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  1. 1. Hirsutism Aboubakr Elnashar Benha University Hospital, Egypt Aboubakr Elnashar
  2. 2. Outline • Introduction • Definition • Causes • Clinical evaluation • Investigations • Treatment • Guidelines Aboubakr Elnashar
  3. 3. Introduction Aboubakr Elnashar
  4. 4. Gynecological, Endocrinological, Cosmetic & Psychogenic: {great anxiety, nature of the disease, social acceptance} Aboubakr Elnashar
  5. 5. Incidence Not known Mediterranean> Asian American females: 10% European: 5% Aboubakr Elnashar
  6. 6. Cycle growth of hair Several months 2 weeks 3 months Aboubakr Elnashar
  7. 7. Types of hair Lanugo Fetal hair Vellus Short, fine, Unpigmented Before puberty Terminal Long, coarse, pigmented arises from vellus hair Clinically, terminal hairs can be distinguished from vellus hairs primarily by their length (i.e.`0.5 cm) and the fact that they are usually pigmented.Aboubakr Elnashar
  8. 8. Non sexual Ambi-sexual Male sexual Sites Lower parts of the scalp, eye brow, lashes, fore-arms, lower legs Temporal & vertical parts of the scalp, axilla, lower pubic hair. Ears, nasal tip, chin, sternum, upper pubic triangle, back. Depend on Growth hormone from pituitary Androgen in low concentration from the adrenals & ovaries in females & adrenals in male Androgen in high concentration Sites of hair Aboubakr Elnashar
  9. 9. Androgen production Androstenedione Testosterone Adrenal DHEA Ovary DHEAS 50% 50% 50% 25% 25% 90% 10% 100% Aboubakr Elnashar
  10. 10. Androgen in the blood Male Normal female Hirsute female Free 3% 1% 2% Albumin 19% 19% 19% SHBG 78% 80% 79% Aboubakr Elnashar
  11. 11. Androgen at target cell (hair follicle) Testosterone (T) 5œ-reductase. Dihydrtestosterone (DHT) Androstanediol Glucuronide 3 alpha androstanediol glucuronide(3 alpha AG) Aboubakr Elnashar
  12. 12. Definitions Aboubakr Elnashar
  13. 13. Virilization: Defiminization: Atrophy of the breast & vagina Musculinization: Hirsutism, deepening of voice temporal balding. Increase: size of the clitoris, muscular mass & libido Aboubakr Elnashar
  14. 14. Aboubakr Elnashar
  15. 15. Main Causes of Virilization 1-CAH 2- Iatrogenic 3- Ovarian tumour 4- Cushing's syndrome. Aboubakr Elnashar
  16. 16. Hirsutism: Latin hirsutus = shaggy, hairy Excessive growth of terminal hair in male sexual sites. Excessive: Socially unacceptable to the patient F& G score >8 Aboubakr Elnashar
  17. 17. Hypertrichosis Excessive growth of (Lanugo, vellus or terminal) hair in non-sexual sites (James et al, 2005) •Cong Acquired •Localized Generalized Congenital hypertrichosis lanuginosa Drug-induced hypertrichosis Aboubakr Elnashar
  18. 18. Aboubakr Elnashar
  19. 19. Hirsutism: •Not an increase in the number of hair follicles but an alteration in their character. •An increase in the transformation of the vellus to terminal hair. {Androgens will convert lanugo & vellus hair to terminal hair}.Aboubakr Elnashar
  20. 20. Hirsutism is a consequence of several factors. An increase in: 1. Androgen production 2. The sensitivity of the androgen receptors at the level of the hair follicle. 3. The activity of 5œ-reductase. Aboubakr Elnashar
  21. 21. Causes Aboubakr Elnashar
  22. 22. A. Ovarian: 1. PCOS: 90% 2. Tumors: 0.5% Virilizing ovarian tumors Luteoma of pregnancy 3. Dysgenesis B. Adrenal:5% 1. Cong adrenal hyperplasia 2. Tumors 3. Cushing syndrome C. Peripheral 1. Idiopathic: Regular ovulation & normal androgen levels 2. Insulin resistance – HAIRAN syndrome: HyperAndrogenic Insulin-Resistant Acanthosis Nigricans – 5H syndromeAboubakr Elnashar
