and aspirin in treatment of juvenile rheumatoid
arthritis 271
Paper 8.2: The treatment of Kawasaki syndrome with intravenous gamma
globulin 274
Paper 8.3: Intra-articular triamcinolone hexacetonide in the management of chronic
arthritis in children 278
Paper 8.4: A USA-USSR double-blind, placebo-controlled trial on methotrexate
in resistant juvenile rheumatoid arthritis 281
Paper 8.5: Preliminary definition of improvement in juvenile arthritis 285
Paper 8.6: Autologous haemopoietic stem-cell transplantation in refractory juvenile
chronic arthritis 288
Paper 8.7: Etanercept in children with polyarticular juvenile rheumatoid arthritis 291
Paper 8.8: Classification of juvenile idiopathic arthritis: second revision, Edmonton,
2001 295
Paper 8.9: Randomized trial of tocilizumab in systemic juvenile idiopathic
arthritis 298
Paper 8.10: Adolescents with chronic disease: transition to adult health care 302

9 Metabolic bone disease 305

Ashok Bhalla and Tehseen Ahmed
Introduction 305
Paper 9.1: Epidemiology of osteoporotic fracture 307
Paper 9.2: Calcium and vitamin D in the prevention of fractures 310
Paper 9.3: Alendronate and reduction of clinical vertebral fractures 313
Paper 9.4: Anabolic therapy in the treatment of osteoporosis 317
Paper 9.5: Atypical femoral fractures 320
Paper 9.6: Bisphosphonates and osteonecrosis of the jaw 325
Paper 9.7: Treatment of Paget’s disease of bone 329
Paper 9.8: Mechanisms of altered calcium homeostasis in sarcoidosis 332
 CONTENTS xiii

10 Ehlers–Danlos syndrome and Marfan syndrome 335

Alan Hakim and Asma Fikree
Introduction 335
Paper 10.1: The clinical and genetic description of Ehlers–Danlos syndrome
as an inherited trait 341
Paper 10.2: Heterogeneity and the classification of Ehlers–Danlos syndrome 343
Paper 10.3: Collagen defects, and genetic linkage in Ehlers–Danlos syndrome 345
Paper 10.4: Genetic linkage in classical Ehlers–Danlos syndrome 347
Paper 10.5: Cardiovascular pathology and Marfan syndrome 349
Paper 10.6: Vascular surgery in Marfan syndrome 351
Paper 10.7: Connective tissue fragility—clinical evidence of the role of transforming
growth factor β in Marfan syndrome 353
Summary 355

Index 357
 Contributors

Nicola Ambrose Despina Eleftheriou

Adolescent and Adult Rheumatologist Arthritis Research UK Centre for
University College Hospital, Adolescent Rheumatology,
London, UK Institute of Child Health,
Tehseen Ahmed University College London, London, UK
Royal National Hospital for Rheumatic Asma Fikree
Diseases, Queen Mary University of London, UK
Bath, UK Hill Gaston
Ashok Bhalla Department of Medicine,
Royal National Hospital for Rheumatic University of Cambridge, UK
Diseases,
Iain Goff
Bath, UK
Department of Rheumatology
Fraser Birrell Northumbria Healthcare NHS Foundation
Institute of Cellular Medicine, Trust, UK
Musculoskeletal Research Group,
Alan Hakim
Newcastle University, UK
Barts Health NHS Trust,
James Bluett London, UK
Centre for Musculoskeletal Research, Queen Mary University of London, UK
Institute of Inflammation
John Ioannou
and Repair,
Arthritis Research UK Centre for
The University of Manchester,
Adolescent Rheumatology University
Manchester Academic Health
College London, London, UK
Science Centre, UK
Haroon Khan
Ian N. Bruce
Department of Rheumatology,
Arthritis Research UK Centre for
Ipswich Hospital NHS Trust, UK
Epidemiology,
Centre for Musculoskeletal Research Elena Nikiphorou
Institute of Inflammation and Repair, Department of Rheumatology,
The University of Manchester, Addenbrooke’s Hospital,
Manchester Academic Health Science Cambridge University Hospitals NHS
Centre, UK Foundation Trust, UK
Lorna Clarson Benjamin Parker
Arthritis Research UK Primary Kellgren Centre for Rheumatology,
Care Centre, Central Manchester University
Keele University, UK Hospitals Foundation Trust, UK
xvi CONTRIBUTORS

Edward Roddy Manchester Academic Health Science

Arthritis Research UK Primary Care Centre, UK
Centre, Suzanne Verstappen
Primary Care Sciences, Centre for Musculoskeletal Research,
Keele University, UK Institute of Inflammation and Repair,
David G. I. Scott The University of Manchester,
Norfolk and Norwich University Manchester Academic Health Science
Foundation NHS Trust Centre, UK
Honorary Professor Adam Young
Norwich Medical School, Department of Rheumatology,
University of East Anglia, UK City Hospital,
Carmel Stober St Albans, UK
Department of Medicine, Richard A. Watts
University of Cambridge School of Consultant Rheumatologist,
Clinical Medicine, UK Ipswich Hospital NHS Trust
Deborah Symmons Honorary Clinical Senior Lecturer,
Centre for Musculoskeletal Research, Norwich Medical School,
Institute of Inflammation University of East Anglia,
and Repair, Department of Rheumatology,
The University of Manchester, The Ipswich Hospital NHS Trust, UK
 Chapter 1

Epidemiology and genetics

James Bluett, Suzanne Verstappen,
and Deborah Symmons

Introduction
Epidemiology
Epidemiology is the study of the distribution and determinants of disease in human popu-
lations. It is applied to describe the prevalence and incidence of a disease, to identify pre-
dictors (genetic and environmental) of the development of disease, and to describe the
consequences of a disease. Understanding the distribution and the burden of diseases
helps health policy makers and the general public to understand the impact of diseases
and injuries across different regions of the world and the need for specific intervention
programmes and better distribution of health care resources. We selected Paper 1.4 as an
excellent example of the estimation of the occurrence/burden of rheumatic and muscu-
loskeletal disorders (RMDs). It was published in The Lancet in 2012 as one of a number
of papers on the global burden of disease, and possible risk factors. This paper showed
that, over the last two decades, the disability-adjusted life years (DALYs) for rheumatoid
arthritis, neck and back pain, and osteoarthritis have increased, whereas the death rate for
rheumatoid arthritis has decreased by ~10%.
Although the Global Burden of Disease study provides the best available estimate of
disease occurrence, these papers also illustrate the challenges epidemiologists face when
estimating the impact of a disease in different countries, and amalgamating data from a
variety of sources, often without case validation. Ideally, to determine prevalence and inci-
dence of a disease, it is important to use validated tools for case definition. We selected two
key papers (Papers 1.1 and 1.2) which demonstrate the development of case definitions for
RMDs. The Kellgren and Lawrence radiological scoring system for osteoarthritis is one of
the first examples of a validated tool in rheumatology. Although the scoring system has
undergone a few minor changes since its introduction 50 years ago, it is often still used to
estimate and compare prevalence rates for osteoarthritis and to assess radiographic dam-
age over time in populations with osteoarthritis in different settings. For rheumatoid arth-
ritis patients, a series of classification criteria sets have been developed by the American
Rheumatism Association/American College of Rheumatology. The 1987 criteria set have
been used extensively, not only to estimate the incidence and prevalence of rheumatoid
2 Epidemiology and genetics

arthritis but also as part of the entry criteria to clinical trials and observational studies.
In the last decade there has been a shift towards earlier classification and treatment of
rheumatoid arthritis. Because of their increased specificity in early rheumatoid arthritis,
the 2010 American College of Rheumatology/European League Against Rheumatism cri-
teria for rheumatoid arthritis are beginning to replace the 1987 criteria in this setting.
Epidemiology studies are also suitable to describe the occurrence and predictors of
long-term consequences of a disease (e.g. co-morbidities, disability, and mortality). Stand-
ardized mortality ratios (SMRs) or standardized incidence ratios (SIRs) are often calcu-
lated, using data from the general population as the reference, to quantify the excess risk
of co-morbidities. Paper 1.3 illustrates one of the first examples of the use of population
registers and record linkage in RMDs. It examined the risk of lymphoma, leukaemia, and
myeloma in patients with rheumatoid arthritis compared to the general population. To
date, this remains one of the largest observational studies showing an increased risk of
lymphoproliferative malignancies in patients with rheumatoid arthritis.

