Hirsutism

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Hirsutism

  1. 1. 1 HIRSUTISM Prof, M.C.Bansal. Founder Principal & Controller; Jhalwar Medical college And hospital, Jhalawar. Ex . Principal & controller; Mahatmagandhi Medical College And Hospital,
  2. 2. EXCESSIVE HAIR GROWTH IT MAY BE EITHER HYPERTRICHOSIS—Excess of hair growth all over the body. HIRSUTISM—Male type sex hair growth in females. VIRILIZATION—Excess sex hair growth and other hyper androgenic effects on female genitalia and body.
  3. 3. 3 DEFINITION HYPERTRICHOSIS : REFERS TO HAIR DENSITY OR LENGTH BEYOND THE ACCEPTED LIMITS OF THE NORMAL FOR THE PARTICUALR AGE,RACE OR SEX. • The excess hair may be generalised or localised and may consist of lanugo, vellus or terminal hair. • It is frequently associated with the use of medication such as antiepileptics
  4. 4. Inherited types CONGENITAL HYPERTRICHOSIS LANUGINOSA – confluent generalised over growth of silvery blonde to grey lanugo hair at birth or early infancy, autosomal dominant, associated dental anomalies. AMBRAS syndrome- longer thicker hair more over the face,ears and shoulders, facial dysmorphism and dental anomalies. CONGENITAL GENERALISED HYPERTRCHOSIS – X linked dominant 4
  5. 5. Acquired types ACQUIRED HYPERTRICHOSIS LANUGINOSA – seen in underlying malignancy DRUG INDUCED – following minoxidil therapy, diazoxide, phenytoin sodium, cyclosporine, topical tacrolimus. POEMS syndrome PORPHYRIA CUTANIA TARDA – hexachlorobenzene, underlying hepatic tumour. 5
  6. 6. Localised hypertrichosis Congenital  Hairy elbow  Spina bifida  Trichomegaly Acquired  Interferon  Repeated trauma  Congenital AV fistula 6
  7. 7. 7 DEFINITION HIRSUTISM : APPEARANCE OF EXCESSIVE COARSE (TERMINAL)HAIR IN A PATTERN NOT NORMAL IN THE FEMALE Definition highlights the abnormal distribution of excess hair growth ,such as facial ,chest or upper abdomen.
  8. 8. Hirsutism in an young girl with PCOD
  9. 9. Abdominal Hair Growth ___PCOD
  10. 10. HIRSUTISM
  11. 11. 11 DEFINITION VIRILIZATION : REFERS TO CONCURRENT PRESENTATION OF HIRSUTISM WITH A BROAD RANGE OF SIGNS SUGGESTIVE OF ANDROGEN EXCESS,SUCH AS ACNE, FRONTOTEMPORAL BALDING, DEEPENING OF THE VOICE , A DECREASE IN BREAT SIZE CLITORAL HYPERTROPHY
  12. 12. 12 INCREASED MUSCLE MASS AMENORREA / OLIGOMENORRHEA Virilization is seen less frequently than hirsutism and may reflect a severe underlying pathologic condition ,such as Male sex hormone producing Ovarian / adrenal tumors Hirsutism and virilization are closely interlinked and hirsutism may actually be the first manifestation of a condition that ultimately will lead to virilization if left untreated
  13. 13. Acne & Hirsutism
  14. 14. Clitoral Enlargement In female hrmophodyte secondary to cogenital adrenal hyperplasia
  15. 15. 15 BASIC FACTS ABOUT HAIR Each hair follicle develops at about 8-10wks of gestation as a derivative of epidermis. Number of hair follicles is set from birth Hair grows from a individual hair follicle that are part of a pilosebaceous gland unit Main difference between sexes is the degree of differentiation of the hair Human hair growth is continuous Hair grows in a mosaic pattern(in a given area ,hair are in different stages of development)
  16. 16. 16 BASIC FACTS ABOUT HAIR Some condition may cause a high level of synchrony between the growth cycles of hair ,leading to the appearance of either massive hair loss (alopecia)or excess hair for a limited period of time
  17. 17. 17 BASIC FACTS ABOUT HAIR Growth cycle of the Hair: ACT Anagen : Growth phase,85- 90 % of the life cycle Catagen : rapid involution Phase Telogen : Quiescent phase The growth phase or the anagen phase is primarily influenced by disorders that stimulate hair growth as well as therapeutic modalities.