  23. 23. A. Ovarian: 1. PCOS: 90% Aboubakr Elnashar
  24. 24. Rotterdam Criteria Of PCOS, 2003 2 out of 3 features are present: 1. Oligomenorrhoea and or Anovulation 2. Clinical Hyperandrogenism and/or hyperandrogenemia. 3. Polycystic ovaries (U/S). After exclusion of other etiologies. Aboubakr Elnashar
  25. 25.  Clinical Hyperandrogenism 1. Hirsutism: The primary clinical indicator of androgen excess . 2. Acne : Potential marker 3. Androgenic alopecia: Poor marker unless with Oligomenorrhoea.  Hyperandrogenemia • FT) or FTI) are the more sensitive methods • Routine measurement of Androstenedione: are not recommended. • DHEAS is raised in small fraction of patient with PCOS .Aboubakr Elnashar
  26. 26. Hirsutism Hirsutism Aboubakr Elnashar
  27. 27. Hirsutism Aboubakr Elnashar
  28. 28. AcneHirsutism Aboubakr Elnashar
  29. 29. PCOS with hirsutism Aboubakr Elnashar
  30. 30. Ovarian orgin. Lateral mammary hirsutism, score 1 Aboubakr Elnashar
  31. 31. Grading scale for female pattern hair loss mild but obvious female pattern hair loss Female androgenic alopecia Frontal and temporal hair loss Aboubakr Elnashar
  32. 32. Rotterdam U/S Criteria of PCOS At least one of the following: • 12 or more follicles measuring 2–9 mm in diameter • increased ovarian volume (>10 cm3).  The distribution of follicles and a description of the stroma are not required for diagnosis.  The presence of a single PCO is sufficient to provide the diagnosis. Aboubakr Elnashar
  33. 33. Hirsutism in a young woman with PCOS. Note the acne lesions and excessive hair on her face and neck. Aboubakr Elnashar
  34. 34. Aboubakr Elnashar
  35. 35. Aboubakr Elnashar
  36. 36. PCOS with hirsutism (Ferriman and Gallwey score 4) on the abdomen Aboubakr Elnashar
  37. 37. Examples of hirsutism affecting the back, chest, and abdomen Aboubakr Elnashar
  38. 38. 2. Ovarian Tumors:0.5% Virilizing ovarian tumors arrhenoblastoma, hilus cell tumor, lipod cell tumor, granulosa cell tumor Luteoma of pregnancy { Not true tumor but an exaggerated reaction of ovarian stroma to chorionic gonadotropins. It is solid, usually unilateral & regress after labour} 3. Ovarian dysgenesis Aboubakr Elnashar
  39. 39. Uterus and adnexa during caesarian section—both ovaries were enlarged (mean diameter 8 cm). Luteoma Aboubakr Elnashar
  40. 40. B. Adrenal:5% 1. Cong adrenal hyperplasia 2. Tumors 3. Cushing syndrome Congenital adrenal hyperplasia Androgen secreting tumor Centipetal obesity in Cushing's syndrome Aboubakr Elnashar
  41. 41. Aboubakr Elnashar
  42. 42. Aboubakr Elnashar
  43. 43. Adrenal SAHA. Central hirsutism, score 2 Adrenal SAHA. Severe papulo-pustular acne and central hirsutism Aboubakr Elnashar
  44. 44. Cushing's Syndrome Aboubakr Elnashar
  45. 45. Aboubakr Elnashar
  46. 46. Centripetal obesity 79-97 Facial plethora 50-94 Glucose intolerance 39-90 Weakness, proximal myopathy 29-90 Hypertension 74-87 Psychological changes 31-86 Easy bruisability 23-84 Hirsutism 64-81 Oligomenorrhea or amenorrhea 55-80 Acne, oily skin 26-80 Abdominal striae 51-71 Ankle edema 28-60 Backache, vertebral collapse, fracture rare Clinical manifestations % Aboubakr Elnashar
  47. 47. Cushing’s Syndrome One should be aware of the possibility of Cushing’s syndrome in women with stigmata of the : PCOS & Obesity as it is a disease of insidious onset and dire consequences Aboubakr Elnashar
  48. 48. Forearm of a women man with Cushing's disease showing multiple ecchymoses due to minimal trauma. 30-year-old woman with Cushing's disease showing round, plethoric "moon" face, facial hirsutism, and increased supraclavicular fat pads Aboubakr Elnashar
