CLINICAL CHEMISTRY 2 – LECTURE

PRELIM TOPIC 3: GONADAL FUNCTION

3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

THE TESTES • The sperm move sequentially through the tubuli recti;
rete testes; ductuli efferentes testes; the head, body, and
• The testes are paired, ovoid organs that serve the dual tail of the epididymis; and, finally, into the vas deferens.
functions of • Various secretory products of the seminal vesicles and
(1) production of sperm and prostate mix with sperm to form the final product: semen.
(2) production of reproductive steroid hormones. In the Seminal vesicle secretions are rich in vitamin C and
embryonic stage, the dominant male sex hormone, fructose, important for the preservation of motility of the
testosterone (T), aids in development and differentiation sperm.
of the primordial gonads. PHYSIOLOGY OF THE TESTICLES
• After puberty, throughout adulthood, and until late in old SPERMATOGENESIS
age, testosterone helps with sperm production and
maintains secondary sexual characteristics. • Sperm are formed from stem cells called spermatogonia.
FUNCTIONAL ANATOMY OF THE MALE The spermatogonia undergo mitosis and meiosis;
REPRODUCTIVE TRACT finally, the haploid cells transform to form mature sperm.
• The mature sperm has a head, body, and tail, which
• The testes are located outside the body, encased by a enables it to swim for the purpose of forming a zygote
muscular sac. Blood flow is governed by an intricate with the haploid ovum. Certain spermatogonia stagger
plexus of arterial and venous blood flow that, together division so that sperm production is uninterrupted and
with contraction of the dartos muscle in the scrotal sac, continuous. The Sertoli cells are polyfunctional cells that
regulates the temperature of the testicles to 2°C below aid in the development and maturation of sperm.
core body temperature. HORMONOGENESIS
• This important function is vital to uninterrupted sperm
production. Also encased in the muscular sheath is the • Testosterone, the predominant hormone secreted by the
spermatic cord, which has the ability to retract the testes, is controlled primarily by two pituitary hormones:
testicles into the inguinal canal in instances of threatened follicle-stimulating hormone (FSH) and luteinizing
injury. The testes themselves are comprised of two hormone (LH).
anatomical units: a network of tubules, known as the • Because these hormones were first described in women,
seminiferous tubules, and an interstitium. they are named in reference to the menstrual cycle. Both
• The tubules contain germ cells and Sertoli cells and are hormones are produced by a single group of cells in the
responsible for sperm production. pituitary called gonadotrophs. FSH acts primarily on
germinal stem cells and LH acts primarily on the Leydig
cells—located in the testicular interstitium—that
synthesize testosterone.
HORMONAL CONTROL OF TESTICULAR
FUNCTION

• The hypothalamus, located in the brain, generates a

hormone called gonadotropin-releasing hormone
(GnRH) in a pulsatile fashion. GnRH is released into the
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

portal hypophysial system that, in turn, determines the and pubis), enhanced linear skeletal growth,
production of LH and FSH from the pituitary gland. development of internal and external genitalia, increased
Impaired pulse generation of GnRH leads to inadequate upper body musculature, and development of larynx and
production of LH and FSH, resulting in hypogonadism. vocal cords with deepening of the voice.
• Testosterone concentration fluctuates in a circadian • Possible mood changes and aggression are undesired
fashion, reflecting the parallel rhythms of LH and FSH effects that may occur during puberty. The linear growth
levels. This fact should be considered when interpreting effects of testosterone are finite, with epiphysial closure
serum levels of testosterone: the highest level is found when genetically determined height is achieved.
at about 8 AM and correlates with most laboratory Hypogonadism during puberty leads to imprecise closure
normal ranges, and the lowest level is found at about 8 of growth plates, leading to excessive height, long limbs,
PM. and disproportionate upper and lower body segments.
CELLULAR MECHANISM OF EFFECT ON SPERMATOGENESIS
TESTOSTERONE ACTION • Stimulation of Leydig cells induces production of
testosterone. Testosterone, acting with FSH, has

• Testosterone enters the cell and converts to paracrine effects on the seminiferous and Sertoli cells

dihydrotestosterone (DHT). inducing spermatogenesis. Exogenous overuse or abuse

• DHT complexes with an intracellular receptor protein of testosterone, such as occurs with some athletes, will

and this complex binds to the nuclear receptor, effecting reduce the high intratesticular concentration of

protein synthesis and cell growth. testosterone, leading to reduction of sperm production.