Genetic epidemiology
A genetic basis underlying a number of RMDs has been established using twin and family
studies. Using rheumatoid arthritis as an exemplar, we have selected and go on to discuss
the milestones that have produced step changes in our knowledge of the genetics under-
lying the development of disease.
Paper 1.5, published in 1987 by Gregerson et al., described the shared epitope hypothesis
to explain the association of the human leukocyte antigen (HLA) DRB1 alleles as the major
risk factor for rheumatoid arthritis; the paper is still widely cited and, until very recently, no
other hypotheses could better explain the association observed. The next major milestone
did not occur until 2004, when Begovich et al. (Paper 1.6) discovered the second-largest
genetic risk for the development of rheumatoid arthritis: a protein-coding change in the
PTPN22 gene. Their research not only identified this genetic variant but also investigated
its biological impact and determined that there is a genetic difference between seropositive
and seronegative rheumatoid arthritis, a potential clue in the disease pathogenesis.
As technological capabilities advanced, in 2007 a consortium of scientists from all over
the UK came together to test genetic variants spanning the whole genome (a genome-wide
association study) in order to establish which genetic markers are associated with a num-
ber of autoimmune diseases, including rheumatoid arthritis. The study (Paper 1.7) val-
idated previous research findings and revealed nine new genetic variants associated with
rheumatoid arthritis, greatly expanding our knowledge of the disease. The results from
the Wellcome Trust Case Control Consortium represented a major advance in the gen-
etic understanding of disease, confirmed the importance of large sample sizes to enhance
power to detect modest genetic effects, and demonstrated how a large group of scientists
and clinicians can work together to enhance our understanding of disease.
From whole genome scanning, genetic studies have returned to focusing on particular
sections of the genome. In 2012, technology and expanding cohort numbers enabled the
investigation of the HLA region with fine mapping to determine the true disease-causing
 INTRODUCTION 3

variants. Raychaudhuri et al. (Paper 1.8) discovered three genetic variants within the HLA
DRB1 gene that increase the risk of rheumatoid arthritis independently of each other and
together and explain the association observed better than the previous shared epitope hy-
pothesis. The variants lie within the peptide-binding grove of the HLA molecule, giving
a vital clue to the importance of antigen presentation in the development of seropositive
rheumatoid arthritis. Outside the shared epitope region, researchers have fine-mapped
areas of previous interest, and in 2012 Eyre et al. (Paper 1.9) characterized, by fine map-
ping, over 40% of the known susceptibility areas to rheumatoid arthritis in one analysis.
This paper was among the first to demonstrate, in rheumatoid arthritis, how genetic stud-
ies can identify novel targets for disease treatment.

Gene–environment interaction
The paradigm for the development of RMDs is that one or more environmental risk factors
act in a genetically predisposed host to produce the disease phenotype. This paper (Paper
1.10) was the first to illustrate, statistically, that a genetic risk factor (the shared epitope)
and an environmental risk factor (smoking) interact to enhance disease susceptibility for
rheumatoid arthritis.
4 Epidemiology and genetics

Paper 1.1: Radiological assessment of osteoarthritis—

the Kellgren and Lawrence score
Reference
Kellgren JH, Lawrence JS. Radiological assessment of osteo-arthrosis. Ann Rheum Dis
1957;16(4):494–502.

Purpose
To develop and validate a system for scoring X-rays for the presence and severity of
osteoarthritis.

Study design
The authors selected standard radiographs to represent 5 grades of osteoarthritis: none (0),
doubtful (1), mild (2), moderate (3), and severe (4) for 11 joint areas. The standard radio-
graphs for Grades 1–4 for the distal interphalangeal (DIP) joints, proximal interphalan-
geal (PIP) joints, metacarpophalangeal (MCP) joints, first carpometacarpal (CMC) joints,
wrist, cervical spine, hip, and knee are reproduced in this paper—a forerunner of the much
used Atlas of Standard Radiographs [1]. The other joint areas assessed were the dorsal and
lumbar spine and the feet. Verbal definitions of the radiological features and the grading
criteria are shown in Table 1.1.

Table 1.1 Kellgren and Lawrence grading system of osteoarthritis

Radiological features
- Formation of osteophytes on the joint margins or, in case of the knee joint, on the tibial spines.
- Periarticular ossicles; these are found chiefly in relation to the distal and proximal interpharangeal
joints.
- Narrowing of joint cartilage associated with sclerosis of subchondral bone.
- Small pseudocystic areas with sclerotic walls situated usually in the subchondral bone.
- Altered shape of the bone ends, particular in the head of the femur.
Grading system:
- Grade 0 (none): No features of osteoarthritis.
- Grade 1 (doubtful): Minute osteophyte, doubtful significance.
- Grade 2 (minimal): Definite osteophyte, unimpaired joint space.
- Grade 3 (moderate): Moderate diminution of joint space.
- Grade 4 (severe): Joint space greatly impaired with sclerosis of subchondral bone.
Source data from Kellgren JH, Lawrence JS. Radiological assessment of osteo-arthrosis. Ann Rheum Dis 1957
Dec;16(4):494–502.
 PAPER 1.1: RADIOLOGICAL ASSESSMENT OF OSTEOARTHRITIS 5

The inter-observer and intra-observer reliability of this scoring system was evaluated by
Kellgren and Lawrence themselves using X-rays from a survey of rheumatic diseases in the
Leigh, Lancashire, population, UK. X-rays of a random sample of 85 people aged 55–64
were read by the two observers by comparing these with the standard radiographs. Eleven
joint areas were evaluated and the intervals between the combined and the independent
readings were two months and one month, respectively, after the independent reading.

Results
Inter-observer agreement ranged from 0.10 for the wrist to 0.83 for the knee. Intra-
observer agreement was higher and ranged from 0.42 for the dorso-lumbar spine to 0.88
for the MCP joints. Although, for most joints, the agreement was high, the estimated preva-
lence of the disease varied widely because of the cumulative effect of observer bias (±31%).

Critique of the Kellgren and Lawrence scoring system

Although the scoring system has been extensively used to define osteoarthritis, it has also
been criticized. First, there are some inconsistencies in the description of the radiographic
features leading to discrepancies in study results [2, 3]. Second, there is quite a large em-
phasis on osteophytes. Third, the scoring system is ordinal, and the lower end of the scale
represents different pathological processes involving different tissues from those at the
higher end of the scale. In more recent years, therefore, based on the Kellgren and Lawrence
system, further subcategorization of specific features of individual joints (i.e. hand joints,
knees, and hips) has been established. In addition, new atlases including standard radio-
graphs and better descriptions of the radiographic features have increased the accuracy to
grade osteoarthritis and have helped to improve the internal and external validity [4].

Significance and importance of the paper

After 50 years the Kellgren and Lawrence scoring system, albeit with some minor modifi-
cations, is still used to estimate incidence and prevalence rates and to assess radiographic
progression in osteoarthritis. In the USA, incidence rates (Kellgren and Lawrence ≥2) of
symptomatic hand, hip, and knee osteoarthritis were obtained among members of the Fal-
lon Community Health Plan, a health maintenance organization in central Massachusetts
[5]. Incident cases had joint symptoms at the time or up to one year before the radiographs
and did not have a history of osteoarthritis. The age- and sex-standardized incidence rate
of hand osteoarthritis was 100 per 100,000 person-years (95% confidence interval (CI),
86–115), for hip osteoarthritis, 88 per 100,000 person-years (95% CI, 75–101), and for
knee osteoarthritis, 240 per 100,000 person-years (95% CI, 218–262). Prevalence rates of
radiographic osteoarthritis have been reported in a few studies. In a Dutch study includ-
ing 6,585 randomly selected inhabitants of Zoetermeer, gender- and age-specific osteo-
arthritis prevalence rates of 22 joints were calculated [6]. The prevalence of radiological
osteoarthritis was highest for the cervical spine and increased from 0.3% in women aged
6 Epidemiology and genetics

20–24 to 84.3% in women aged 75–79. In men a similar increase was observed, from 0.7%
to 84.8%. Seventy-five per cent of the women had osteoarthritis (grade ≥2) of their DIP
joints. Severe osteoarthritis was most common in those aged >45 years, and the prevalence
rate exceeded the 20% for the cervical spine and lumbar spine, DIP joints of hands, and,
in women only, MCP joints, first CMC joints, first metatarsophalangeal joints, and knees.
Since the Kellgren and Lawrence score is based on an ordinal scoring system, it is more
difficult to determine annual progression than to assess changes in joint space narrowing
over time. In a systematic review, the annual radiographic progression was calculated as
percentage with change of at least one grade [7]. Including both data from observational
studies and clinical trials, the overall mean risk of Kellgren and Lawrence annual progres-
sion of at least one grade was 5.6 ± 4.9%, with a higher risk associated with shorter disease
duration, and with cohorts that included both incident and prevalent cases. This overview
also showed that patients with a Kellgren and Lawrence score ≥2 at inclusion into a study
have a higher risk of progression than those recruited with a Kellgren and Lawrence score
≥1 (6.2% vs 3.3%).