  49. 49. C. PERIPHERAL 1. Idiopathic: Regular ovulation & normal androgen levels 2. Insulin resistance – HAIRAN syndrome: HyperAndrogenic Insulin-Resistant Acanthosis Nigricans – 5H syndrome acanthosis nigricans. Aboubakr Elnashar
  50. 50. Aboubakr Elnashar
  51. 51. 3. Aromatase deficiency 4. Glucocorticoid resistance 5. Hyperprolactinema can cause an increase in DHEAS. TT with bromocriptin: dec PRL & DHEAS Aboubakr Elnashar
  52. 52. Hirsutism Anabolic steroids Danazol Metoclopramide Methyldopa Phenothiazines Progestins Reserpine Testosterone Hypertrichosis Cyclosporine Diazoxide Hydrocortisone Minoxidil Penicillamine Phenytoin Psoralens Streptomycin Hunter, 2003 D. Drugs Aboubakr Elnashar
  53. 53. Clinical evaluation Aboubakr Elnashar
  54. 54. Primary objective: 1. Confirm diagnosis 2. Determine degree 3. Exclude life threatening diseases Aboubakr Elnashar
  55. 55. History .Virilization, psychological .Onset & duration: Rapidly progressive virilization: androgen secreting tumors .Menstrual history: PCOS, Pregnancy .Family history: Hair patterns are similar in families .Drug intake Aboubakr Elnashar
  56. 56. Examination .General: Thyroid disease, Cushing syndrome, Signs of virilization, Signs of insulin resistance e.g. acanthosis nigricans. Aboubakr Elnashar
  57. 57. .Breast: Galactorrhea {Hyperprolactinaemia can be accompanied by increase in adrenal androgen} .Pelvic: mass Aboubakr Elnashar
  58. 58. Degree of hirsutism Photography or scoring systems a. Ferriman & Gallwey(1961): 9 areas upper lip, chin, chest upper abdomen, lower abdomen, upper arm, thighs, upper back, lower back/buttocks minimal=1, mild=2, moderate=3, severe=4 >8 = hirsutism 15 = organic cause Aboubakr Elnashar
  59. 59. Degree of hair growth (Ferriman & Gallwey,1961) Aboubakr Elnashar
  60. 60. Aboubakr Elnashar
  61. 61. b. Macnight (1964): divided the body into 7 areas: Face Neck Shoulders Chest Abdomen back Aboubakr Elnashar
  62. 62. Investigations Aboubakr Elnashar
  63. 63. Total testosterone: measures the ovarian & adrenal activity. When testing for elevated androgen levels: measure an early morning plasma total testosterone level as the initial test. Aboubakr Elnashar
  64. 64. Free testosterone Good correlation with total production rate (= secretion rate + peripheral conversion rate) Good correlation with degree of virilization If the plasma total testosterone is normal in the presence of risk factors for hyperandrogenism or the presence of hirsutism that progresses despite therapy: measuring an early morning plasma total and free testosterone Free androgen index(FAI)= TX 100 / SHBG if > 4.5: PCOS •Not done routinely in presence of hirsutism Aboubakr Elnashar
  65. 65. 17 OHP: an intermediate metabolite in steroidogensis in the adrenals. In patients with a high likelihood of congenital adrenal hyperplasia [positive family history, member of a high-risk ethnic group such as Ashkenazi Jews (prevalence 1 in 27), Hispanics (1 in 40), and Slavics (1 in 50)], we recommend measurement of an early morning follicular phase level of 17-hydroxyprogesterone.  DHEAS: Good marker of Adrenal A production Not essential Aboubakr Elnashar
  66. 66. DHES is not essential (Speroff,2005) 1. If 17 OHP is normal: adrenal enzyme defect can be excluded . 2. Moderate elevations of DHES can be suppressed by suppression of ovulation. 3. DHES > 700 ug/dl is rare & is associated with high levels of T 4. Imaging of the adrenals is more cost-effective than measuring DHES. Aboubakr Elnashar