  18. 18. 18 BASIC FACTS ABOUT HAIR Three types of Hair : Lanugo : Body hair seen in the fetus and newborn Vellus : Fine adult hair covering the body Terminal hair : Thick pigmented hair of scalp and pubic area Thickness of the terminal hair varies form one individual to other depending upon genetic, and possibly nutritional
  19. 19. 19 BASIC FACTS ABOUT HAIR Androgen sensitive hair : depend upon androgen input for hair growth. Face,neck,chest,abdomen,axillary,upper arms ,inner thighs and pubic hair,+ part of the scalp hair. Less Androgen independent : Forearms ,hands .lower legs
  20. 20. ANDROGEN INDUCED HAIR GROWTH 20 adrenal pitutary ovary ACTH LH TESTOSTERONE HAIR FOLLICLE
  21. 21. Androgens are C-19 steroids produced in: • Adrenal gland • Ovary • Androgens are metabolised in:  Skin  Adipose tissue  Liver  Placenta 21
  22. 22. 22 Testosterone Androstendione DHA DHAS ADRENAL CORTEX OVARY 50 50 90 10 99 50 25 25 Origin of circulating androgens
  23. 23. The production rate of testosterone in the normal female is 0.2 to 0.3 mg/day Normal total testosterone concentration in serum is below 0.8ng/ml 23
  24. 24. Hair & sebaceous Follicle Response to Hyperandrogenism
  25. 25. 25 PRESENTATION OF HIRSUTISM HIRSUTISM ALONE HIRSUTISM AND ASSOCIATED PILOSEBACEOUS UNIT OVERACTIVITY (ACNE) HIRSUTISM AND OVULATORY DISORDERS HIRSUTISM AND SIGNS OF VIRILIZATION
  26. 26. 26 PRESENTATION OF HIRSUTISM Hirsutism alone is the greatest challenge,patients usually go to dermatologist Hirsutism wIth acne is frequently develop in teenage girls Hirsutism with ovulatory disorders comes mostly to gynecologist Hirsutism with virilization requires immediate work-up
  27. 27. 27 CAUSES OF HIRSUTISM Excess androgen production Relative circulating androgen excess and low binding globulins Excess end organ response Patient perception
  28. 28. 28 DISORDERS OF EXCESS ANDROGEN PRODUCTION Source of androgen : Exogenous Endogenous (most common) Two primary endogenous sources : Adrenal glands Ovaries
  29. 29. Mechanism of excessive hair growth Main stimulus- Testosterone Testosterone – binds – androgen receptors 29 Activation of 5 alpha reductase DHT TERMINAL HAIR ANDROSTENEDION
  30. 30. ANDROGEN Lengthen Anagen phase Increase hair follicle size Increase hair follicle diameter Increase sebum secretion 30
  31. 31. 31 Normal women Hirsute women 80% SHBG 79% SHBG 19% Albumin 19% Albumin 1% Free 2% Free
  32. 32. Causes of hirsutism Androgenic ( 75-85% ) Non Androgenic Idiopathic 32
  33. 33. ANDROGENIC PCOD(70-80%) Hyperandrogenism - 6.8% The hyperandrogenic insulin-resistant acanthosis nigricans syndrome (HAIR-AN) - 3 % 21-hydroxylase non-classicaI adrenal hyperplasia (late- onset CAH) - 1.6% Hypothyroidism - 0.7% 21-hydroxylase-deficient congenital adrenal hyperplasia - 0.7% Hyperprolactinemia - 0.3% Androgenic tumors - 0.2% Cushing’s syndrome - 0-1% 33
  34. 34. NON ANDROGENIC Acromegalics. chronic skin problems, Non-androgenic anabolic drugs. Danazol (Danocrine) Norplant Metoclopramide (Reglan) Anabolic steroids Methyldopa (Aldomet) Phenothiazines Progestins Reserpine (Serpasil) Testosterone 34
  35. 35. Tumor related causes of hirsutism Tumors of the ovaries and the adrenal glands secrete excess hormones including androgen. Ovarian tumors Adrenal tumors Granulosa -theca cell tumors Adrenal adenoma Arrhenoblastoma Adrenal carcinoma Gonadoblastomas Lipoid cell tumors ACTH secreting tumors Dysgerminoma Brenner's tumor 35
  36. 36. 36 COMMON CAUSES OF ECTOPIC ACTH SECRETION Small cell carcinoma of the lung 50% Endocrine tumors of foregut origin 35% Thymic carcinoid Islet cell tumor Medullary carcinoma thyroid Bronchial carcinoid Pheochromocytoma 5% Ovarian tumors 2%
  37. 37. Miscellaneous causes of hirsutism Functional adrenal hyperandrogenism Hypereactio luteinalis of pregnancy - transient increase in androgen levels during pregnancy Thecoma of pregnancy - Transient androgen secreting tumor during pregnancy True hermaphroditism - condition where both male and female internal sex organs are present 37