References
1 Kellgren JH., Lawrence JS. The epidemiology of chronic rheumatism. Atlas of standard radiographs.
Oxford: Blackwell Scientific;1963.
2 Spector TD, Cooper C. Radiographic assessment of osteoarthritis in population studies: whither
Kellgren and Lawrence? Osteoarthr Cartil 1993;1(4):203–6.
3 Arden N, Nevitt MC. Osteoarthritis: epidemiology. Best Pract Res Clin Rheumatol 2006;20(1):3–25.
4 Altman RD, Gold GE. Atlas of individual radiographic features in osteoarthritis, revised. Osteoarthr
Cartil 2007;15(Suppl A):A1–56.
5 Oliveria SA, Felson DT, Reed JI, Cirillo PA, Walker AM. Incidence of symptomatic hand, hip,
and knee osteoarthritis among patients in a health maintenance organization. Arthritis Rheum
1995;38(8):1134–41.
6 van Saase JL, van Romunde LK, Cats A, Vandenbroucke JP, Valkenburg HA. Epidemiology of
osteoarthritis: Zoetermeer survey. Comparison of radiological osteoarthritis in a Dutch population
with that in 10 other populations. Ann Rheum Dis 1989;48(4):271–80.
7 Emrani PS, Katz JN, Kessler CL, et al. Joint space narrowing and Kellgren-Lawrence progression in
knee osteoarthritis: an analytic literature synthesis. Osteoarthr Cartil 2008;16(8):873–82.
 PAPER 1.2: RHEUMATOID ARTHRITIS AND LYMPHOMA 7

Paper 1.2: The association between rheumatoid arthritis

and lymphoma
Reference
Isomäki HA, Hakulinen T, Joutsenlahti U. Excess risk of lymphomas, leukemia and mye-
loma in patients with rheumatoid arthritis. J Chron Dis 1978;31(2):691–6.

Purpose
To compare the incidence of malignancy in patients entitled to free medication for
rheumatoid arthritis in Finland with that in the general Finnish population matched for
age and gender.

Population studied
The population studied comprised patients on the Finnish Social Insurance Institution’s
Population Data Register (started in 1965) as being entitled to reimbursable medication
for ‘rheumatoid arthritis’. The term ‘rheumatoid arthritis’ included systemic connective
tissue disease until 1970 (1.7% of cases) and ankylosing spondylitis since 1970 (2.2% of
all cases).

Study design
This paper describes a longitudinal observational study using population registers. Details
of patients entitled to reimbursable medication for ‘rheumatoid arthritis’ from 1967–1973
were linked to the Finnish Cancer Registry in order to identify all new cancer cases diag-
nosed from 1 January 1967 or the date of the first rheumatoid arthritis prescription until
31 December 1967 or death. The numbers of various types of malignancy observed were
compared with those expected in the general Finnish population matched for age and sex.

Results
The study follows 11,483 men and 34,618 women with ‘rheumatoid arthritis’ for 213,911
years. The authors report 1,202 incident malignancies as compared to the 1,137.89
expected.
The authors report that the incidence of cancer of the respiratory organs, lymphoma,
myeloma, and leukaemia was increased in men with rheumatoid arthritis (Table 1.2). Al-
though the overall incidence of malignancy was not increased in women, the incidence of
Hodgkin’s disease, lymphoma, and myeloma was increased.

Critique of the paper

There are two weaknesses in the composition of the rheumatoid arthritis cohort: (i) no
case definition was used beyond the requirement of medication for a condition labelled
as rheumatoid arthritis by the physician in charge of the case, and (ii) there was ‘contam-
ination’ of the cohort with cases of connective tissue disorder and ankylosing spondylitis.
8 Epidemiology and genetics

Table 1.2 Occurrence of malignancies by site

Sex Primary site Observed Expected P value SIR (95% CI)*

number number
Male All 407 354.11 <0.01 1.14 (1.04–1.27)
Respiratory organs 171 132.75 <0.01 1.28 (1.10–1.50)
Hodgkin’s disease 5 2.28 NS 2.10 (0.71–5.12)
Lymphoma 13 4.84 <0.01 2.69 (1.43–4.59)
Myeloma 7 3.26 <0.05 2.15 (0.86–4.42)
Leukaemia 18 7.10 <0.01 2.54 (1.50–4.01)
Female All 795 783.78 NS 1.01 (0.94–1.09)
Hodgkin’s disease 14 4.54 <0.01 3.08 (1.69–5.17)
Lymphoma 25 9.34 <0.01 2.68 (1.73–3.95)
Myeloma 21 9.49 <0.01 2.21 (1.37–3.38)
Leukaemia 27 18.74 NS 1.44 (0.95–2.10)
* CI, confidence interval; SIR, standardized incidence ratio. Calculated using a Poisson distribution around the observed
number. Not presented in the original paper.

In addition, the paper was published before the widespread calculation of relative risk and
95% CI. We have included these in Table 1.2 for completeness. In addition the authors do
not address the possible reasons for the link beyond speculating that in some way patients
are susceptible to both rheumatoid arthritis and lymphoproliferative malignancies.

Significance and importance of the paper

This is one of the earliest examples in rheumatology of the use of population registers and
record linkage to address an important epidemiological question. The Scandinavian coun-
tries are ideally placed to conduct such studies as the use of a unique identification number,
and the existence of a large number of population-based registers makes linkage relatively
straightforward. This was the first study to use this design to address the hypothesis of an
increased risk of lymphoproliferative malignancies in patients with rheumatoid arthritis
and remains the second largest study conducted to date [1]. A meta-analysis published in
2008 of 14 studies published between 1990 and 2007 found an overall twofold increase risk
of lymphoma in rheumatoid arthritis (SIR: 2.08; 95% CI, 1.80 –2.39)—very similar to that
reported by Isomäki [2]. In recent years we have seen an elegant demonstration that the
risk of lymphoma in rheumatoid arthritis is associated with cumulative disease activity and
exposure to immunosuppressive medications such as azathioprine [3, 4]. There was con-
siderable concern at the time of their introduction that anti-tumour necrosis factor therapy
might further increase the risk of lymphoma—but this has not been borne out with time.
The Isomäki paper continues to provide a useful benchmark with which to compare more
recent studies conducted in an era when treatment of rheumatoid arthritis has improved
dramatically and one might therefore expect the excess risk of lymphoma to diminish.
 PAPER 1.2: RHEUMATOID ARTHRITIS AND LYMPHOMA 9

References
1 Parikh-Patel A, White RH. Risk of cancer among rheumatoid arthritis patients in California. Cancer
Causes Control 2009;20(6):1001–10.
2 Smitten AL, Simon TA, Hochberg M, Suissa S. A meta-analysis of the incidence of malignancy in
adult patients with rheumatoid arthritis. Arthritis Res Ther 2008;10(2):45.
3 Baecklund E, Iliadou A, Askling J, et al. Association of chronic inflammation, not its treatment, with
increased lymphoma risk in rheumatoid arthritis. Arthritis Rheum 2006;54(3):692–701.
4 Asten P, Barrett J, Symmons D. Risk of developing certain malignancies is related to duration
of immunosuppressive drug exposure in patients with rheumatic diseases. J Rheumatol
1999;26(8):1705–14.
10 Epidemiology and genetics

Paper 1.3: The American Rheumatism Association 1987 revised

criteria for the classification of rheumatoid arthritis
Reference
Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association
1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum
1988;31(3):315–24.