  67. 67. 3 alpha androstanediol glucuronide •Metabolite of DHT •Good marker of peripheral androgen action •Inc {increased activity of 5 alpha reductase} {end organ hypersensitivity} •Not done routinely: 1. No change in diagnosis & treatment, 2. Values overlap in 20% Aboubakr Elnashar
  68. 68. Endocrine Society, 2008 Aboubakr Elnashar
  69. 69. Testosterone (ng/dl) >200 <200 U/S of the ovary Anovulation (PRL, endom biopsy) Adenxal mass Nothing Laparotomy CT of the adrenala & ovaries Laparotomy Aboubakr Elnashar
  70. 70. Ovarian tumors should be suspected 1. Rapid onset of virilization 2. Unilateral adenxal mass 3. Testosterone >200 ng/dl. •TVS, CT or MRI. Aboubakr Elnashar
  71. 71. Screening for late onset adrenal hyperplasia •Incidence: 1-5% •Clinical indication of ACTH stimulation test: Strong family history Severe hirsutism from puberty Flatness of the breast Hypertension Short stature Aboubakr Elnashar
  72. 72. 17 oh P(ng/dl) morning < 200 > 200 Rules out adrenal hyperplasia ACTH stimulation test (0.25 21-hydroxylase deficiency mg ACTH I.V.& 17 oh P at time zero & after 1 hour) Normal Abnormal Rules out adrenal hyperplasia Adrenal hyperplasia Aboubakr Elnashar
  73. 73. Screening for Cushing syndrome •Rare •Indications: Centripetal obesity, buffalo hump Moon face, Virilization Pigmented stria, Hypertension Aboubakr Elnashar
  74. 74. Dexamethazone suppression test ( 1 mg orally at bed time) Free cortisol (ug/dl > 6 < 6 long term dexamethazone test Normal Aboubakr Elnashar
  75. 75. PCOS T LH/FSH usually inc 2/1 Late-onset CAH 17-OH-P >200 ng/dL Androgen-secreting ov tumor Total T >200 ng/dL Androgen-secreting ad tumor DHEAS >700 g/dL Cushing syndrome Cortisol Increased Exogenous androgen use Toxicology screen Increased Aboubakr Elnashar
  76. 76. Treatment Aboubakr Elnashar
  77. 77. Androgen Excess Society,2012 Aboubakr Elnashar
  78. 78. Lines of treatment I. General II. Specific III. Local IV. Surgery Aboubakr Elnashar
  79. 79. I. General •Reassurance: •explain the condition, treatment regimen & the time required •Stop smoking •Weight reduction: {Inc SHBG: Dec FT} Keep BMI around 21 kg / m2 Dec the risk of DM & CVD Aboubakr Elnashar
  80. 80. II. Specific I. Ovarian suppression: 1. OCPs 2. Progestagen 3. GnRha II. Adrenal suppression: Corticosteroids III. Antiandrogens: 1. Spironolactone 2. Cyproterone acetate 3. Flutamide 4. Ketoconazole IV. 5 alpha reductase inhibitors: Finasteride V. Insulin sensitizer: MetforminAboubakr Elnashar
  81. 81. I. Ovarian suppression 1. Oral contraceptive pills The first line of therapy Mechanism: P: suppress ov steroidogenesis E: inc SHBG: dec FT Aboubakr Elnashar
  82. 82. Best type: Avoid OCs containing norethisterone or levonorgestrel less androgenic or antiandrogenic high estrogen Diane (cyproterone acetate), Yasmin (Drospirenone) Clordion, Gestafortin, Lormin, NonOvlon, Normenon, Verton (Chlormadinone acetate) Gynera (gestodene), Marvelon (desogestrel), Cilest (norgestimate). Effect: 1. Dec T after 1-3 mo. 2. Additional benefitsAboubakr Elnashar
  83. 83. We do not suggest one particular OCP over another for treating hirsutism (Endocrine Society, 20108) most androgenic progestin: Levonorgestrel, norethisterone low androgenicity: norgestimate and desogestrel progestins with antiandrogenic activity drospirenone and CPA One small trial did not demonstrate a difference in hirsutism efficacy between an OCP containing levonorgestrel and one containing desogestrel Levonorgestrel may adversely affect metabolic biomarkers when compared with other less androgenic progestins, but there are no data to suggest that these effects are associated with adverse clinical outcomes.Aboubakr Elnashar
