hirsutism
TRANSCRIPT
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HIRSUTISM
Prof, M.C.Bansal.
Founder Principal & Controller;
Jhalwar Medical college And hospital, Jhalawar.
Ex . Principal & controller;
Mahatmagandhi Medical College And Hospital,
Sitapura, Jaipur.
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.
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DEFINITIONHYPERTRICHOSIS : 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
Inherited typesCONGENITAL 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
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Acquired typesACQUIRED HYPERTRICHOSIS
LANUGINOSA – seen in underlying malignancyDRUG INDUCED – following minoxidil therapy,
diazoxide, phenytoin sodium, cyclosporine, topical tacrolimus.
POEMS syndrome PORPHYRIA CUTANIA TARDA –
hexachlorobenzene, underlying hepatic tumour.
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Localised hypertrichosisCongenital
Hairy elbowSpina bifidaTrichomegaly
Acquired InterferonRepeated traumaCongenital AV fistula
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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.
Hirsutism in an young girl with PCOD
Abdominal Hair Growth ___PCOD
HIRSUTISM
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DEFINITIONVIRILIZATION : 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 SIZECLITORAL HYPERTROPHY
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INCREASED MUSCLE MASS AMENORREA / OLIGOMENORRHEAVirilization is seen less frequently than hirsutism and may reflect a severe underlying pathologic condition ,such as Male sex hormone producing Ovarian / adrenal tumorsHirsutism 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
Acne & Hirsutism
Clitoral Enlargement In female hrmophodyte secondary to cogenital adrenal hyperplasia
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BASIC FACTS ABOUT HAIREach hair follicle develops at about 8-10wks of gestation as a derivative of epidermis.Number of hair follicles is set from birthHair grows from a individual hair follicle that are part of a pilosebaceous gland unitMain difference between sexes is the degree of differentiation of the hairHuman hair growth is continuousHair grows in a mosaic pattern(in a given area ,hair are in different stages of development)
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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
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BASIC FACTS ABOUT HAIR
Growth cycle of the Hair: ACTAnagen : Growth phase,85- 90 % of the life cycleCatagen : rapid involution PhaseTelogen : Quiescent phase
The growth phase or the anagen phase is primarily influenced by disorders that stimulate hair growth as well as therapeutic modalities.
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BASIC FACTS ABOUT HAIR
Three types of Hair :Lanugo : Body hair seen in the fetus and newbornVellus : Fine adult hair covering the bodyTerminal 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
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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
ANDROGEN INDUCED HAIR GROWTH
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adrenal
pitutary
ovary
ACTH LH
TESTOSTERONE
HAIR FOLLICLE
Androgens are C-19 steroids produced in:• Adrenal gland• Ovary • Androgens are metabolised in: Skin Adipose tissue Liver Placenta
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Testosterone Androstendione DHA DHAS
ADRENAL
CORTEX
OVARY
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50
90
10
99
50
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Origin of circulating androgens
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
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Hair & sebaceous Follicle Response to Hyperandrogenism
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PRESENTATION OF HIRSUTISM
HIRSUTISM ALONEHIRSUTISM AND ASSOCIATED PILOSEBACEOUS UNIT OVERACTIVITY (ACNE)HIRSUTISM AND OVULATORY DISORDERSHIRSUTISM AND SIGNS OF VIRILIZATION
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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
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CAUSES OF HIRSUTISM
Excess androgen production
Relative circulating androgen excess and low binding globulins
Excess end organ response
Patient perception
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DISORDERS OF EXCESS ANDROGEN PRODUCTION
Source of androgen :
Exogenous
Endogenous (most common)
Two primary endogenous sources :
Adrenal glands
Ovaries
Mechanism of excessive hair growth
Main stimulus- Testosterone
Testosterone – binds – androgen receptors
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Activation of 5 alpha reductase
DHT
TERMINAL HAIR
ANDROSTENEDION
ANDROGEN
Lengthen Anagen phase
Increase hair follicle size
Increase hair follicle diameter
Increase sebum secretion
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Normal women Hirsute women
80% SHBG 79% SHBG
19% Albumin 19% Albumin
1% Free 2% Free
Causes of hirsutism
Androgenic ( 75-85% )
Non Androgenic
Idiopathic
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ANDROGENICPCOD(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
NON ANDROGENICAcromegalics.
chronic skin problems,
Non-androgenic anabolic drugs.