Purpose
The 1987 American Rheumatism Association/American College of Rheumatology criteria
for rheumatoid arthritis were developed in order to improve specificity and sensitivity and
additionally to improve simplicity, as compared to the 1958 American Rheumatism Asso-
ciation criteria. [1–4]

Participants and patients

In this study, 262 consecutive patients with rheumatoid arthritis and 262 control patients
with a rheumatic disease other than rheumatoid arthritis (e.g. osteoarthritis, systemic
lupus erythematosus, psoriatic arthritis, or other), including both new and established pa-
tients, were selected by the nine rheumatologist members of a subcommittee of the Diag-
nostic and Therapeutic Criteria Committee of the American College of Rheumatology
and 32 other rheumatologists. The certainty of the patient having rheumatoid arthritis was
estimated by the rheumatologist on a 10 cm visual analogue scale.

Study design
The evaluated criteria set included the individual items of the old American Rheumatism
Association and New York criteria (Table 1.3) for rheumatoid arthritis and items con-
sidered to be important by the committee following a Delphi method procedure. Two stat-
istical approaches were applied to develop the classification criteria. First, combinations of
variables which were most sensitive and specific to the classification of rheumatoid arth-
ritis were selected by means of Boolean algebra; for example, a patient would be classi-
fied as having rheumatoid arthritis if at least X out of Y criteria were present. The second
method involved selecting variables which best discriminated rheumatoid arthritis pa-
tients from controls using a ‘classification tree’. All analyses were repeated for patients with
‘new’ disease and for patients with established disease. Finally, the specificity of the two
methods was tested against 137 consecutive subjects enrolled in a USA prospective study.

Results
Items selected by the committee included morning stiffness, pain on motion in joints,
swelling in ≥3 joint areas, symmetric swelling, subcutaneous nodules, abnormal rheuma-
toid factor, and radiological findings. The accuracy, calculated as the mean of sensitivity
and specificity, of these individual items varied from 50.3 for pain on motion of the distal
interphalangeal joint to 87.4 for swelling of ≥3 joint areas upon physical examination. The
 PAPER 1.3: AMERICAN RHEUMATISM ASSOCIATION REVISED CRITERIA 11

Table 1.3 Comparison of items included in the American

Rheumatism Association criteria and the New York criteria

Item American Rheumatism New York

Association criteria criteria
Morning stiffness X
Joint pain X X
One joint swollen X
Two joints swollen X
Symmetric swelling X
Joint swelling X
Rheumatoid nodules X
Serum rheumatoid factor X X
Mucin clot X
Synovial biopsy X
Nodule biopsy X
Radiographic findings X X

Table 1.4 The 1987 revised criteria for the classification of rheumatoid arthritis (list format)*

Criterion Definition
1. Morning stiffness Morning stiffness in and around the joints, lasting at least one hour before
maximal improvement.
2. A
 rthritis of three At least three joint areas simultaneously have had soft tissue swelling or
or more joint areas fluid (not bony overgrowth alone) observed by a physician. The 14 possible
areas are right or left PIP, MCP < wrist, elbow, knee, ankle, and MTP joints.
3. Arthritis of hand joints At least one area swollen in a wrist, MCP, or PIP joint.
4. Symmetric arthritis Simultaneous involvement of the same joint areas (as defined in Criterion 2)
on both sides of the body (bilateral involvement of PIP, MCP, or MTP joints is
acceptable without absolute symmetry).
5. Rheumatoid nodules Subcutaneous nodules, over bony prominences, or extensor surfaces, or in
juxtaarticular regions, observed by a physician.
6. S erum rheumatoid Demonstration of abnormal mounts of serum rheumatoid factor by any
factor method for which the result has been positive in <5% of normal controls.
7. Radiographic changes Radiographic changes typical of rheumatoid arthritis on posterior/anterior
hand and wrist radiographs, which must include erosions or unequivocal
bony decalcification localized in or marked adjacent to the involved joints
(osteoarthritis changes alone do not qualify).
* For classification purpose, a patient shall be said to have rheumatoid arthritis if he/she has satisfied at least four of
these seven criteria. Criteria 1 through 4 must have been present for at least 6 weeks. Patients with Criterion 2 clin-
ical diagnoses are not excluded. Designation as classic, definite, or probable rheumatoid arthritis is not to be made;
DIP, distal interphalangeal; PIP, proximal interphalangeal; MCP, metacarpophalangeal; MTP, metatarsophalangeal.
Source data from Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised cri-
teria for the classification of rheumatoid arthritis. Arthritis Rheum 1988 Mar;31(3):315–24.
12 Epidemiology and genetics

final seven criteria and their definitions included in the 1987 criteria for rheumatoid arth-
ritis are shown in Table 1.4. To be classified as having rheumatoid arthritis, patients had
to satisfy at least four out of these seven criteria. The criteria included in the classification
tree were slightly different and did not include morning stiffness or rheumatoid nodules
(Figure 1.1) [5]. Compared to the 1958 American Rheumatism Association and New York
criteria, the sensitivity and specificity improved for the revised classification criteria and
classification tree to 91.2% and 93.5%, respectively, for sensitivity and to 89.3% and 89.3%,
respectively, for specificity.

Arthritis of 3
or more joints
Yes No

X-ray changes RF
(swelling of MCP joints) (wrist swelling)

No Yes

RF
(wrist swelling) Symmetry

No No

Yes Yes Yes No

Swelling of MCP Swelling of MCP
and wrist or wrist

Yes No Yes No

RA RA RA IP RA RA IP IP

Fig. 1.1 Tree format of the American College of Rheumatology 1987 criteria for the classification
of rheumatoid arthritis, as applied to patients with inflammatory polyarthritis; IP, inflammatory
polyarthritis; MCP, metacarpophalangeal; RA, rheumatoid arthritis; RF, rheumatoid factor.

Critique of the 1987 criteria

The main criticism of the 1987 criteria for rheumatoid arthritis is that they were developed
in a cohort of patients with established rheumatoid arthritis. The specificity of the criteria
was especially low in patients with early rheumatoid arthritis. The pooled sensitivity and
specificity of the 1987 criteria in early rheumatoid arthritis (<1 year disease duration) were
77% (68%–84%) and 77% (68%–84%), respectively, for the list format and 80% (72%–
88%) and 33% (24%–43%), respectively, for the tree format [6]. In established rheumatoid
arthritis, the pooled sensitivity and specificity were respectively 79% (71%–85%) and 90%
(84%–94%), respectively, versus 80% (71%–85%) and 93% (86%–97%), respectively. In the
 PAPER 1.3: AMERICAN RHEUMATISM ASSOCIATION REVISED CRITERIA 13

last decade it has been shown that early and aggressive treatment of inflammatory arthritis
is clinically more beneficial, resulting in less accrual joint damage and long-term disability
[7–9]. If the 1987 criteria for rheumatoid arthritis are used to determine which patients
should be included in treatment studies, or even as a guide in clinic for treatment deci-
sions, those who might benefit most from early intensive treatment would be excluded.
For these reasons, new criteria showing better specificity were developed and published
in 2010 [10–12].
A further criticism is in the selection of the comparison cohort. Many of the patients
included in the comparison cohort had non-inflammatory conditions which are easily
distinguishable from rheumatoid arthritis. In studies of criteria development, the com-
parison group should have diseases which have features in common with the disease
under study.
Finally, unlike the 1958 criteria, there are no exclusions included in the 1987 criteria.
Thus it is possible, for example, for someone with classical gout to also be classified as hav-
ing rheumatoid arthritis if they happen to fulfil the 1987 criteria.

Significance and importance of the paper

In the 30 years following the publication of the 1987 criteria for rheumatoid arthritis, the
criteria have been used extensively as entry criteria in clinical trials and for observational
studies. This has facilitated generalisability of the results of such studies. Due to a lack
of diagnostic criteria for rheumatoid arthritis, the criteria have also been widely used in
practice for diagnosis. Furthermore, incidence rates, based on the 1987 criteria, have been
reported among different populations, ranging from 0.1 cases per 1,000 for France to 0.5
cases per 1,000 for the USA [13]. Prevalence rates range from 1.8 cases (crude rate) per
1,000 in Yugoslavia to 10.7 cases per 1,000 in the USA.