  84. 84. OCPs containing either 30–35 g ethinyl estradiol or the lower-dose 20-g preparations may be used for suppression of ovarian androgens. There are no clinical trials of 20-g OCPs for hirsutism, but these lower-dose preparations appear to be as effective as the 30- to 35-g preparations for acne. Aboubakr Elnashar
  85. 85. 2. Progestins Indication: If pills is contraindicated or unwanted Mechanism: inhibit ov steroidogenesis, inc clearance of androgen, inhibit 5 alpha reductase dec SHBG:inc FT Dose: DMPA: 150 mg IM / 3 mo. MPA: 30 mg PO / d Effect: comparable to OCPs Aboubakr Elnashar
  86. 86. 3. Gn Rh analogue Indications: Failure of usual management Overweight with severe hirsutism Dose: leuprolide acetate depot: IM / mo. The initial stimulatory effect can be avoided by starting therapy in the luteal phase when Gnt are already suppressed by elevated progesterone levels. Once maximal response has been obtained OCP or antiandrogen for long term suppression of hair growth. Treatment should be limited to 6 mo. Aboubakr Elnashar
  87. 87. Mechanism of action: Side effects: of estrogen deficiency Use with OCPs: {avoid problems associated with E deficiency & add benefits} Effects: highly effective & better than OCP alone Aboubakr Elnashar
  88. 88. II. Adrenal suppression Glucocorticoids Indication: 1.High not moderate elevation of DHEAS (Sperof,2005) 2. CAH Mechanism: inhibit ACTH dependant androgen Aboubakr Elnashar
  89. 89. Dose: Nocturnal {maximal suppression of the CNS adrenal axis that peaks during sleep} Dexamethazone: 0.3 mg or 0.25 mg/ other evening Prednisone: 3 mg Adrenal hyperplasia: higher doses Effects: 1. No cortisol suppression 2. No Cushingoid side effects Aboubakr Elnashar
  90. 90. Aboubakr Elnashar
  91. 91. III. Antiandrogens 1. Spironolactone (Aldactone) Dose: 100-200 mg/d remission: dec dose to 25-50 mg 100-200 mg/d from D1-D21 Mechanism : on receptor ovary & adrenals Liver kidney Aboubakr Elnashar
  92. 92. Side effects: minimal. Mens irregularities, mastalgia, feminization of male fetus, transient diuresis, hyperkalemia, ?carcinogenic Use with OCP: 1. Dramatic effect, but not impressively better 2. Prevent feminization of male fetus 3. Regular menstruation Effects: maximal by 6mo Cessation : relapse Aboubakr Elnashar
  93. 93. 2. Cyproterone acetate (androcure) Dose: 50-100 mg from D5 to D15 & EE2: 30-50 ug from D5 to D25. Dec dose after remission Mechanism: on receptors Progestational effect Weak corticosteroid effect Aboubakr Elnashar
  94. 94. Side effects: mens irregularities, mastalgia, feminization of male fetus, loss of libido, fatigue, edema, weight gain, decrease HDLP & cholesterol, glucose intolerance. Use with EE2 or OCPs Effects: maximal by 3mo improvement in 60-90% Cessation: relapse Aboubakr Elnashar
  95. 95. 3. Flutamide (Eulexin) Indication: under tertiary center supervision Severe cases Failure of spironolactone & OCPs Dose: 250 - 500 mg/d Mechanism: antiandrogen. Aboubakr Elnashar
  96. 96. Side effects: dryness of the skin, increase appetite hepatotoxicity, expensive. It is unsuitable for treatment of hirsuitism (Speroff, 2005) Use with OCPs: 1. Add benefit 2. Avoid block androgen receptors in male fetus. Effects: Similar or better than Spironolactone We do not recommend one antiandrogen over another, except that we recommend against the use of flutamide. Aboubakr Elnashar
  97. 97. Aboubakr Elnashar
  98. 98. IV. 5 alpha reductase inhibitors Finasteride (Proscar) Indication: under tertiary center supervision. Severe cases Mode of action: Inhibit 5 alpha reductase activity: blocking conversion of T to DHT. Dose: 2.5 - 5 mg /d Aboubakr Elnashar