PHYSIOLOGIC ACTIONS OF TESTOSTERONE EFFECT ON SECONDARY SEXUAL

PRENATAL DEVELOPMENT • Testosterone has growth-promoting effects on various

target tissues. The secondary sex characteristics that

• Early in development, embryos have primordial develop during puberty are maintained into late

components of the genital tracts of both sexes. The adulthood by testosterone.

primitive gonads become distinguishable at about the DISORDERS OF SEXUAL DEVELOPMENT AND

seventh week of embryonic stage. Both chorionic TESTICULAR HYPOFUNCTION

gonadotropins and fetal LH stimulate production of (Hypergonadotropic Hypogonadism)

testosterone by the fetal Leydig cells. Exposure of KLINEFELTER’S SYNDROME

testosterone to the Wolffian duct leads to differentiation
of the various components of the male genital tract. • Klinefelter’s syndrome occurs in about 1 of 400 men and
Sertoli cells produce müllerian regression factor, which is caused by the presence of an extra chromosome.
aids in regression of the female primordial genital tract. • The most common karyotype is 47, XXY. Men with this
• The scrotal skin is rich in 5-reductase, which converts disorder have small (2.5 cm), firm testicles.
testosterone to DHT. Fetal exposure to drugs that block • Gynecomastia (enlargement of the male breast) can also
this hormone leads to feminization of the male fetus. be present at the time of diagnosis. Due to reduced
POSTNATAL DEVELOPMENT production of testosterone, FSH and LH levels are
elevated.

• Testicular function is reactivated during puberty after a • These men also have azoospermia and resultant sterility.

period of quiescence to produce testosterone that results Men with mosaicism may produce some sperm and
in development of secondary sex hair (face, chest, axilla, pregnancies have been reported with such men.
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

• Elevated levels of FSH and LH induced increased TESTICULAR INJURY AND INFECTION
aromatase activity, resulting in elevated estrogen levels.
Men with Klinefelter’s syndrome may have reduced • Post pubertal mumps infection can result in mumps
bone density and breast cancer. orchitis and permanent testicular injury.
TESTICULAR FEMINIZATION SYNDROME • Testicular damage due to viral orchitis and HIV infection
has also been reported. Radiation and chemotherapy for
• Testicular feminization syndrome is the most severe cancer can also result in long-term damage.
form of androgen resistance syndrome, resulting in lack SERTOLI CELL-ONLY SYNDROME
of testosterone action in the target tissue.
• As a result of the lack of testosterone effect, the physical • Sertoli cell–only syndrome is characterized by a lack of
development pursues the female phenotype, with fully germ cells. Men present with small testes, high FSH
developed breast and female distribution of fat and hair. levels, azoospermia, and normal testosterone levels.
• Most men present for evaluation of primary amenorrhea, • Testicular biopsy is the only procedure to confirm this
at which time the lack of female internal genitalia diagnosis.
becomes apparent. HYPOGONADOTROPIC HYPOGONADISM
• The testicles are often undescended, and failure to KALLMANN’S SYNDROME
promptly remove these organs results in malignant
transformation. • Kallmann’s syndrome is a result of an inherited, X-
• Biochemical evaluation reveals normal levels of linked recessive trait that manifests as hypogonadism
testosterone with elevated FSH and LH levels. There is during puberty. The frequency of this syndrome is 1 of
no utility or response to administration of exogenous 10,000 males.
testosterone. • The associated defects, such as anosmia (inability to
5A-REDUCTASE DEFICIENCY smell) and midline defects (cleft palate and lip), should
alert the clinician to suspect this disorder.
• The genotype in 5-reductase deficiency is XY. • Certain men also have red-green color blindness,
• A reduction in levels of the enzyme 5-reductase results congenital deafness, or cerebellar dysfunction.
in decreased testosterone levels. HYPERPROLACTINEMIA
• Physical development is similar to the female
phenotype until puberty when residual enzyme activity • Prolactin elevation resulting from any cause (drug
sufficiently converts testosterone to induced or prolactin-producing tumors of the pituitary)
dihydrotestosterone, resulting in development of a male can result in hypogonadotropic hypogonadism.
phenotype. AGE
MYOTONIC DYSTROPHY
• There is a gradual reduction in testosterone after age 30,
• Myotonic dystrophy is inherited in an autosomal with an average decline of about 110 ng/dL every
dominant fashion and presents with hypogonadism, decade. The Baltimore Longitudinal Study of Aging
muscle weakness, frontal balding, diabetes, and muscle revealed reduced total testosterone levels of 19% at age
dystonia. Testicular failure typically presents in the 60, 28% at age 70, and 49% at age 80,16,17 with free
fourth decade of life. testosterone levels much lower in these men.
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