  38. 38. Genetics There are very obvious family and racial differences in hirsutism patients. In some women, the skin is very sensitive to even low levels of androgens and their follicles produce primarily terminal (coarse and dark) hair. 38
  39. 39. 39 DISORDERS OF EXCESS ANDROGEN PRODUCTION ADRENAL ANDROGEN EXCESS May be linked to genetically determined steroid synthesis enzyme deficiency Malignant adrenal neoplastic process Other conditions like Cushing’s syndrome
  40. 40. 40 DISORDERS OF EXCESS ANDROGEN PRODUCTION ADRENAL ANDROGEN EXCESS Three recognised adrenal enzyme deficiencies : 21 alpha Hydroxylase defieiency 11-beta-Hydroxylase deficiency 3-beta-ol-dehydrogenase deficiency Classical forms are usually presented in prenatal or neonatal period as ambiguous genitalia in female Nonclassic forms are linked with hirsutism
  41. 41. The enzyme deficiency causes reduction in end-products, accumulation of hormone precursors & increased ACTH production. The clinical picture reflects the effects of inadequate production of cortisol & aldosterone and the increased production of androgens & steroid metabolites. 41
  42. 42. 42
  43. 43. 43  ACTH ↑  Cortisol ↓  Aldosterone ↓  17-OH-progesterone↑  Testosterone ↑  Urinary 17-ketosteroids↑ ESSENTIALS OF DIAGNOSIS
  44. 44. 44 In less severe forms (late onset CAH) Genitalia is normal at birth. Precocious pubic hair & Clitoromegaly Excess facial or body hair appear later in childhood, often accompanied by tall stature GIRLS WITH CAH Varying virilizing symptoms ranging from oligomenorrhea to hirsutism and infertility
  45. 45. 45 DISORDERS OF EXCESS ANDROGEN PRODUCTION 21-alpha-Hydroxylase deficiency: Most common ,<1% to >10% Prevalence depends on ethnic origin(common in slavs,1/50 Hispanics 1/40, ashkenazi jews 1/27 Cushing’s syndrome :Hirsutism with weight gain and growth retardation as the primary manifestation,with acne and other cutaneous problems
  46. 46. causes 46 ACTH-dependent States ACTH-secreting pituitary tumor ( Cushing’ s disease ) 90-95% Pituitary CRH-secreting neoplasm ( ectopic CRP syndrome ) Nonpituitary ACTH-secreting neoplasm ( ectopic ACTH syndrome ) ACTH-independent States Adrenal adenoma/carcinoma Micronodular /macronodular adrenal disease Exogenous Sources Glucocorticoid intake Psychiatric Conditions (Pseudo-Cushing Disorders) Depression Alcoholism
  47. 47. 47 CLINICAL FEATURES OF GLUCOCORTICOID EXCESS Weight gain 90% “ Moon facies” 75 Hypertension 75 Violaceous striae 65 Hirsutism 65% Glucose intolerance 65 Proximal muscle weakness 60 Plethora 60 Menstrual dysfunction 60 Acne 40 Easy bruising 40 Osteopenia 40 Dependent edema 40 Hyperpigmentation 20 Hypokalemic metabolic alkalosis 15
  48. 48. 48 DISORDERS OF EXCESS ANDROGEN PRODUCTION OVARIAN ORIGIN Most common cause is POLYCYSTIC OVARIAN SYNDROME Other Neoplastic ovarian disease
  49. 49. PCOS In 70-80 % cases of hirsutism 5-10% of women in reproductive age Fulfills the Rotterdam criteria Hyperandrogenism Amenorrhoea /oligomenorrhoea USG features of PCOD Anovulation Infertility Obesity 49
  50. 50. Pathogenesis dpankar 50
  51. 51. Increased ovarian androgen biosynthesis in the polycystic ovary syndrome results from abnormalities at all levels of the hypothalamic–pituitary–ovarian axis. The increased frequency of luteinizing hormone (LH) pulses in the polycystic ovary syndrome appears to result from an increased frequency of hypothalamic gonadotropin-releasing hormone (GnRH) pulses. The latter can result from an intrinsic abnormality in the hypothalamic GnRH pulse generator, favoring the production of luteinizing hormone over follicle- stimulating hormone (FSH) in patients with the polycystic ovary syndrome, in whom the administration of progesterone can restrain the rapid pulse frequency 51