  99. 99. Side effects: very minimal. Teratogenic Use with OCPs: To avoid risk on male fetus & added benefits. Effects: Flutamide or Spironolactone is more effective Drugs in this class: Finasteride 5 mg (Proscar} Finasteride 1 mg (Propecia) Dutasteride (Avodart) Aboubakr Elnashar
  100. 100. V. Insulin sensitizer Metformin •PCOS IH: {insulin resistance} (Unluhizarci et al, 2004). •1500 mg/d •Dec serum insulin & T. Dec F&G score (Kazerooni et al, 2003 ; Kelly & Gordon, 2003) •Metformin Vs Dianette (EE2: 35 ug + cyproterone acetate: 2 mg) Dianette was more effective (Harborne et al, 2003). Aboubakr Elnashar
  101. 101. Cochrane library (2003) •Cyprotrone acetate was compared to (spironolactone, flutamide, finastride, GnRHa, Ketconazole): No differences in clinical outcomes Spironolactone 100 mg/d is superior to finastride 5 mg/d & low dose cypr acetate 12.5 mg/d (first 10 days of the cycle) up to 12 months after the end of the treatment Aboubakr Elnashar
  102. 102. III. Local Suppress hair growth: Eflornithine Hydochloride (Vaniqa) Remove hair pigment: Bleaching Temporary depilation: shaving, chemical depilators Temporary epilation: plucking, waxing Permanent removal: Electrolysis, Laser & intense pulsed light Aboubakr Elnashar
  103. 103. 1. Suppress hair growth Eflornithine 13.9% (Vaniqa) cream •Inhibits ornithine decarboxylase (an enzyme in hair dermal papilla that is essential for hair growth). •Face, neck Can be used with other tt e.g. lasers, intense pulsed light Regrowth can take 2 ms: Must be continued indefinitely to prevent regrowth S effects: stinging, burning, tingling Aboubakr Elnashar
  104. 104. 2. Bleaching (remove hair pigment) •Hydrogen peroxide, often combined with amonia. •Face, arms Hair lightens & softens, inexpensive Hair discoloration, skin irritation, Lack of effectiveness Aboubakr Elnashar
  105. 105. 3. Temporary depilation (remove part of hair) a. Shaving: •All areas Inexpensive, effective & does not cause change in hair quality, quantity or texture. Daily need, skin irritation, quick regrowth folliculitis, time consuming, beard stubbleAboubakr Elnashar
  106. 106. b. Chemical depilators: •Break down & dissolve hair by hydrolysing disulhide bonds. •Extremities, groin, face Quick, inexpensive, effective Regrowth in days, skin irritation Aboubakr Elnashar
  107. 107. 4. Temporary epilation (remove the entire hair) a. Plucking: •Face, eyebrows, nipples, bikini area Effective for small amount, inexpensive, regrowth can take weeks Pain, skin irritation, postinflam pigmentation, folliculitis, slow, ingrown hairs, scarring Aboubakr Elnashar
  108. 108. b. Waxing: group plucking •Face, eyebrows, groin, trunk, extremities Regrowth can take 6 weeks Pain, postinflam pigmentation, scarring, slow, expense, irritation, folliculitis Aboubakr Elnashar
  109. 109. 5. Permanent removal (destruction of the dermal papilla) a. Electrolysis: •Needle is inserted into the hair follicle & a current is used to destroy the dermal papilla. •All areas, usually the face May give permanent removal Pain, scarring, painful, repeat treatments needed time consuming, expensive, pigmentation Aboubakr Elnashar
  110. 110. b. Laser & intense pulsed light •Selective phototricholysis. A light source sufficient to penetrate to the follicular bulge & the papillae is directed at the hair by probe. •All areas May give permanent hair reduction, efficient, painless Dark hair required, expensive, scarring, skin pigmentation, repeated treatments usually necessary Aboubakr Elnashar
