ANSWER
The correct answer is alopecia areata (choice “d”), the causes of which are discussed below. It typically manifests with sudden-onset complete hair loss in a well-defined area or areas.
Androgenetic alopecia (choice “a”) is incorrect, since its onset is remarkably gradual and the areas it affects are patterned differently from those seen with alopecia areata.
Kerion (choice “b”) is the name of an edematous, inflamed mass in the scalp triggered by fungal infection (tinea capitis) and is almost always accompanied by broken skin and palpable lymph nodes in the area.
Lichen planopilaris (choice “c”) is lichen planus of the scalp and hair follicles, an inflammatory condition that can involve hair loss of variable size and shape, but not in the same well-defined pattern seen here.
DISCUSSION
There are dermatologists who specialize in diseases of the scalp, especially those resulting in hair loss. In addition to the differential diagnoses mentioned, they see conditions such as lupus, trichotillomania, and reactions to hair care products.
Alopecia areata (AA) seldom needs the attention of these specialists, except in atypical cases. The total hair loss in these well-defined, oval-to-round areas presents fairly acutely, with obviously excessive hair loss noted not only in the scalp but also in the comb, brush, or sink. Although AA is quite common (and thus well known to barbers and hairdressers), it is still often a total and very distressing mystery to the patient. Stress is one of the factors theorized to trigger it—but unfortunately, the more stressed the patient is about the hair loss, the worse it gets.
In the vast majority of cases, the condition resolves, the hair returns, and the grateful patient breathes a sigh of relief. Recurrences, however, are not at all uncommon. A tiny percentage of AA patients go on to lose all the hair in their scalp (alopecia totalis), and an even smaller percentage of those patients go on to lose every hair on their body, permanently (alopecia universalis).
Much has been reported about the cause, which appears to be autoimmune in nature, with an apparent hereditary predisposition. About 10% to 20% of affected patients have a positive family history of AA, and those with severe AA have a positive family history about 16% to 18% of the time.
The theory of an autoimmune basis is also strongly supported by the significantly increased incidence of other autoimmune diseases (especially thyroid disease and vitiligo) in AA patients and their families. But T-cells almost certainly play a role too: Reductions in their number are usually followed by resolution of AA, while increases have the opposite effect. Increased antibodies to various portions of the hair shaft and related structures have now been tied to AA episodes, but these may be epiphenomenal and not causative.
One constant is the perifollicular lymphocytic infiltrate surrounding anagen phase follicles of AA patients. When corticosteroids are administered (eg, by intralesional injection, orally, or systemically), it is this infiltrate that is thereby dissipated, promoting at least temporary hair regrowth. Topically applied steroid preparations are not as helpful, and no known treatment has a positive effect on the ultimate outcome.
Fortunately, most cases of AA resolve satisfactorily with minimal or no treatment. Numerous treatments have been tried for AA, including minoxidil, topical sensitizers (eg, squaric acid, dintrochlorobenzene), and several types of phototherapy. Studies of the efficacy of the various treatments is complicated by the self-limiting nature of the problem.
Predictors of potentially poor outcomes include youth, atopy, extent of involvement, and the presence of ophiasis, a term used to describe extensive involvement of the periphery of the scalp.