• Age is also associated with elevation of SHBG by about • Clinical signs and symptoms of hypogonadism (e.g., loss
1% per year. Total testosterone levels may be normal in of secondary sexual characteristics, osteoporosis) should
aging men but the free (unbound) levels of testosterone be corroborated with low testosterone levels, particularly
are more reliable indicators of biochemical reduction. when testosterone replacement therapy is considered.
• The associated features of reduced secondary sex hair TESTOSTERONE REPLACEMENT THERAPY
growth, loss of muscle bulk and strength, and loss of PARENTERAL TESTOSTERONE
bone density are corroborative evidence indicative of the
lack of tissue effects of testosterone. • This is the most widely available and cost-effective mode
• Testosterone deficiency is a constellation of clinical of administration. The cypionate and enanthate esters of
features of hypogonadism combined with low serum testosterone are available for intramuscular injection.
testosterone levels. The combination of biochemical and • The peak level is achieved in 72 hours and the effect
clinical evidence of testosterone should prompt lasts for a period of 1–2 weeks. Weekly administration
consideration of testosterone replacement in older men. provides for a lower peak and less fluctuation within the
PITUITARY DISEASE normal range of testosterone levels. Usual dosing is 50–
100 mg weekly or 200–250 mg once every 2 weeks.
• Acquired hypogonadism can follow injury to the • Testosterone dose should be based on lean body mass,
pituitary as a result of tumors, surgical trauma, vascular not on body weight, and is best reached by administering
injury, autoimmune hypophysitis, or granulomatous or a standard dose of testosterone with minor dose
metastatic disease. escalations based on serum testosterone levels measured
• Hemochromatosis is a rare cause of pituitary midpoint between two injections.
dysfunction. • The goal is to maintain this middose level at midpoint of
DIAGNOSIS OF HYPOGONADISM the normal ranges.
TRANSDERMAL TESTOSTERONE THERAPY
• Both clinical and biochemical features must be met to
make the diagnosis of hypogonadism. Testosterone • This mode of administration provides more physiologic
levels have a circadian rhythm and the time of sampling levels of testosterone.
must be considered. Multiple estimation of free and • The patch is permeability enhanced to aid in the
bound testosterone levels should be done on different absorption of testosterone through normal skin. Local
days before a diagnosis of hypogonadism is made. skin irritation can occur and limit patch use.
• The distinction between primary (disease or destruction TESTOSTERONE GEL
of the testes) versus secondary (disease or destruction of
the pituitary) is relatively easy to make. • This hydroalcoholic gel preparation is applied to
• FSH and/or LH19 levels are elevated in primary nongenital skin once daily. The absorption is gradual and
hypogonadism and are inappropriately normal or low provides blood levels of testosterone in the normal range
with secondary etiologies. Pituitary MRI should be done for 24 hours.
in secondary hypogonadism in young individuals. Older • The main concern with this preparation is potential
individuals often have secondary or tertiary transmission to female partners or children on close skin
(hypothalamic) dysfunction as a result of reduced contact.
hypothalamic pulse generator frequency, resulting in low
or inappropriately normal FSH and/or LH levels.
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

