Male Androgenetic Alopecia

Excerpt

Male androgenetic alopecia (MAA) is the most common form of hair loss in men, affecting 30-50% of men by age 50. MAA occurs in a highly reproducible pattern, preferentially affecting the temples, vertex and mid frontal scalp. Although MAA is often regarded as a relatively minor dermatological condition, hair loss impacts self-image and is a great cause of anxiety and depression in some men. MAA is increasingly identified as a risk factor for arterial stiffness and cardiovascular disease. A familial tendency to MAA and racial variation in the prevalence is well recognized, with heredity accounting for approximately 80% of predisposition. Normal levels of androgens are sufficient to cause hair loss in genetically susceptible individuals. The key pathophysiological features of MAA are alteration in hair cycle development, follicular miniaturization, and inflammation. In MAA, the anagen phase decreases with each cycle, while the length of telogen remains constant or is prolonged. Ultimately, anagen duration becomes so short that the growing hair fails to achieve sufficient length to reach the surface of the skin, leaving an empty follicular pore. Hair follicle miniaturization is the histological hallmark of androgenetic alopecia. Once the arrector pili muscle, that attaches circumferentially around the primary follicle, has detached from all secondary follicles and primary follicles have undergone miniaturization and detachment, hair loss is likely irreversible. While many men choose not to undergo treatment, topical minoxidil and oral finasteride are approved by the Food and Drug Administration (USA) for the treatment of MAA. Both medications prevent further hair loss, but only partially reverse baldness, and require continuous use to maintain the effect. Topical minoxidil is well tolerated as a 2% or 5% solution or 5% foam. There is initially accelerated hair loss for several weeks due to telogen hairs falling out. Minor adverse effects include itching of the scalp, dandruff, and erythema. Finasteride is a potent and selective antagonist of the type II 5 alpha reductase, and is not an anti-androgen. 5 alpha reductase converts testosterone into dihydrotestosterone (DHT). DHT binding to the scalp hair follicle androgen receptors produces MAA. A daily oral finasteride dose of one milligram reduces scalp dihydrotestosterone by 64% and serum dihydrotestosterone by 68%. Adverse effects, including sexual dysfunction (erectile dysfunction, low libido, anorgasmia) are uncommon, and most often resolve without discontinuing treatment. Permanent sexual adverse effects have been reported on social media and internet forums; however, the true incidence is unknown. Dutasteride inhibits type I and type II 5 alpha reductase, and it might be superior to finasteride in improving hair growth in young males. However, adverse sexual side effects are more common with dutasteride than with finasteride. Combining medications with different mechanisms of action enhances the efficacy. Topical antiandrogens, prostaglandin analogues, topical antifungals, growth factors, and laser treatment are all emerging medical treatments for MAA, yet lack the necessary research to confirm efficacy and safety. Hair transplantation involves removal of hair from the occipital scalp and re-implantation into the bald vertex and frontal scalp. With modern techniques, graft survival in excess of 90% can be reliably achieved. A combination of these therapeutic options is now available for men experiencing MAA, with favorable cosmetic outcomes possible. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.