Androgenic alopecia (AA) is caused by androgen effects on hair follicles in genetically susceptible women and men. The thinning often begins between ages 12 and 40 years.
Walter Futterweit MD, FACP, FACE is Clinical Professor of Medicine, Division of Endocrinology, Mount Sinai School of Medicine and President of Androgen Excess-Polycystic Ovary Syndrome Society (AE-PCOS).
The Annual Meeting of AE-PCOS will be in Orlando, FL, October 13-14, 2011. For program, see www.ae-society.org/meetings
Androgenic alopecia (AA) is caused by androgen effects on hair follicles in genetically susceptible women and men (1). The thinning often begins between ages 12 and 40 years. In susceptible hair follicles, dihydrotestosterone (DHT), whose precursor is testosterone (T), binds to the androgen receptor, and the hormone-receptor complex activates the genes responsible for the gradual transformation of large terminal hair follicles to miniaturized small and thin follicles.
Both young women and young men with AGA have higher levels of the enzyme 5-alpha reductase which block significant formation of T to DHT. Less of the androgen receptor is present in frontal hair follicles and in denser hair of the occipital follicles. The presence of another pathway of T metabolism is by an enzyme called aromatase which goes to estrogens, and minimizes the DHT effect on the androgen receptor. This enzyme is present in higher concentrations in the occipital and frontal areas of the scalp resulting in less hair loss in women than men.
The diagnosis of AGA in women is supported by an early age of a gradual onset, usually retention of the occipital area and frontal hairline, and the presence of small shorter and finer miniaturized hairs. Most women with AGA have normal menses and pregnancies. Hormonal testing is usually not extensively performed unless symptoms and signs of androgen excess are present such as excessive body hair growth (hirsutism), severe unresponsive cystic acne, masculinization, or a milky breast discharge due to high serum prolactin levels (1). In view of the fact that alopecia is a common first complaint in 10% of women with androgen excess including polycystic ovary syndrome and adrenal disorders (2), many clinicians order T, DHT, prolactin, and adrenal androgens to ensure the absence of excess male hormones.
Androgenetic alopecia in women is not usually accompanied by rapid and markedly increased shedding such as is seen in telogen effluvium (TE) (3,4). Hairs converting from the growing (anagen) phase to a resting (telogen) phase may follow childbirth, major illness, severe stress, thyroid dysfunction, infection, or other causes such as iron and zinc deficiencies in vegetarians (3). The number of hairs shed is misleading in women who seldom comb their hair after shampooing, leaving it to dry naturally. Later when they comb their hair many loose hairs appear on the fingers. TE not infrequently may be associated in women with AA. A tug test pulling gently in TE is positive for 5 hairs or more, unlike AA. The prognosis of TE is usually good if diagnosed early and the factor(s) responsible for its presence treated or removed. With the latter, the hairs often regenerate in 6-12 months or less.
TREATMENT OPTIONS IN ANDROGENIC ALOPECIA
In my view, minoxidil as 2% Rogaine should be used, routinely and constantly, twice a day in AA. One should note that in the first 2 months of use, it may cause some additional hair loss. Use of the 5% Rogaine (by prescription) may cause local irritation and increased hirsutism via absorption.
A common treatment of AA, similar to that of hirsutism, is the combination of spironolactone varying from 100-200 mg daily in divided doses, with a nonandrogenic oral contraceptive. Hair loss may stabilize with reduction of interval of regrowth after local treatment, thinner hair diameter, and reduction of darker hair pigment. Improvement may often be delayed for at least 6 months. Significant hair regrowth is infrequent in AA with this treatment as with other antiandrogens. Clearly flutamide is the most effective antiandrogen, but caution must be used in view of potential severe hepatotoxicity in perhaps 1 of 2000 women. Varying results with any antiandrogen treatment are reported, and some are reported superior to others (5). These may reflect different ethnic groups and other environmental factors. Other than the USA, some claim that cyproterone acetate is more effective than other treatments. This is also stated for other antiandrogen treatments in conjunction with an oral contraceptive.
A recent trend using 5-alpha reductase inhibitors in AA is associated only with relatively few well designed studies. Most studies to date are those relating to the use of 2.5-5.0 mg finasteride daily (6). Little is written about dutasteride, the more potent 5-a reductase inhibitor experimentally. Cautious use also is warranted in view of paucity of studies and the fact that they enhance aromatase conversion to estrogens. Future studies will be helpful in deciding their value and safety.
Empathy and mutual understanding of the effect of alopecia is vital in treating women with alopecia. Helping to increase their self-esteem is an important role for the physician and the women they treat. An important role for hair transplants may be of value in severely affected and depressed women. Most antiandrogen treatments with oral contraceptives and minoxidil tend to stabilize hair loss but regrowth is limited. The future role of 5a-reductase inhibitors may be helpful, but this should be clarified in the next few years. The role of multiple antiandrogen drug combinations is also not yet fully studied.
1) Camacho-Martinez FM. Hair loss in women. Semin Cutan Med Surg 2009;100:741-3
2) Futterweit W, Dunaif A, Yeh HC, Kingsley P. The prevalence of hyperandrogenism in 109 consecutive female patients with diffuse alopecia. J Am Acad Dermatol 1988:19:831-6
3) Futterweit W. Polycystic ovary syndrome: a common reproductive and metabolic disorder necessitating early recognition and treatment. Prim Care 2007;34:761-89
4) Azziz R, Carmina E, Dewailly D et al. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 2009;91:456-88.
5) Redmond GP. Clinical evaluation of the woman with an androgenic disorder. In: Redmond GP, editor. Androgenic disorders. New York; Raven Press; 1995, p. 1-20.
6) Schweiger ES, Boychenko O, Bernstein RM. Update on the pathogenesis, genetics and medical treatment of patterned hair loss. J Drugs Dermatol 2010;9:1412-9