Danazol (Danocrine)
Norplant
Metoclopramide (Reglan)
Anabolic steroids
Methyldopa (Aldomet)
Phenothiazines
Progestins
Reserpine (Serpasil)
Testosterone
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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
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COMMON CAUSES OF ECTOPIC ACTH SECRETION
Small cell carcinoma of the lung 50%
Endocrine tumors of foregut origin35% Thymic carcinoid
Islet cell tumor
Medullary carcinoma thyroid
Bronchial carcinoid
Pheochromocytoma 5%
Ovarian tumors 2%
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
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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.
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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
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DISORDERS OF EXCESS ANDROGEN PRODUCTION
ADRENAL ANDROGEN EXCESSThree recognised adrenal enzyme deficiencies :21 alpha Hydroxylase defieiency11-beta-Hydroxylase deficiency3-beta-ol-dehydrogenase deficiencyClassical forms are usually presented in
prenatal or neonatal period as ambiguous genitalia in female
Nonclassic forms are linked with hirsutism
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.
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ACTH ↑ Cortisol ↓ Aldosterone ↓ 17-OH-progesterone↑ Testosterone ↑ Urinary 17-ketosteroids↑
ESSENTIALS OF DIAGNOSIS
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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
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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
causes
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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
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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 60Menstrual dysfunction 60Acne 40Easy bruising 40Osteopenia 40Dependent edema 40Hyperpigmentation 20Hypokalemic metabolic alkalosis
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DISORDERS OF EXCESS ANDROGEN PRODUCTION
OVARIAN ORIGIN
Most common cause is
POLYCYSTIC OVARIAN SYNDROME
Other
Neoplastic ovarian disease
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
Obesity49
Pathogenesis
dpankar 50
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
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. 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.
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. 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.
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Lab.Evaluation of Hirsutism
Three basic hormonal evaluation
1. Total testosterone
2. DHEAS
3. 17-hydroxyprogesterone
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
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The Testosterone level
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RELATIVE ANDROGEN EXCESS AND SHBG
<3 % TESTOSTERONE IS FREEMostly bound to Sex hormone binding globuline(SHBG)Dcrease in SHBG leads to Excess free TestosteroneCauses of Reduced SHBG : PCOS(Chronic anovulation) and Obesity
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EXCESS REPONSIVITY TO ANDROGEN
TESTOSTERONE5-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 CELLSRECEPTOR
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Flowchart for investigation of hirsutism
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BASIC APPROACH TO THE DIAGNOSIS OF HIRSUTISM
AND VIRILIZATION
SYMPTOMS AND HISTORYSIGNSPHYSICAL EXAMINATIONINVESTIGATION
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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
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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
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APPROACH TO DIAGNOSIS
Physical examinationEstablish presence of hirsutism and quantifying itPresence of acne and virilization and rule out hypertrichosisSkin hyperpigmentation,acanthosis nigricans suggests insulin resistance.Often associated with PCOD
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APPROACH TO DIAGNOSIS
Measurement of weight and height and blood pressure: defects relates to adrenal enzyme defectsGalactorrhoeaTanner staging : Hirsutism before Tanner stage 3 to 4 is alarming and suggests a serious pathologyVisual genital examination for virilization
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APPROACH TO DIAGNOSISDegree 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
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APPROACH TO DIAGNOSIS
INVESTIGATION:FOR VIRILIZATION :Work-up focuses of the identification on the
source of androgen excessRule out exogenous androgenEvidence of endogenous androgen excess: Serum total testosteroneSerum dehydroepiandrosterone sulfate
(DHEAS)
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APPROACH TO DIAGNOSIS
INVESTIGATION:
FOR VIRILIZATION
Imaging studies:Pelvic sonography
Adrenal imaging(USG,CT)
Specialized studies :
Selective venous catherization(adrenal or ovarian)
Radioisotope studies
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Any ageRapid onsetHirsutes++Virilism+AmenorrhoeaDHEAS ↑↑(>700µg/100ml)T- normal or ↑Dexa suppression test- negativeIVPCT-scanMRI
Any ageRapid onsetHirsutes++Virilism+AmenorrhoeaT- ↑( >200 ng/100ml)DHEAS- normal SonographyLaparoscopybiopsy
ADRENAL TUMOR OVARIAN TUMOR
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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 preferredDHEASIn selected cases : 17-OHP(fasting morning sample)