BUCCAL TESTOSTERONE FUNCTIONAL ANATOMY OF THE OVARIES

• This plastic tablet is placed along the gum line twice • The ovaries are oval organs that lie in the pelvic fossa,
daily. formed by the posterior and lateral pelvic wall, and attach
• Local discomfort and the need for twice-daily dosing to the posterior surface of the broad ligament by the
sometimes limit use. peritoneal fold, otherwise known as the mesovarium.
MONITOR TESTOSTERONE REPLACEMENT • They are positioned near the fimbrial end of the fallopian
THERAPY tubes, which are connected to the uterine cavity.
• An adult ovary averages 2–5 cm in length, weighs an

• Prostate-specific antigen (PSA), blood counts, and average of 14 grams, and typically contains 2–4 million

lipid levels should be checked 3–6 months after primordial follicles.

initiation of testosterone replacement and at least yearly • These primordial follicles are present at birth; however,

thereafter. maturation is blocked until puberty. Following the onset

• Routine clinical evaluation for leg edema, worsening of of puberty, each ovarian cycle is marked by recruitment

sleep apnea, and prostate enlargement is also of a few primordial follicles for maturation.

recommended. • Typically, all but one of these follicles will then atrophy,

• Pharmacologic use of testosterone may also reduce in a process termed the follicular phase.

sperm count by reducing the intratesticular testosterone

concentration that is manyfold higher than serum
concentrations.
• If PSA elevation is noted after testosterone replacement,
prostate evaluation with possible biopsy is
recommended. Active prostate cancer is a
contraindication to testosterone replacement.
THE OVARIES

• The ovaries are paired organs that, like the male gonads,
perform the dual functions of gamete (ovum) and steroid
hormone production.
• Unlike in the male, the primordial reproductive cells in
• The single remaining follicle—known as the Graafian
the female typically produce a solitary gamete. Ovarian
follicle—is composed of an outer and inner layer (the
and menstrual events are carefully synchronized by a
theca externa and theca interna, respectively) encasing a
complex interplay of hormones among the
central fluid-filled cavity and a layer of cells known as
hypothalamus, pituitary, and ovaries to prepare the
the granulosa layer.
uterus for implantation of an embryo. In the absence of
• The maturing ovum attaches to the inside of the follicle
implantation, the uterine lining is shed, resulting in
via cells derived from granulosa cells, called cumulus
menses.
cells. During the luteal phase of the ovarian cycle, the
• The length of the menstrual cycle is the time between any
Graafian follicle releases its ovum in response to ovarian
two consecutive cycles. The typical duration is 28 (3)
stimulation by LH.
days with average menstrual flow about 2–4 days.
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