References
1 Bennett GA, Cobb S, Jacox R, Jessar RA, Ropes MW. Proposed diagnostic criteria for rheumatoid
arthritis. Bull Rheum Dis 1956;7(4):121–4.
2 Cobb S, Merchant WR, Warren JE. An epidemiologic look at the problem of classification in the field
of arthritis. J Chronic Dis 1955;2(1):50–4.
3 Cobb S, Thompson DJ, Rosenbaum J, Warren JE, Merchant WR. On the measurement of prevalence
of arthritis and rheumatism from interview data. J Chronic Dis 1956;3(2):134–9.
4 Ropes MW, Bennett GA, Cobb S, Jacox R, Jessar RA. 1958 Revision of diagnostic criteria for
rheumatoid arthritis. Bull Rheum Dis 1958;9(4):175–6.
5 Lunt M, Symmons DP, Silman AJ. An evaluation of the decision tree format of the American College
of Rheumatology 1987 classification criteria for rheumatoid arthritis: performance over five years in a
primary care-based prospective study. Arthritis Rheum 2005;52(8):2277–83.
6 Banal F, Dougados M, Combescure C, Gossec L. Sensitivity and specificity of the American College
of Rheumatology 1987 criteria for the diagnosis of rheumatoid arthritis according to disease duration:
a systematic literature review and meta-analysis. Ann Rheum Dis 2009;68(7):1184–91.
7 Combe B, Landewe R, Lukas C, et al. EULAR recommendations for the management of early
arthritis: report of a task force of the European Standing Committee for International Clinical Studies
Including Therapeutics (ESCISIT). Ann Rheum Dis 2007;66(1):34–45.
Exploring the Variety of Random
Documents with Different Content
 242 DESSERTS, CUSTARDS AND CREAMS TRIFLE Sponge
cake, soaked in sherry wine; chopped figs and a pint of almond
custard, large cup of strawberry jam, one pint of cream, whipped,
for top. GINGER CREAM Cut four ounces of prepared ginger in dice;
put one ounce of gelatine into a saucepan with a pint of milk and
four tablespoonfuls of sugar. Let it boil slowly, stirring all the time till
the gelatine is dissolved, then add ginger. When cool add one pint of
whipped cream. Pour in dampened mould to form. PINEAPPLE
CREAM One can of pineapple (grated), three ounces of loaf sugar,
half a pint of water, three-quarters of an ounce of gelatine, one and
a half pints of cream. Drain syrup from pineapple and put in half a
pint of water and sugar in sauce-pan. When dissolved add fruit,
boiling ten minutes, then add gelatine and boil ten minutes longer.
When entirely cold add the cream, well whipped, and pour in
moulds. RUSSIAN CREAM 1 box gelatine. f cups sugar. 1 qt. milk. 4
eggs. Soak gelatine in cup of milk, add to rest of milk, heated. Add
yolks of eggs and sugar. Cook until smooth. Remove from stove and
add whites of eggs. Pour in mould to cool. SAUCE Three eggs, three
ounces sugar, half pint of whipped cream measured after being
whipped, half glass of chartreuse ; whip eggs and sugar over boiling
water for ten minutes; then remove and whip until cold, then add
cream and chartreuse.
 DESSERTS, CUSTARDS AND CREAMS 243 SOUFFLE 2 oz.
butter. oz. flour. Yolks of 4 eggs. Whites of 6 eggs. 1 teaspoonful
vanilla. 2 oz. chocolate. 2 oz. sugar. 1 gill cream. Melt butter and
flour, then add cream; cook two minutes; add chocolate and stir till
melted. Remove from fire and let cool, then add yolks and, just
before steaming, add whites stiffly beaten; fold them in gently;
steam one hour and a half. Steam in mould placed in saucepan of
hot water; let water come half way up mould ; put mould in bottom
of saucepan and cover with a greased paper, and then cover
saucepan. Do not let water boil. Six lemons, four eggs (the whites),
two pints sugar. Make a thick syrup of one pint sugar and about one
pint water; when cold, thin with the juice of six lemons, and water
enough to make it a rich lemonade. When it is half frozen add boiled
icing, made as follows: One pint sugar moistened with water, and
boiled until it is a soft candy; whilst hot add the stiff beaten whites
of four eggs. Flavor with vanilla and a little citric acid or cream tartar,
and beat hard until thick and smooth, and add to the half frozen
lemonade. Soak gelatine for several hours in pint of cold water, grate
the rinds of lemons, add with the juice of the lemons the LEMON
SHERBET WINE JELLY 1 box gelatine. 1 pt. cold water. 1 cup sugar.
2 lemons. 2 eggs. 1 pt. hot water. ^ cup wine. Wine glass whisky.
 244 DESSERTS, CUSTARDS AND CREAMS whites and shells
of two eggs, hot water (not boiling), wine, whisky, some cinnamon
and sugar and let all boil ; skim and strain through flannel bag, add
large cup sugar and remainder of wine and put in mould to cool.
LEMON JELLY 1 box gelatine. 1 pt. sugar. 1 pt. hot water. 2 lemons,
juice and rind. ■J pt. wine. Whites 3 eggs. Soak gelatine for one
hour in a pint of cold water, then add hot water, wine, sugar, lemons,
juice and thinly pared rind. Boil for one-half a minute and strain.
This with wine left out. Whites of three eggs (beaten to a stiff froth
and stirred in before quite cold), and put in mould. FRUIT JELLY 1
box gelatine. 1 cup sugar. 2 lemons. •J pt. cold water. pts. boiling
water. Fruits : Peaches, bananas, oranges, sliced. Dissolve gelatine in
one-half pint cold water, add sugar and lemon juice, with boiling
water. Let this stand until the jelly begins to thicken, then pour a
little into the mould: place on it a layer of peaches, cut any shape
desired. Put in more jelly and fruit, alternately until the mould is
filled. Place on ice to set and serve with whipped cream. Care should
be taken to allow each layer of fruit and jelly to set before putting in
another, so that the fruit will not fall together. PRUNE JELLY One pint
of prunes, half a box of gelatine, sugar to taste, and a pinch of salt.
Wash the prunes, then boil slowly till
 DESSERTS, CUSTARDS AND CREAMS 245 soft in sufficient
water to cover. Take out the stones, sweeten to taste ; add essence
of vanilla, or if preferred the juice and rind of a lemon, and the juice
of two oranges. Soak the gelatine till soft, then add the above, stir
all well together, and pour into a mould and let stand till it is very
cold. One pound of prunes, well washed, then covered with water
and allowed to soak for six hours. Put on to boil in same water until
tender; add sugar, and boil ten minutes; strain and remove stones.
