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Summary of 'The Bearded Lady'

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Summary of 'The Bearded Lady' JOURNAL OF INSURANCE MEDICINE VOLUME 23, No. 1 SPRING 1991 SUMMARY OF "THE BEARDED LADY" A report by Eugene S. Rotatori, MD (Travelers Insurance Com- testosterone. He demonstrated the enzymatic defects which pany), of a presentation to the Insurance Medical Group of New can cause impaired transformation of these substances, result- England given by Bruce Bower, MD, on October 31, 1990. ing in the over-production of some metabolites and the under- production of the intended hormone. The latter causes a loss of the normal feedback control mechanism. The ovary and the Dr. Bruce Bower, Head of Endocrinology at the Hartford adrenal gland both produce testosterone and androstendione, Hospital, presented a concise but comprehensive review of the but estradiol is only ovarian in origin, while hyperandrogenic state in females. He distinguished between dehydroepiandrosterone (DHEA) and DHEA-S are formed hypertrichosis and hirsutism -- the former being androgen- only in the adrenal gland. independent body hair and the latter androgen-dependent hair growth on the face, chin, chest, etc. Hypertrichosis is not Analgous to the thyroid hormone, testosterone circulates in a an indication for an endocrine work-up. Hirsutism is too bound form which is metabolically inactive. The level of "free" frequently casually dismissed as an inconsequential problem testosterone is calculated by determining the difference in total while paradoxically it is often over-evaluated by laboratory and bound testosterone levels. A decreased bound testosterone studies. The condition has a significant emotional impact and level is frequently misinterpreted to mean the absence of andro- interfaces with many specialities. Internists, gynecologists, gen excess. Dr. Bower suggested that the only essential labo- and primary care physicians see those people and often as- ratory studies are a free and total serum testosterone and a sume that the other physicians have obtained appropriate serum DHEA-S (this has replaced the "old" 17-ketosteroid studies. The perception of hirsutism in the presence of normal studies). These studies will document the presence of an ex- hair growth is another problem but was not discussed during cessive amount of testosterone and the DHEA-S result will this presentation. pinpoint the origin to either the ovary or the adrenal. Other studies frequently obtained but not critical for diagnostic pur- Androgens are a normal component of a woman’s endocrine pose are serum FSH/LH, 17-OH progesterone, and andro- milieu; only an excess amount causes body responses such as stenedione. The latter does not discriminate between adrenal acne, menstrual irregularities, decrease in breast size, and or ovarian origin. A precursor to angrogen, 17-OH progester- other signs of "defeminization." It is unusual for hirsutism to one measurements can be useful to detect an enzyme defi- occur in the pediatric age group or in younger adults; tumor ciency in this metabolic pathway. of the ovary or adrenals must be ruled out in these situations. In the menopausal age group, there is a "relative" excess of The therapy of hirsutism depends on the etiology of the an- androgen as estrogen production wanes. In the peri-adoles- drogen excess. If adrenal in origin, dexamethasone can be used cents, hirsutism is usually benign, although the polycystic to suppress the level, while anovulatory drugs are indicated ovary syndrome and the use of anabolic steroids must be when it is ovarian in origin. It goes without saying that malig- suspected. The degree of hair growth is not an indication of nancies of these organs are appropriately treated in addition the magnitude of any androgen abnormality. to the treatment for hirsutism. Endogenous androgen over-production may be adrenal or A recent development in hirsutism is the finding that cells in ovarian in origin, although there is an idiopathic form in the hair follicle can be the site of metabolic transformation of which an excess cannot be detected by laboratory methods. androgen precursors to its biologically active forms. This ac- The exogenous form is due to the use of anabolic steroids. tion can be blocked by spironolactone and flutamide. The Using colored slides, Dr. Bower traced the metabolic pathways latter androgen receptor antagonist is not yet commercially and eventual formation of aldosterone, cortisol, and dihydro- available in the United States..
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