• When the ovum is extruded, the Graafian follicle the luteal phase, and deficiency results in failure of
undergoes a morphologic change with hypertrophy of the implantation of the embryo.
theca and granulose cells to become the corpus luteum. ANDROGENS
This process is called luteinization.
• The corpus luteum is rich in cholesterol and acts as a • Ovaries produce the androgens androstenedione,
substrate for continued production of progesterone and dehydroandrostenedione, testosterone, and
estrogen, maintaining the endometrium for conception. dihydrotestosterone, all of which are carbon-19
If conception or implantation fails to occur, the compounds.
endometrium is shed and the corpus luteum atrophies to • Excess production of ovarian androgens in women leads
an atretic follicle. to excess hair growth (hirsutism), loss of female
HORMONAL PRODUCTION BY THE OVARIES characteristics, and—in severe cases—development of
ESTROGEN overt male secondary sexual features (masculinization or
virilization).
• Naturally synthesized estrogens are carbon-18 • Unlike estrogen, which is not produced in the ovary after
compounds. The principal estrogen produced in the menopause, ovarian androgen synthesis continues well
ovary is estradiol. Estrone and estriol are primarily into advanced age.
metabolites of intraovarian and extra glandular THE MENSTRUAL CYCLE
conversion. Estrogens promote breast, uterine, and
vaginal development and also affect the skin, vascular • By convention, the menstrual cycle is considered to start
smooth muscles, bone cells, and the central nervous on the first day of menses (day 1).
system. • The menstrual cycle consists of two phases of parallel
• The lack of estrogen that naturally occurs with the onset events occurring at the ovaries and endometrium. Within
of menopause leads to atrophic changes in these organs. the ovaries, these events are known as the follicular and
During the reproductive period, it is estrogen that is luteal phases, while the concurrent endometrial events
responsible for follicular phase changes in the uterus, are known as the proliferative and secretory phases.
with deficiency resulting in irregular and incomplete THE FOLLICULAR PHASE
development of the endometrium.
PROGESTERONE • The follicular phase begins with the onset of menses and
ends on the day of LH surge. Early in the follicular phase,
• Progesterone is a carbon-21 compound within the steroid the ovary secretes very little estrogen or progesterone. A
family and is produced by the corpus luteum. rise in FSH, however, stimulates estrogen production.
• Progesterone induces the secretory activity of those • The estrogen secreted by the developing follicle within
endometrial glands that have been primed by estrogen, the ovary stimulates uterine epithelial cells, blood vessel
readying the endometrium for embryo implantation. growth, and endometrial gland development to increase
Other effects include thickening of the cervical mucus, the thickness of the endometrium.
reduction of uterine contractions, and the thermogenic • The intense secretory capacity of the uterine glands
effect, in which basal body temperature rises after provides a secretion that aids the implantation of the
ovulation. This effect is of clinical use in marking the embryo.
occurrence of ovulation.
• Progesterone is the dominant hormone responsible for
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

THE LUTEAL PHASE PUBERTY DEVELOPMENT IN THE FEMALE

• Estrogen levels peak 1 day before ovulation, at which • As with males, puberty in females consists of a sequence
point a positive feedback system results in an LH surge. of hormonally mediated events resulting in the
• The start of the luteal phase is marked by the extrusion development of secondary sexual characteristics and
of the ovum approximately 36 hours after this LH surge attainment of final adult height.
with subsequent luteinization of the Graafian follicle to • Thelarche (development of breast tissue) is typically the
form the corpus luteum. earliest sign of sexual development, followed by
• The corpus luteum secretes progesterone to aid in the development of pubic hair.
implantation of the embryo. • Menarche, or initiation of menses, occurs an average of
• In the absence of fertilization, a gradual decline in the 2–3 years after the onset of puberty.
production of progesterone and estrogen by the corpus MENSTRUAL CYCLE ABNORMALITIES
luteum there is a loss of endometrial blood supply; this
results in shedding of the endometrium approximately 14 • The menstrual cycles ranges from 25 to 35 days, with an
days after ovulation occurred. average 28-day duration. The average age of menopause
• The typical duration of menstrual bleeding is 3–5 days, in the United States is between 45 and 55 years of age
with blood loss averaging 50 mL. Onset of menses marks with the median at age 53.
the end of the luteal phase. • Amenorrhea is defined as the absence of menses.
HORMONAL CONTROL OF OVULATION Primary amenorrhea describes when a woman has never
menstruated, while secondary amenorrhea is used to
• The central control of FSH and LH secretion resides in describe a woman who has had at least one menstrual
the GnRH pulse generator of the arcuate nuclei and cycle followed by absences of menses for a minimum of
medial preoptic nuclei of the hypothalamus. 3–6 months.
• Positive and negative feedback responses exist among • Oligomenorrhea refers to infrequent of irregular
estrogen, progesterone, LH, and FSH production. It is menstrual bleeding, with cycle lengths in excess of 35–
because of the lack of estrogen after menopause that both 40 days.
FSH and LH levels rise. • Uterine bleeding in excess of 7 days is dysfunctional and
• During reproductive years, FSH levels are elevated early is termed menorrhagia.
in the follicular phase. • In a patient with infertility, the diagnosis of inadequate
• A midcycle surge in LH production stimulates a series of luteal phase is made when the luteal phase is less than 10
events that culminates in ovulation, with FSH levels days or when an endometrial biopsy indicates the
falling after this event. progression of endometrial changes is delayed or out of
• Any injury to the hypothalamus or the presence of either phase, resulting in implantation failure. The multiple
psychosocial or physical stressors leads to changes in causes of male and female infertility are shown in Table
these hormonal cues and results in anovulation and 21-4.
amenorrhea.
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