Take gelatine soaked in one cup of water. Put on stove juice from
prunes equal to two and a half cupfuls; add juice of lemon and
orange. When this commences to boil add gelatine and prunes. Turn
into mould and serve when cold with whipped cream. One pound of
stewing prunes, wash well and leave them to soak about an hour. In
the meantime put half a package of gelatine to soak, then take the
prunes and put them on a saucepan on the fire, well covered with
water and about half a cupful of sugar. Boil for about an hour. Strain
the juice from the prunes, then add the gelatine to the juice and put
on the fire to boil up. Cover the prunes with the juice and gelatine
mixed, put in hot in a mould and leave till cold. Serve with whipped
cream. PRUNE JELLY 1 lb. prunes. 1 lb. sugar. 1 oz. gelatine. 1
orange. 1 lemon. Whipped cream. PRUNE JELLY APPLE SPONGE 1 lb.
apples. J oz. gelatine. 1 lb. sugar. Juice of 2 lemons. Kind of 1
lemon. J pt. boiling water.
 246 DESSERTS, CUSTARDS AND CREAMS Boil the water
and sugar in a saucepan until dissolved. Peel and slice the apples
thinly, and add to the syrup, and stew until tender. Add gelatine, and
strain all through a sieve; add lemon juice and rind and beat until
cool. Beat the whites of three eggs stiffly and add to the mixture,
and beat all until cold. Put into a mould; serve with custard.
COMPOTE OF CHESTNUTS (FRANC ATELLI) 50 chestnuts. 3 oranges.
1 qt. milk and water. \ pt. cream. 12 oz. sugar. Maraschino. Oranges
quartered and soaked in maraschino. Whipped cream. Remove husks
and skin from the chestnuts, and boil gently in the milk and water
until like floury potatoes, and strain them. Boil the sugar until it purls
on the surface and flavor with vanilla bean ; add the chestnuts and
work all together vigorously, and rub through a potato masher on to
a dish. Pile up whipped cream in the centre of a dish, and gently
strew the chestnuts on top of the cream in a conical form; garnish
with orange quarters at the base of the cream and nuts. PRINCE OF
WALES DESSERT Take sponge cakes, stale preferred ; dip in sherry
or syrup and line a mould with them. Take three-quarters pound
cornflour, one ounce arrowroot, and mix together; add one pint
boiling milk and cook a few minutes; add one teaspoon vanilla and
pour this into the lined basin. When cold turn out. Put a large
spoonful of red currant jelly on the top, and sprinkle well with
chopped pistachio nuts. This may be varied by putting the cakes
soaked in raspberry juice or wine in a glass dish; fill as above over
the top of this. When cold spread whipped cream; decorate with
cherries
 DESSERTS, CUSTARDS AND CREAMS 247 and chopped
citron peel. Serve very cold and in the glass dish in which it was
made. The latter looks very pretty when complete. One quart milk,
yolks two eggs, one cup white sugar, two tablespoons cornstarch,
one-half large cup of caramel. Stir all together carefully, cooking in a
double boiler. Serve cold, with whipped cream. To make the caramel.
— Two cups white sugar, one-half cup water. Put on a hot fire in a
frying-pan, and stir constantly until it burns a dark brown color and
becomes liquid. Remove from the fire and add one-half large cup of
boiling water. Set away when cool in a jar for use. .Will keep for
weeks. Pour boiling water over a quart of plums, let them stand long
enough to soften the skins, but not to break them open ; pour off
the water and when cool peel and remove the stones, taking care to
save all the juice. Soak half a box of gelatine in a cup of cold water.
Stew the plums until tender after adding a cup of water ; sweeten to
taste ; then stir the whole while hot into the gelatine. Serve with
whipped cream. Lemon juice or wine may be used with the water, if
liked. One quart of cream, one small cup of sugar, one tablespoonful
of vanilla. Mix sugar and flavoring with cream. When the sugar is
dissolved strain into the freezer. CARAMEL CUSTARD PLUM SHAPE
PHILADELPHIA ICE CREAM SPANISH CREAM 1 box gelatine. 1J pts.
milk. 3 eggs, beaten separately. 3 tablespoonfuls sugar.
 248 DESSERTS, CUSTARDS AND CREAMS Dissolve gelatine
on top of kettle, boil milk ; add gelatine, stirring it in quickly, then
add yolks of eggs, beaten with sugar. When well scalded take off the
fire and stir the whites in, well beaten; flavor to taste and put into
mould. BURNT CREAM 1 qt. milk. 1 lb. brown sugar. 4 tablespoonfuls
cornstarch. -J pt. cream, whipped. A few walnut meats. Boil milk, stir
in cornstarch, add a few broken walnuts. Put in a saucepan one
pound of brown sugar, let it brown as dark as possible, then add the
milk ; after the milk is thick beat well together and turn into a
mould. Decorate with half walnuts around, or solitaire moulds with a
half walnut on top, whipped cream around dish. APPLE CHARLOTTE
\ lb. breadcrumbs. \ lb. brown sugar. 1 lb. apples. 1 grated rind of
lemon. 2 oz. suet, chopped. Butter a pie dish and sprinkle it with
sugar. Mix suet and bread-crumbs together, put a layer of apple in
small pieces, sugar and rind of lemon, then suet and crumbs; repeat
until dish is full. Bake thirty or forty minutes. Turn out. GINGER
CREAM Make a custard of a gill of milk, one ounce of sugar, the
beaten yolks of three eggs. Stir in a double boiler until thick, let it
cool, then add one gill of the syrup from the jar of preserved ginger,
and two ounces of the ginger cut up; add three-quarters ounce, full
weight, of gelatine melted in as little water as possible. Last of all
add one-half pint of
 DESSERTS, CUSTARDS AND CREAMS 249 whipped cream.
Mix gently until well blended, pour into a mould and set on ice. RICH
CHOCOLATE TORTE (GERMAN) $ lb. chocolate. Yolks of 7 eggs. i lb.
pounded almonds. Bread or cracker crumbs. J lb. sugar. Beat yolks
very light with sugar, add chocolate, melted, almonds pounded, and
last the whites of eggs beaten very stiff. Butter a flat shallow pan
with unsalted butter, and sift in finely rolled cracker or bread crumbs.
Pour in the mixture and cook half an hour in a moderate oven. Must
be cut while hot into cubes. Will keep well for weeks.
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DESSERTS, CUSTARDS AND CREAMS WRITTEN RECIPES