  52. 52. . By whatever mechanism, the relative increase in pituitary secretion of luteinizing hormone leads to an increase in androgen production by ovarian theca cells. Increased efficiency in the conversion of androgenic precursors in theca cells leads to enhanced production of androstenedione, which is then converted by 17 -hydroxysteroid dehydrogenase (17 ) to form testosterone or aromatized by the aromatase enzyme to form estrone. Within the granulosa cell, estrone is then converted into estradiol by 17. 52
  53. 53. . Numerous autocrine, paracrine, and endocrine factors modulate the effects of both luteinizing hormone and insulin on the androgen production of theca cells; insulin acts synergistically with luteinizing hormone to enhance androgen production. Insulin also inhibits hepatic synthesis of sex hormone–binding globulin, the key circulating protein that binds to testosterone and thus increases the proportion of testosterone that circulates in the unbound, biologically available, or "free," state. Testosterone inhibits and estrogen stimulates hepatic synthesis of sex hormone–binding globulin. The abbreviation scc denotes side-chain cleavage enzyme, StAR steroidogenic acute regulatory protein, and 3 -HSD 3 -hydroxysteroid dehydrogenase. Solid arrows denote a higher degree of stimulation than dashed arrows. 53
  54. 54. 54 Lab.Evaluation of Hirsutism Three basic hormonal evaluation 1. Total testosterone 2. DHEAS 3. 17-hydroxyprogesterone
  55. 55. Normal ranges Total testosterone 20-80 ng/dl Free testosterone 0.3-1.9 ng/dl Bioavailable testosterone 0.8- 10 ng/dl Free androgen index ( T/SHBG x 100) Androgen producing tumor > 200 ng/dl 55 The Testosterone level
  56. 56. 56 RELATIVE ANDROGEN EXCESS AND SHBG <3 % TESTOSTERONE IS FREE Mostly bound to Sex hormone binding globuline(SHBG) Dcrease in SHBG leads to Excess free Testosterone Causes of Reduced SHBG : PCOS(Chronic anovulation) and Obesity
  57. 57. 57 EXCESS REPONSIVITY TO ANDROGEN TESTOSTERONE 5-ALPHA – REDUCTASE DIHIDROTESTOSTERONE Excessive response of the receptor to DHT(may be due to mutation of the highly polymorphic region in gene of the receptor located on X Chromosome Over activity of the 5-alpha-reductase (Type –1 and Type 2,type –1 is involved in hirsutism ) TARGET CELLS RECEPTOR
  58. 58. 58 Flowchart for investigation of hirsutism
  59. 59. 59 BASIC APPROACH TO THE DIAGNOSIS OF HIRSUTISM AND VIRILIZATION SYMPTOMS AND HISTORY SIGNS PHYSICAL EXAMINATION INVESTIGATION
  60. 60. 60 APPROACH TO DIAGNOSIS Patient may present with ovulatory problems and hirsutism may not be reported There may be normal hair pattern but patient complains about hirsutism Evident virilization should investigated at once
  61. 61. 61 APPROACH TO DIAGNOSIS Careful history regarding the timing of onset and chronological progression Precocious puberty with androgen excess suggests adrenal enzyme defect Family history : androgen excess disorders
  62. 62. 62 APPROACH TO DIAGNOSIS Physical examination Establish presence of hirsutism and quantifying it Presence of acne and virilization and rule out hypertrichosis Skin hyperpigmentation,acanthosis nigricans suggests insulin resistance.Often associated with PCOD
  63. 63. 63 APPROACH TO DIAGNOSIS Measurement of weight and height and blood pressure: defects relates to adrenal enzyme defects Galactorrhoea Tanner staging : Hirsutism before Tanner stage 3 to 4 is alarming and suggests a serious pathology Visual genital examination for virilization
  64. 64. 64 APPROACH TO DIAGNOSIS Degree and extent FERRIMAN GELLWAY SCORE score Quantifies the extent of hair growth in 9 most androgenic sensitive sites Hair growth is graded 0-4 at each site Score of 8 or more (max 36) indicates hirsutism
  65. 65. 65