  111. 111. Aboubakr Elnashar
  112. 112. IV. Surgery •Tumor •LOD Discrepant & variable response. Modest & sustained improvement in 25% (Amer et al, 2002). Aboubakr Elnashar
  113. 113. Guidelines Endocrine Society 2008 Diagnosis of hirsutism 1. We suggest against testing for elevated androgen levels in women with isolated mild hirsutism because the likelihood of identifying a medical disorder that would change management or outcome is low (2). Aboubakr Elnashar
  114. 114. 2. We suggest testing for elevated androgen levels in women with (2) • Moderate or severe hirsutism • Hirsutism of any degree when it is sudden in onset, rapidly progressive, or when associated with any of the following: – menstrual irregularity or infertility – central obesity – acanthosis nigricans – rapid progression – clitoromegaly Aboubakr Elnashar
  115. 115. Treatment of hirsutism 1. For women with patient-important hirsutism despite cosmetic measures, we suggest either pharmacological therapy or direct hair removal methods (2). The choice between these options depends on (a) patient preferences, (b) The extent to which the area of hirsutism that affects wellbeing is amenable to direct hair removal, and (c) access to and affordability of these alternatives. Aboubakr Elnashar
  116. 116. 2.Pharmacological treatments a. Monotherapy For the majority of women, we suggest oral contraceptives to treat patient-important hirsutism (2) because of its teratogenic potential, we recommend against antiandrogen monotherapy unless adequate contraception is used (1| ). For women who cannot or choose not to conceive, we suggest the use of either oral contraceptive preparations (OCPs) or antiandrogens The choice between these options depends on patient preferences regarding efficacy, side effects, and costs.Aboubakr Elnashar
  117. 117. We suggest against the use of flutamide therapy (2). We suggest against the use of topical antiandrogen therapy for hirsutism (2). We suggest against using insulin-lowering drugs as therapy for hirsutism (2). Aboubakr Elnashar
  118. 118. For women with hirsutism who do not have classic or nonclassic congenital adrenal hyperplasia due to 21-hydroxylase deficiency (CYP21A2), we suggest against glucocorticoid therapy (2). We suggest glucocorticoids for women with hirsutism due to non classic congenital adrenal hyperplasia (NCCAH) who have a suboptimal response to OCPs and/or antiandrogens, cannot tolerate them, or are seeking ovulation induction (2). Aboubakr Elnashar
  119. 119. We suggest against using GnRH agonists except in women with severe forms of hyperandrogenemia, such as ovarian hyperthecosis, who have a suboptimal response to OCPs and antiandrogens (2). For all pharmacologic therapies for hirsutism, we suggest a trial of at least 6 months before making changes in dose, changing medication, or adding medication (2). Aboubakr Elnashar
  120. 120. b. Combination therapy If patient-important hirsutism remains despite 6 or more months of monotherapy with an oral contraceptive, we suggest adding an antiandrogen (2). Aboubakr Elnashar
  121. 121. 3. Direct hair removal methods For women who choose hair removal therapy, we suggest laser/photoepilation (2). For women undergoing photoepilation therapy who desire a more rapid initial response, we suggest adding eflornithine cream during treatment (2). For women with known hyperandrogenemia who choose hair removal therapy, we suggest pharmacologic therapy to minimize hair regrowth (2). Aboubakr Elnashar
  122. 122. Benha University Hospital, Egypt Email: elnashar53@hotmail.com Aboubakr Elnashar