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DESSERTS, CUSTARDS AND CREAMS WRITTEN KECIPES

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DESSEETS, CUSTARDS AND CREAMS WRITTEN KECIPES

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DESSERTS, CUSTARDS AND CREAMS WKITTEN RECIPES

 PASTRY, PIES AND TARTS Use the very best materials in
making pastry ; the shortening should be fresh, sweet, and hard;
the water cold (ice water is best), the paste rolled on a cold board,
and all handled as little as possible. "When the crust is made, it
makes it much more flaky and puff much more to put it in a dish
covered with a cloth, and set in a very cold place for half an hour, or
even an hour ; in summer, it could be placed in the ice box. A great
improvement is made in pie-crust by the addition of about a heaping
teaspoonful of oaking-powder to a quart of flour, also brushing the
paste as often as rolled out, and the pieces of butter placed thereon,
with the white of an egg, assist it to rise in leaves or flakes. As this is
the great beauty of puff-paste, it is as well for housekeepers to try
this method. If currants are to be used in pies, they should be
carefully picked over, and washed in several waters, dried in a towel,
and dredged with flour before they are suitable for use. Raisins, and
all dried fruits for pies and cakes, should be seeded, stoned, and
dredged with flour, before using in cooking. Almonds should be
blanched by pouring boiling water upon them, and then slipping the
skin off with the fingers. In pounding them, always add a little rose
or orange water, with fine sugar, to prevent their becoming oily.
Great care is requisite in heating an oven for baking pastry. If you
can hold your hand in the heated oven while you count twenty, the
oven has just the proper temperature, and 254
 PASTRY, PIES AND TARTS 255 it should be kept at this
temperature as long as the pastry is in ; this heat will bake to a light
brown, and will give the pastry a fresh and flaky appearance. If you
suffer the heat to abate, the under crust will become heavy and
clammy, and the upper crust will fall in. Another good way to
ascertain when the oven is heated to the proper degree for puff-
paste ; put a small piece of the paste in previous to baking the
whole, and then the heat can thus be judged of. Pie-crust can be
kept a week, and the last be better than the first, if put in a tightly
covered dish, and set in the icechest in summer, and in a cool place
in winter, and thus you can make a fresh pie every day with little
trouble. In baking custard, pumpkin or squash pies, it is well, in
order that the mixture may not be absorbed by the paste, to first
partly bake the paste before adding it, and when stewed fruit is used
the filling should be perfectly cool when put in, or it will make the
bottom crust sodden. This quantity gives enough for three or four
pies. Cottolene makes good pastry. The shortening may be mixed,
but the flavor is better where butter alone is used. The richness of
pastry depends upon the amount of shortening used. Sift the salt
and flour together, reserving a little flour for the board. With a knife,
cut the butter into the flour. Add the water a little at a time, and mix
it in lightly with the knife ; turn it on to the board, and roll it twice —
that is, after it is rolled out once, fold it together and roll it again. If
the paste is wanted richer for the top crust, put bits of butter over
the paste when rolled; fold and roll it again several PLAIN PASTRY
FOR PIES 1 qt. flour. 1 cupful butter. 1 cupful cold water. 1
teaspoonful salt. (Half butter and half lard or cottolene will do.)
 256 PASTRY, PIES AND TARTS times. Fold the paste, and
put it in the ice-box for an hour before using, keeping it covered. In
making pastry everything should be cold, the handling light, and the
hands used as little as possible. Paste will keep several days in a cool
place, but should be rolled in a napkin, so it will not dry and form a
crust. To Put a Pie Together. — Roll the paste one-eighth inch thick,
and a little larger than the tin. Dust the pan with flour ; place the
paste on it, letting it shrink all it will. Lift it from the sides to fit into
place, and press it as little as possible. Cut a narrow strip of paste,
and lay around the edge ; moisten it so it will stick. Brush the top of
the bottom crust with white of egg, so the filling will not soak in and
make it heavy. Put in the filling, and cover with another sheet of
pastry. Moisten the top of the strip of pastry so the top crust will
adhere to it ; this gives three layers around the edge. Trim and press
them lightly together. Cut several slits in the top crust to let the
steam escape in cooking. A thin piece of paste cut into fancy shape
can be placed in the centre for ornament if desired. PASTEY FOE
TAEXS OE OPEN PIES 2 cups flour. 1 tablespoonful sugar. | cupful
butter. Yolks of 2 eggs. i teaspoonful salt. Water. Sift the flour, salt,
and sugar together. Cut in the butter as directed above. Mix in the
beaten yolks, then enough water to make a paste which is not very
stiff ; roll it two or three times, then wrap it in a cloth, or cover it
closely, and put it in the ice-box for an hour. This gives enough paste
for four small tarts. ICING FOE PASTEY To ice pastry, which is the
usual method adopted for fruit tarts and sweet dishes of pastry, put
the white of an egg on
 PASTRY, PIES AND TARTS 257 a plate, and with the blade
of a knife beat to a stiff froth. When the pastry is nearly baked,
brush it over with this, and sift over some pounded sugar ; put it
back into the oven to set the glaze, and in a few minutes it will be
done. Great care should be taken that the paste does not catch or
burn in the oven, which it is very liable to do after the icing is laid
on. Or make a meringue by adding a tablespoonful of white sugar to
the beaten white of one egg. Spread over the top, and slightly
brown in the oven. 2 tablespoonfuls cornstarch. \\ cups water. Grate
the rind and squeeze the juice of the lemons; beat eggs light and
melt the butter. Mix all together. Make a puff paste and line the tins
with the pastry. Brush over with the white of an egg and fill with the
lemon mixture and bake. LEMON PIE AND TAETS 2 lemons. 2 eggs.
2 cups sugar, scant. Butter size of egg. MINCE MEAT FOE PIES 5 lbs.
beef. 3 lbs. suet. 3 lbs. raisins. 3 lbs. currants. \ pk. apples. 1 cup
molasses. 1 cup beef liquor. 1 pt. brandy. 1 tablespoonful salt. 2 lbs.
sugar. 1 dessertspoonful each cinnamon, cloves, ginger, allspice.
Chop beef, suet, apples, raisins, add spices and mix well; then add
liquid ingredients. Cook for four or five hours on back of stove.
 258 PASTRY, PIES AND TARTS OLD. COUNTRY MINCE
MEAT 2 lbs. raisins. 1 small nutmeg. 3 lbs. currants. 2 lbs. apples.
lbs. lean, chopped beef. 2 lemons, juice of one anl 3 lbs. beef suet,
chopped. rind of two. 2 lbs. brown sugar. J pt. brandy. 6 oz. mixed
candied peel. Stone the raisins and chop; wash the currants and dry;
slice the peel thinly, grate the nutmeg, pare, core, and mince the
apples, peel lemon and strain the juice. Get all your dry ingredients,
including of course the beef (uncooked) and suet, well mixed; add
the lemon-juice and brandy last, and press the mixture into a jar
that will exclude the air. Set away for a fortnight before using.
MINCE MEAT (WITH BEEF) 2 lbs. boiled beef (chopped). 2 lbs.
powdered sugar. 2 lbs. beef suet. 1 qt. whisky. 4 lbs. apples. 1
wineglass rose water. 2 lbs. raisins. 2 grated nutmegs. 2 lbs.
currants. -J oz. cinnamon. 1 teaspoonful salt. i oz. each cloves and
mace. 2 oranges, large. J lb. citron, sliced. Chop beef, suet, oranges,
apples. Add spices, then liquids and cook 3 or 4 hours, slowly. Keep
in jars tightly covered and set in a dry, cool place. MINCE MEAT IN
1812 1 lb. chopped suet. 1 teacupful brandy. 1 lb. chopped beef. 2
lbs. sultana raisins. 1 qt. apple cider. 2 lbs. currants. 1 pt. molasses.
J lb. citron or lemon peel. 1 pt. preserved grapes. Allspice,
cinnamon, and 1 lb. brown sugar. cloves to taste.
 PASTRY, PIES AND TARTS 25S Simmer for half a day on the
back of the stove till thoroughly cooked. Put in a cool place in an
earthen jar. If a very moist mince meat is preferred, add cider to
each pie when baking ; have crust very short. MINCE MEAT
(WITHOUT BEEF) 1 lb. chopped suet. 2 lbs. seeded raisins. 2 lbs.
currants. 2 lbs. apples. 2J lbs. sugar. 2 nutmegs grated. 1
teaspoonful salt. 4 lemons boiled (with seeds removed). Grated
yellow rind of 2 raw lemons. J lb. citron. ■J lb. orange. J pt. sherry. 1
teaspoonful each powdered J pt. brandy, mace and ginger. Mix all
together, then stir in well half sherry and brandy. Cook several hours.
MINCE MEAT 4 lbs. raw beef, chopped. 6 lbs. suet, chopped. 1 pk.
sour apples. 6 lbs. brown sugar. 4 lbs. seeded raisins. Spices to
taste. 2 lbs. currants. f lb. citron. 1 tablespoonful salt. 6 lemons,
juice. Pulp and peel of 2 lemons. Can be kept a year. SWEET
POTATO CUSTARD PIE 1 pt. mashed sweet potato. $j cup butter. 1
teacup sweet milk. 1 cup sugar. Yolks of 4 eggs. A little nutmeg or
cinnamon. Cream sugar and butter together, mix with potatoes,
flavor with nutmeg or cinnamon. Add beaten yolks and milk.
 260 PASTRY, PIES AND TARTS Beat the whites to a stiff
froth and stir in, pour in pie-pan lined with crust and bake quickly.
LEMON FILLING FOR TAETS, CAKES, ETC. 1 cup sugar. 1 cup boiling
water. 1 egg. 1 dessertspoonful cornstarch. Grated rind and juice of
1 lemon. Beat sugar and egg to a cream, add rind and juice of
lemon, previously prepared, also cornstarch, and blend thoroughly.
Then pour in slowly cup of water, which must be boiling. Put on the
fire in a double saucepan and allow it to simmer for ten minutes.
The filling is then ready for use. Orange may be used instead of
lemon. LEMON PIE 1 lemon, grated. Butter size of egg. 1J