HYPOGONADOTROPIC HYPOGONADISM HYPERGONADOTROPIC HYPOGONADISM

• Hypogonadotropic hypogonadism, or gonadotropin • Hypergonadotropic hypogonadism is characterized by

(FSH and LH) deficiency resulting in decreased sex ovarian failure resulting in elevation of FSH
steroid production, is a common cause of secondary concentrations, with or without LH elevations. Ovarian
amenorrhea. failure occurs naturally between 45 and 55 years of age
• There are many physiologic and pathologic causes of in American women. When the depletion of oocytes and
hypogonadotropic hypogonadism, including weight loss follicles occurs at the expected time, it is termed
as associated with anorexia nervosa or various disease menopause. Menopause is a natural, inevitable event that
processes, intense physical exercise (commonly termed results in elevation of FSH and LH levels, with low
runner’s amenorrhea), and pituitary tumors that disrupt levels of estrogen.
secretion of FSH or LH. • Premature ovarian failure is defined as primary
• Prolactin production by prolactinomas can have similar hypogonadism in a woman before the age of 40 and can
effects. be a result of congenital chromosomal abnormality (e.g.,
• Any secondary cause of chronic hypogonadism can Turner’s syndrome) or premature menopause.
induce pathologic bone loss, resulting in osteopenia or, • Patients with Turner’s syndrome do not complain of the
if severe, osteoporosis. same hot flashes experienced by patients with secondary
hypergonadotropic hypogonadism. Premature
menopause can occur in isolation or in association with
other endocrine gland failure such as
hypoparathyroidism, hypothyroidism, or
hypoadrenalism.
 CLINICAL CHEMISTRY 2 – LECTURE
PRELIM TOPIC 3: GONADAL FUNCTION
3RD YEAR | 1ST SEMESTER A.Y 2023-2024 Minerva Diane Dichoso, RMT, MSc

POLYCYSTIC OVARY SYNDROME laboratory evaluation in a woman born in the United

States.
• This common disorder can present in many ways: • It is estimated that about 5%–10% of American women
infertility, hirsutism, chronic anovulation, glucose have hirsutism, which can be quantified using a
intolerance, hyperlipidemia or dyslipidemia, and measurement technique known as the Ferriman-Gallwey
hypertension. Scale that identifies nine areas (lip, chin, sideburn region,
• The onset is often perimenarchial (premenarchial), neck, chest, abdomen, upper and lower back, and thigh)
chronic, and notable for its slow progression. for assessment and allots points on a scale of 1–4 based
Investigations for this disorder involve estimation of free on hair thickness and pigmentation. A score of higher
testosterone, SHBG, FSH, LH, fasting glucose, insulin, than 8 is consistent with a diagnosis of hirsutism.
and lipid levels.
• Ovarian ultrasound reveals multiple cysts in many
patients (about 30% of patients do not have ovarian
cysts).
• Most patients with this disorder are overweight;
however, patients with polycystic ovary syndrome
(PCOS) of eastern Asian or South American descent are
of normal weight.
• Most symptoms and laboratory abnormalities are
reversed with weight loss and increased physical activity.
The drug Glucophage (metformin), commonly used for
the treatment of diabetes, is useful in this condition, even
in the absence of diabetes. Although not U.S. Food and
Drug Administration approved for this use, it reportedly
normalizes menstrual cycles and improves conception
rates.
HIRSUTISM

• Hirsutism is abnormal, abundant, androgen-sensitive

terminal hair growth in areas in which terminal hair
follicles are sparsely distributed or not normally found in
women. Most commonly, hirsutism is idiopathic in
etiology (60% of cases), with PCOS the next most
common cause (35%).
• Hirsutism should only be considered in the context of a
woman’s ethnic origin. Women of Italian, eastern
European, eastern Indian, and Irish descent possess more
androgen-sensitive terminal hair than do most northern
European women, making a careful elicitation of ethnic
background important prior to initiation of an extensive