  66. 66. 66 APPROACH TO DIAGNOSIS INVESTIGATION: FOR VIRILIZATION : Work-up focuses of the identification on the source of androgen excess Rule out exogenous androgen Evidence of endogenous androgen excess: Serum total testosterone Serum dehydroepiandrosterone sulfate (DHEAS)
  67. 67. 67 APPROACH TO DIAGNOSIS INVESTIGATION: FOR VIRILIZATION Imaging studies:Pelvic sonography Adrenal imaging(USG,CT) Specialized studies : Selective venous catherization(adrenal or ovarian) Radioisotope studies
  68. 68. 68 Any age Rapid onset Hirsutes++ Virilism+ Amenorrhoea DHEAS ↑↑(>700µg/100ml) T- normal or ↑ Dexa suppression test- negative IVP CT-scan MRI Any age Rapid onset Hirsutes++ Virilism+ Amenorrhoea T- ↑( >200 ng/100ml) DHEAS- normal Sonography Laparoscopy biopsy ADRENAL TUMOR OVARIAN TUMOR
  69. 69. 69 APPROACH TO DIAGNOSIS INVESTIGATION : HIRSUTISM: Goal is to rule out serious potential life threatening conditions and gain information that helps in treatment Evaluation of Androgen excess: Testosterone ,total preferred DHEAS In selected cases : 17-OHP(fasting morning sample)
  70. 70. 70 APPROACH TO DIAGNOSIS Evaluation of accompanying medical disorder Ovulation disorder :FSH,LH Thyroid dysfunction:TSH Hyperprolactinemia :PRL Other investigations ( inselected cases) Androgen production :Androstenedione, 3-alpha Androstenediol glucuronide Provocative tests : Corticotropin stimulation tests,Insulin resistance determination
  71. 71. Differentation of hyperandrogenism 71 Diagnosis Menstrual Total DHAS LH 17OHP Sourse of Pattern Testoste- Androgen rone PCOS Irregular Elevated mildly Elevated Normal OVARY elevated CAH Irregular Elevated Often Usually Markedly Adrenals Normal Normal elevated Idiopatic Regular Normal Normal Normal Normal Skin hirsutism
  72. 72. 72 THERAPEUTIC OPTIONS VIRILIZATION GOAL: Identify the underlying cause and correcting it Usually related to malignant process and requires surgical approach
  73. 73. 73 THERAPEUTIC OPTIONS HIRSUTISM GOAL: The prevention of further stimulation of hair growth Cosmetic correction of the problem
  74. 74. 74 THERAPEUTIC OPTIONS BASIC STEPS OF MANAGEMENT OF HIRSUTISM ARE: DEFINE THE PROBLEM QUANTIFY THE DEGREE OF HIRSUTISM INDENTIFY THE PATHOPHYSIOLOGY CORRECT THE PROBLEM,WHETHER ACUTE OR CHRONIC DEFINE SUCESSWITH THE PATIENT FOLLOW UP
  75. 75. 75 THERAPEUTIC OPTIONS Regular follow up is indicated at appropriate intervals,usually every 3- 6 months
  76. 76. 76 THERAPEUTIC OPTIONS GENERAL MEASURES : Eliminating causative factors Optimizing weight Weight Reduction Associated with reduction of hyperinsulinemia and androgen excess.BMI should not be > 25 Manage hair Bleaching Cutting or shaving Electrolysis Laser epilation
  77. 77. 77
  78. 78. Removal of the source 78 Adrenal or ovarian tumour – surgically treated Cushing disease – Adrenalectomy Radiation to pituitary Removal of ACTH producing tumor Iatrogenic cases – Offending drug to be stopped
  79. 79. 79 THERAPEUTIC OPTIONS Management of excess ovarian androgen production : Standard therapy is :combined E+P,most commonly OCs It reduces ovarian androgen production It increases SHBG It induces competition at the cellular level for binding to the androgen receptor
  80. 80. 80 THERAPEUTIC OPTIONS Choice of OC EE + Norgestimate approved in USA Cyproteroneacetate used as progesterone component in Ocs Cyproterone acetate: A progestin that also has strong antiandrogenic action. Inhibits gonadotrophin secretion and interferes with androgen action on target organs by competing for androgen receptors Dosage- 100mg from D5-D14 with ethinyloestradiol 30µg, from D 5 to D25
  81. 81. OVARIAN SUPPRESSION BY LONG ACTING GnRH ANALOGUE Can be used for functional ovarian androgen overproduction and even for malignant condition But to be used for long with back-up Treatment is expensive and results are inconsistent Use is reserved for patients resisting to initial therapy. 81
