Case. 24 year old female presented to your office complaining of excess hair growth on her face and abdomen. Questions?

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Transcription:

Hirsutism

Case 24 year old female presented to your office complaining of excess hair growth on her face and abdomen Questions?

Started around puberty with gradual progression Irregular menstrual cycle Acne No dark striae, thin skin, or bruising No frontal balding, voice deepening, increased muscle mass, clitoromegaly Ethnicity: Caucasian No family history of excess body hair

PMH: GERD PSH: Appendectomy SH: Unremarkable FH : DM Meds: Omeprazole Review of systems: Unremarkable

Physical exam: BP 122/72 HR 71 RR 17 Temp 96.8 Height: 5.4 ft, Weight: 172 lb, BMI: 29.5 Excess of dark and coarse hair on the chin and abdomen

Labs?

Labs: Testosterone 91 (6-82) DHEA Sulfate 296 (65-380) 17 OH progesterone: 83 (20-100) Prolactin 19 (3-26) FSH 6.5, LH 11.2 TSH 2.72, F T4 1.2 Fasting BS 97, A1c 5.7

Hirsutism

Hirsutism is defined by the presence of an excessive quantity of androgendependent terminal hair growth on the upper lip, chin, chest, abdomen, back and buttocks It must be differentiated from hypertrichosis Hypertrichosis is the excessive diffuse growth of androgen independent hair that is vellus (fine, soft, not pigmented) Hypertrichosis could be familial or caused by a drug, examples of which include phenytoin, minoxidil and cyclosporine Hypertrichosis also can occur in patients with some systemic illnesses, such as hypothyroidism, anorexia nervosa, malnutrition, porphyria, and dermatomyositis

Pathogenesis of hirsutism Androgens increase hair follicle size, hair fiber diameter, and the proportion of time terminal hairs spend in the growth phase Androgen excess in women leads to increased hair growth in androgen sensitive sites except the scalp where it manifests with hair loss Nearly all hirsute women have an increased production rate of androgens

Androgens responsible for hirsutism Testosterone excess is usually of ovarian origin Dehydroepiandrosterone (DHEA) and its sulfated form (DHEAS) excess are of adrenal origin Androstenedione excess can be of either adrenal or ovarian origin

Ethnicity and hirsutism The definition of normal hair growth must also consider race and ethnicity Most Asian and Native American women have little body hair While Mediterranean on average have substantially greater quantities of body hair The most important consideration, whatever the woman's background, is whether the pattern of hair growth has changed or the rate of growth has increased

EVALUATION

History Menstrual history: regularity, presence of symptoms of ovulation Time course of symptoms: The age at onset, the rate of progression Weight history Medication history: Drugs that have androgenic effects include danazol, oral contraceptives that contain androgenic progestins Family history

Physical examination Hirsutism vs hypertrichosis Ferriman-Gallwey score: method to grade hair growth Nine androgen-sensitive sites are graded from 0 to 4 95 % of women have a score below 8 Scores above 8 suggest an excess of androgen-mediated hair growth that should be confirmed by hormonal evaluation

Physical examination Body habitus: height, weight and BMI Skin: acne, temporal balding, striae, thin skin, bruising, and acanthosis nigricans Signs of virilization: deepening of the voice, frontal balding, increased muscle mass, and clitoromegaly Abdominal and pelvic examination: could reveal a mass

Laboratory testing Not all women with hirsutism need biochemical testing The Endocrine Society Clinical Practice Guidelines recommend biochemical testing in women with: Moderate or severe hirsutism Hirsutism of any degree if it is sudden in onset and rapidly progressive, or associated with irregular menses, obesity, or evidence of virilization

Common approach for initial laboratory evaluation includes: Total testosterone, DHEAS and prolactin followed by additional testing when indicated Testing for late onset congenital adrenal hyperplasia with a serum 17-OH progesterone in women with early onset of hirsutism, family history and in women from high risk ethnic groups (Hispanics, Yugoslavs, and Ashkenazi Jews) LH/FSH when suspecting PCOS Testing for cushings syndrome when there is a suspicion

IMAGING Pelvic ultrasonography to look for a polycystic ovary and to screen for ovarian androgen-secreting tumors Abdomen CT or MRI to look for adrenal mass if DHEAS is markedly elevated or there is other evidence of excess adrenal steroid production

TREATEMENT Hirsutism can be mild and requires only reassurance and cosmetic therapy It sometimes causes psychological distress and requires extensive intervention

Endocrine Society guidelines Treatment decisions should be based upon the degree and severity of the hirsutism The recommendation is to start pharmacologic therapy or direct hair removal methods in clinically significant hirsutism The choice between the two approaches depends upon the woman's preference, location and size of the affected area and the availability and affordability of direct hair removal methods (electrolysis or laser)

Pharmacological therapy Estrogen-progestin contraceptives are the preferred initial therapy (increases SHBG and decreases free androgens) Antiandrogens (spironolactone, finasteride): decreases testosterone to dihydrotestosterone conversion It can be added in women taking contraceptives but without optimal response after six months It should not be used in women of reproductive age unless reliable contraception is used because of their potential teratogenic effect in a male fetus

Cosmetic and mechanical treatments Cosmetic methods (shaving, plucking, bleaching, waxing): It can be used alone or in addition to drug therapy Permanent hair reduction (electrolysis and laser): Hair is likely to re-grow in women with underlying hyperandrogenemia especially without pharmacologic therapy

Questions?