from Southern Medical Journal

Daniel J. Hogan, MD, Matthew Chamberlain, MD, Section of Dermatology, Louisiana State University School of Medicine, Shreveport.

Abstract

Background. Male pattern baldness, or androgenetic alopecia (AGA) in men, occurs with varying severity and age of onset. Two new treatments widely available as alternatives to 2% minoxidil are 1 mg finasteride and topical 5% minoxidil. Finasteride is a 5 alpha-reductase inhibitor available by prescription only; 5% minoxidil is available over the counter.
Methods. We searched MEDLINE to identify all articles on AGA and its pharmacologic therapies.
Results. We found limited information on AGA in peer review medical journals. Associated diseases include psychologic disorders and coronary heart disease. Hair growth is unpredictable and limited for all pharmacologic therapies, with the vast majority of treatment studies being industry sponsored.
Conclusion. AGA is not easy to treat. Finasteride and 5% minoxidil offer new therapeutic options to the balding man. Treatment options may improve as new drugs are further investigated.

Introduction

Men with male pattern baldness (MPB) or androgenetic alopecia (AGA) seek treatment from a range of physicians -- particularly family physicians and dermatologists.^[1] The incidence of MPB is estimated to be from 23% to 87%.^[2] It may develop any time after puberty. The mode of inheritance remains unclear, but is more likely to be polygenic than autosomal dominant.^[3,4] The relatively strong concordance for baldness between fathers and sons is not consistent with a simple mendelian autosomal dominant inheritance.^[4] The high prevalence of AGA, its distribution in the general population, the higher risk of AGA as the number of affected relatives increases, and the high risk of inheritance from an affected parent argue in favor of polygenic inheritance.^[3,4]

MPB does not occur in men with a genetic deficiency of type II 5 alpha-reductase, which converts testosterone to dihydrotestosterone (DHT).^[5] Type I 5 alpha-reductase isoenzyme is present in the skin.^[6] The type II isoenzyme is present in hair follicles and the prostate.^[6,7] The genes encoding type I and type II 5 alpha-reductase isoenzymes are not associated with male pattern baldness.^[4] The clinical pattern of hair loss is apparently the result of genetically determined distribution of androgen-sensitive hair follicles transformed from terminal to miniaturized follicles.

Androgens, especially DHT, play a crucial role in the pathogenesis of MPB. DHT is the most potent of the circulating androgens in human plasma and is a major testosterone metabolite in human skin as well.^[8] One of the early findings in MPB is an increased percentage of hairs in the telogen, or quiescent, phase of the hair cycle due to shortening of the anagen, or growing phase.^[2] Diagnostic histopathologic features of MPB include a near normal number of hairs but reduced terminal and increased vellus hairs with a terminal:vellus hair ratio of 2:1 rather than the normal terminal: vellus hair ratio of 7:1.^[9] The anagen/telogen ratio is reduced in AGA from 14:1 to 5:1.^[9] In MPB the follicular growth cycle is altered, with shortened anagen growth and a reduced diameter or miniaturization of the follicle with patchy perivascular and perifollicular inflammation.^[9] The average decrease in hair diameter in Japanese men is 1.1 microns per year.^[10] Inflammatory infiltrates center around the infundibular hair follicle epithelium in the vicinity of the sebaceous duct orifice, the putative site of hair follicular stem cells.^[11] Inflammation of this site is associated with permanent alopecia with fibrosis.^[11] Left untreated, androgen-dependent alopecia progressively deteriorates.^[12] Black men have less severe male pattern baldness than white men.^[13] In both groups, increasingly severe male pattern baldness is associated with increased chest hair.^[13]

Other less common causes of hair loss must be ruled out when diagnosing AGA in men. These disorders include alopecia areata, telogen effluvium, hair loss due to thyroid disease, adverse drug effects, nutritional deficiency states, scalp or hair trauma, discoid lupus erythematosus, lichen planus, and structural hair shaft abnormalities.^[14] This can be done with a thorough history and physical examination, as well as laboratory tests to support relevant findings and scalp biopsies for transverse as well as vertical sections for histopathologic examination and direct immunofluorescence staining of predominantly lesional skin.^[15]

Men with AGA are classified into different stages based on the severity of disease by the Hamilton-Norwood scale (Figs 1 and 2).^[16,17] Women are classified by a separate scale (Ludwig scale) and usually have less severe disease with sparing of the anterior hairline.^[18,19] This article will focus on AGA in men.