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APPROACH TO DIAGNOSIS
Evaluation of accompanying medical disorderOvulation disorder :FSH,LHThyroid dysfunction:TSHHyperprolactinemia :PRL
Other investigations ( inselected cases)Androgen production :Androstenedione,
3-alpha Androstenediol glucuronideProvocative tests : Corticotropin stimulation tests,Insulin resistance determination
Differentation of hyperandrogenism
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Diagnosis Menstrual Total DHAS LH 17OHP Sourse of
Pattern Testoste- Androgens ronePCOS Irregular Elevated mildly Elevated Normal OVARY elevated
CAH Irregular Elevated Often Usually Markedly Adrenals Normal Normal elevated
Idiopatic Regular Normal Normal Normal Normal Skinhirsutism
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THERAPEUTIC OPTIONS
VIRILIZATION
GOAL: Identify the underlying cause and correcting it
Usually related to malignant process and requires surgical approach
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THERAPEUTIC OPTIONS
HIRSUTISM
GOAL:
The prevention of further stimulation of hair growth
Cosmetic correction of the
problem
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THERAPEUTIC OPTIONS
BASIC STEPS OF MANAGEMENT OF HIRSUTISM ARE:DEFINE THE PROBLEMQUANTIFY THE DEGREE OF HIRSUTISMINDENTIFY THE PATHOPHYSIOLOGYCORRECT THE PROBLEM,WHETHER ACUTE OR CHRONICDEFINE SUCESSWITH THE PATIENTFOLLOW UP
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THERAPEUTIC OPTIONS
Regular follow up is indicated at appropriate intervals,usually every 3- 6 months
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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
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Removal of the source
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Adrenal or ovarian tumour – surgically treated
Cushing disease –
Adrenalectomy
Radiation to pituitary Removal of ACTH producing tumor
Iatrogenic cases – Offending drug to be stopped
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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
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THERAPEUTIC OPTIONSChoice of OC
EE + Norgestimate approved in USACyproteroneacetate 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
Side effects: Nausea, fatique, weight gain, loss of libido, mastalgia
OVARIAN SUPPRESSION BY LONG ACTING GnRH ANALOGUECan be used for functional ovarian androgen overproduction and even for malignant conditionBut to be used for long with back-up
Treatment is expensive and results are inconsistent
Use is reserved for patients resisting to initial therapy.
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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
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Drosperinone in PCOSCLINICAL BENEFITS
Helpful in treatment of Hirsutism Excellent cycle controlDecreases acne No weight gain.
METABOLIC BENEFITSNo effect on carbohydrate metabolismNo deterioration in the glycemic and insulinemic response to glucose load.No effect on serum lipid concentration.Safe for long term use
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THERAPEUTIC OPTIONS
MANAGEMENT OF EXCESS ADRENAL ANDROGEN PRODUCTION
Metabolic correction of the disorder,usually with exogenous steroids
Dexamethasone,mostly used,But LIMITED ROLE
Glucocorticoids
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Mode of action Suppress pituitary adrenal axis -
suppression of endogenous ACTH secretion
Use –
In adrenal or mixed adrenal and ovarian hyperandrogenism
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
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Glucocorticoid preparations used in monotherapy & combined with antiandrogens
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THERAPEUTIC OPTIONS
Management directed to the target organ and cells
Competition with Androgen receptors:Spironolactone,Flutamide, Ketoconazole,Cyproterone acetate
5-alpha reductase Inhibitors :Finasteride
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CPA
50-100 mg/day on menstrual cycle days5-15 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
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THERAPEUTIC OPTIONSandrogen receptors
competitorsSPIRONOLACTONE:
Best studied and as Gold standardMechanism :Androgen receptors blockadeSuppression of Androgen biosynthesisIncreased metabolic clearance of teststerone ( Testosterone Estrogen )50-200 mg/day in two divided dosesSpironolactone + OC is well established regimen
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THERAPEUTIC OPTIONSandrogen receptors
competitorsFLUTAMIDE :
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.
CIMETIDINE= 300mg BD
LEAST POTENT ANDROGEN RECEPTOR BLOCKER
Clinical reports disappointing.
CLINICALLY NOT EFFECTIVE.
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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.
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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
Cosmetic treatments for Hirsutism
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Bleaching - can cause irritation, purities, skin discolorationShaving - 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 dermatitisElectrolysis - painful, erythema, inflammation, scarringLaser
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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
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Hirsutism is a symptom of underlying cause
Commonest cause is PCO
Progression may hint to diagnosing tumor
Treatment – Medicines/ Cosmetic
To summarise