  82. 82. 82 THERAPEUTIC OPTIONS Long acting GnRH analogues used But there is doubt that this therapy will be beneficial over Ocs INSULIN SENSITIZING AGENTS: For PCO with acanthosis nigicans Commonly used agent is : Metformin and Troglitazone,Pioglitazone,Rosiglitazone
  83. 83. 83 Drosperinone in PCOS CLINICAL BENEFITS Helpful in treatment of Hirsutism Excellent cycle control Decreases acne No weight gain. METABOLIC BENEFITS No effect on carbohydrate metabolism No deterioration in the glycemic and insulinemic response to glucose load. No effect on serum lipid concentration. Safe for long term use
  84. 84. 84 THERAPEUTIC OPTIONS MANAGEMENT OF EXCESS ADRENAL ANDROGEN PRODUCTION Metabolic correction of the disorder,usually with exogenous steroids Dexamethasone,mostly used,But LIMITED ROLE
  85. 85. Glucocorticoids 85 Mode of action Suppress pituitary adrenal axis - suppression of endogenous ACTH secretion Use – In adrenal or mixed adrenal and ovarian hyperandrogenism
  86. 86. Glucocorticoid Dosage Frequency Hydrocortisone 10-20 mg Twice daily Prednisone 2.5-5 mg Nightly or a alternate days Dexamethasone 0.25-0.50 mg Nightly 86 Glucocorticoid preparations used in monotherapy & combined with antiandrogens
  87. 87. 87 THERAPEUTIC OPTIONS Management directed to the target organ and cells Competition with Androgen receptors:Spironolactone,Flutamide, Ketoconazole,Cyproterone acetate 5-alpha reductase Inhibitors :Finasteride
  88. 88. 88 CPA 50-100 mg/day on menstrual cycle days 5-15 with ethinyl estradiol 20-35 mg on days 5-25 Spironolactone 100-200 mg/day (given in divided doses twice daily) Finasteride 2.5-5 mg/day Flutamide 250-500 mg/day (high dose) 62.5 to - <250 mg (low dose) DOSES
  89. 89. 89 THERAPEUTIC OPTIONS androgen receptors competitors SPIRONOLACTONE: Best studied and as Gold standard Mechanism :Androgen receptors blockade Suppression of Androgen biosynthesis Increased metabolic clearance of teststerone ( Testosterone  Estrogen ) 50-200 mg/day in two divided doses Spironolactone + OC is well established regimen
  90. 90. 90 THERAPEUTIC OPTIONS androgen receptors competitors FLUTAMIDE : Blocks the androgen receptors Decreases androgen production May have therapeutic value in cases of PCOS Usually used with Ocs KETOCONAZOLE: Equally effective but danger of liver toxicity Last resort of treatment.
  91. 91. CIMETIDINE= 300mg BD LEAST POTENT ANDROGEN RECEPTOR BLOCKER Clinical reports disappointing. CLINICALLY NOT EFFECTIVE. 91
  92. 92. Recent Eflornithien: vaniqua (13.9% cream) US FDA approved It irreversibly inhibits ornithine decarboxylase (ODC), an enzyme that catalyzes the rate- limiting step for follicular polyamine synthesis, which is necessary for hair growth. Improvement occurs gradually over a period of 4-8 weeks or longer. Most reported adverse reactions consisted of minor skin irritation. 92
  93. 93. 93 THERAPEUTIC OPTIONS SELECTING BEST THERAPY: Correct underlying medical problem Correct thyroid/hyperprolactinemia PCO :oral contraceptives Ocs + spironolactone is usually the choice 75 –80% patients shows response Atleast 6 months is needed for evidence of response
  94. 94. Cosmetic treatments for Hirsutism 94 Bleaching - can cause irritation, purities, skin discoloration Shaving - Shaving does not lead to worsening of hirsutism and is a good short-term solution for facial hair. - Does not affect the rate or duration of anagen phase, or diameter of hair - But yields a blunt tip – illusion of thicker hair Plucking, Waxing - scarring, folliculitis, hyperpigmentation Depilatory creams - Irritant dermatitis Electrolysis - painful, erythema, inflammation, scarring Laser
  95. 95. 95 THERAPEUTIC OPTIONS If response is seen in 6 months then treatment should be continued for further 6 months and in most cases for number of years
  96. 96. 96 Hirsutism is a symptom of underlying cause Commonest cause is PCO Progression may hint to diagnosing tumor Treatment – Medicines/ Cosmetic To summarise

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