tablespoonf uls cornstarch. 1 cup hot water. , f cupful sugar. Yolks of
2 eggs. Cook in double boiler, let it cool a little, then put in yolks
last, after the other ingredients are well cooked. To prepare the
lemon, grate off the outside, taking care to get only the yellow (the
white is bitter), then squeeze out the juice. Bake your pie crust first,
then add lemon filling; keep the whites for the meringue. Whip up
the whites stiff, add a little pulverized sugar, then spread on top of
pie, and put in the oven for a few minutes. PIE CBUST Three cups
flour sifted with two teaspoonfuls baking powder, one teaspoonful of
salt, two cups of lard, one cup water.
 PASTRY, PIES AND TARTS 261 CREAM PIE 1 cup sweet
mil°k. Butter size of egg. 1 small eup sugar. 1 tablespoonful flour.
Yolks of 3 eggs. Boil until it thickens, stirring constantly. Then fMl the
shell (which has previously been baked) with the mixture, and ice
with the whites of eggs. Place in oven a few minutes until icing
begins to brown. MARTHA WASHINGTON PIE 4 oz. blanched
almonds. 4 oz. powdered sugar. 2 eggs. 2 oz. macaroons. 2 oz.
melted butter. J gill rum. \ saltspoonful ground cinnamon. 6 drops
orange flower wafer. Pound almonds in a mortar with two ounces of
powdered sugar, adding gradually one raw egg. When well pounded
add two ounces more of sugar, melted butter, rum, ground
cinnamon, orange flower water and break in another egg. Pound for
five minutes and add well-pounded macaroons. Line a pie plate with
good paste, pour in the preparation and bake; decorate with candied
fruits. TARTS (Apricot, Plum, Apple, Berry.) Roll the paste one-eighth
of an inch thick, lay it on a deep pie-dish ; let it shrink all it will, and
use as little pressure as possible in fitting it to the tin. Cut the paste
an inch larger than the dish, and fold it under, giving a high twisted
edge. Prick the paste on the bottom in several places with a fork.
Lay over it a thin paper, and fill the tart with rice, dried peas, beans,
cornmeal, or any dry material convenient.
 262 PASTRY, PIES AND TARTS Brush the edge with egg,
and bake it in a moderate oven. When done remove the rice, or
other filling, and the paper. Brush the bottom with white of egg. This
will insure a dryunder crust. If apricots or peaches are to be used,
peel and cut them in halves, lay them evenly over the tart with the
centre side up. Place the half of a blanched almond in each one to
represent the pit. Put the juice of the fruit into a saucepan on the
fire ; if there is no juice use a cupful of water. Sweeten to taste, and
when it boils add to each cupful of juice one teaspoonful of
arrowroot dissolved in a little cold water, and let it cook until clear ;
then pour it around the fruit, but not over it, as the fruit should lie
on top and show its form. Place in the oven only long enough to
cook the fruit tender. If canned fruit is used, cook the juice and
arrowroot until a little thickened and clear ; then pour it around the
fruit, and let cool. It will not need to be put in the oven. When plums
or cherries are used, remove the pits carefully, and place the fruit
close together, with the whole side up. For apple tarts, cut the
apples in even quarters or eighths; stew them in sweetened water,
with a little lemon juice added, until tender. Lay them overlapping in
even rows or circles in the tart. To a cupful of water in which the
apples were stewed add a teaspoonful of arrowroot, and cook until
clear ; pour it over the apples, sprinkle with sugar, nutmeg, and
cinnamon. With berries, the fruit may be stewed or not before being
placed in the tart; then strips of paste are laid across it, like lattice-
work, and the paste brushed with egg. Bake long enough to cook
the fruit and the strips of paste. When cold place a fresh berry on
each piece of crust where it crosses; or place a drop of meringue on
the crusts, and the berries in the openings. The California canned
fruits make very good pies. One can of fruit will make two pies. Tart-
rings are better to
 PASTRY, PIES AND TARTS 263 use than pie-tins, as the
sides are straight. Place them on a baking-sheet, or tin, before lining
them with pastry. ORANGE PIE Juice and grated yellow rind 1 cupful
sugar. of 1 orange. 1 tablespoonful flour. § cupful milk J saltspoonful
salt. 3 eggs. Beat the yolks and the sugar together ; add the flour,
the milk, and the grated rind and juice of the orange. Place it on the
fire in a double boiler, and stir until it is a little thickened ; then pour
it into an open or tart pie, and bake thirty minutes. The crust of the
pie should be brushed with white of egg before adding the thickened
mixture. The tart crust may be first baked, as directed above, if
preferred. Cover the top with meringue made with the whites of the
eggs and sweetened with three tablespoonfuls of sugar. Pile it on
irregularly, or press it through a pastry-bag into fancy shapes. Place
it in the oven a moment to brown. A little more flour may be used if
the pie is wanted more solid. PLAIN APPLE PIE Fill a pie with apples
sliced thin, using enough to make the pie at least an inch thick when
done. Add a little water to the apples, and cover with a top crust,
which is a little richer than the under one. This is done by rolling out
a part of the same paste, covering it with bits of butter, folding it
together, and rolling it again, repeating the operation two or three
times. Cut a few slits in the paste to let out the steam while cooking.
Brush the top with beaten yolk of egg. When the pie is baked, and
while it is still hot, lift off carefully the top crust; add sugar, nutmeg,
and a little
 264 PASTRY, PIES AND TARTS butter, and mix them well
with the apples. Keplace the top crust, and dust it with powdered
sugar. Apple pies seasoned in this way are better than when
seasoned before being baked. PUMPKIN PIE 2J cups pumpkin,
cooked. 2 cupfuls milk. 2 eggs. 1 tablespoonful molasses. 1
teaspoonful each salt, butter, cinnamon and ginger. Sugar to taste.
To pulp add milk, salt, butter, cinnamon, and ginger, molasses, eggs,
and sugar. Add the beaten eggs last and after the mixture is cold.
Pour it into an open crust and bake slowly forty to fifty minutes.
Squash pies are made in the same way, but are not the same in
flavor, although they are often given the name of pumpkin pies.
CEEAM PIE 3 eggs. 2J cups milk. 1 cupful sugar. 2 tablespoonfuls
flour. 1 teaspoonful baking powder, f cupful sugar. 1 cupful flour. 1
egg. Cream for filling: 1 teaspoonful vanilla. Sift the flour and baking
powder together ; beat the yolks and sugar together; add the flour
and lastly the whipped whites of the eggs. Bake this cake mixture in
two layers, and place between them when cold, and just before
serving, a thick layer of whipped cream. Have the top piece covered
with a boiled icing, or use between the cakes a cream filling made as
follows: Cream for Filling. — Scald the milk; turn it on to the beaten
egg; return it to the fire; add the flour moistened with a little milk,
and the sugar, and stir until thickened.
 PASTRY, PIES AND TARTS 265 Let it cool before adding it to
the cake. Serve with whipped cream if desired. COCOANUT PIE 1 pt.
milk. 3 eggs, yolks. i grated cpcoanut. 3 tablespoonfuls sugar. 2
tablespoonfuls cornstarch. 1 teaspoonful vanilla. Line a tin basin
which is two inches deep with pie paste, and bake it. Scald the milk
and turn it on to the yolks and sugar beaten together; return it to
the fire; add the cornstarch moistened with cold milk, and stir until
well thickened; add vanilla, and the whites of two eggs whipped to a
froth; cook one minute to set the egg, then remove, and when
nearly cold and stiffened stir in the cocoanut. Brush the bottom of
the baked pie-crust with white of egg ; cover it with a thin layer of
grated cocoanut and turn in the thickened custard. Cover the top
with meringue made with the white of one egg. Eeturn it to the oven
one minute to color the meringue. Let the pie stand long enough to
get firm and cold before serving. If the grated cocoanut is not added
until the custard has stiffened, it will not sink to the bottom.
CRANBERRY PIE Chop one cupful of cranberries and a half cupful of
seeded raisins together into small pieces ; add to them a cupful of
sugar, a half cupful of water, a tablespoonful of flour, and a
teaspoonful of vanilla. Bake with an upper and under crust. This
resembles cherry pie. LENT PIES Two tablespoons of ground rice to
one pint of new milk, add five eggs and sweeten to taste, flavoring
with two bay leaves. Cover pie plates with a good crust, pour in
mixture and bake.
 266 PASTRY, PIES AND TARTS LEMON FILLING FOR PIE
One lemon, juice and rind grated; yolks of two eggs, one cup of
water, one cup of sugar, one heaping teaspoonful of cornstarch. Put
in a double boiler and boil thick. Save the whites for top. PUMPKIN
PIE 6 cups cooked pumpkin. 3 eggs. 2 cups sugar. | cup molasses. 2
finely rolled crackers. 1 teaspoonful ginger. \ nutmeg. Cinnamon and
salt to taste. Put pumpkin in a pan with eggs, sugar, molasses
(maple preferred), crackers, ginger, nutmeg, cinnamon and salt; stir
well, add enough rich milk to thin. Bake in pastry shape. PUMPKIN
PIE Three-quarters cupful of pumpkin (well mashed), one and a half
cupfuls of milk, half cupful of sugar, one egg, half a teaspoonful of
ginger, nutmeg, cinnamon and cloves. WALDORF PUMPKIN PIE 3
pts. pumpkin pulp. 1 tablespoonful ginger. 2 tablespoonfuls flour. 1
teaspoonful salt. 4 eggs. 2 qts. milk. 1 lb. sugar. Cook all together
until well thickened; meanwhile make crust and line pie dish. Bake in
a moderate oven one hour. PIE CRUST One-half pound flour, one-
half pound butter, one-quarter pint cold water, yolk of one egg, juice
of one-half lemon. Sift the flour thoroughly, then add a pinch of salt
and two ounces of butter. Mix the yolk of egg and lemon juice with
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