Abstract
The precise event that begins the cascade of changes leading to hair loss in defined patches of hair-bearing skin (alopecia areata) remains unknown. The alteration of immune function responsible for alopecia also is unknown. Defects in immune function are present in patients with alopecia areata, but no one defect is present in all patients, and many have no derangement of the immune system. This situation is not unlike that seen with discoid lupus erythematosus. In discoid lupus erythematosus, most patients do not later develop lupus erythematosus, although some individuals who initially manifest discoid lesions later develop nephritis (the percentage is low). Some patients with discoid lupus erythematosus are found to have a variety of autoantibodies. With alopecia areata, up to 83 per cent of patients have a single patch of hair loss or only a few such patches, and the prognosis for recovery is good. 17 But others are at risk for more significant medical events in the future, most likely involving endocrine organs. Awareness of the possible connection between these endocrine diseases, immune system dysfunction, and the cutaneous marker of alopecia areata may someday allow identification of the initial event that can trigger the processes which unfold slowly, sometimes over many years, as in the case referred to anecdotally at the beginning of this article. That patient represents the full spectrum of the syndrome (an immunocutaneous endocrinopathy) and differs from one with an uncomplicated case of cutaneous alopecia areata, just as an individual with the full spectrum of findings in systemic lupus erythematosus differs from one with purely cutaneous features. The difference with alopecia areata is the long time course over which the disease evolves and our current inability to adequately identify who is at risk for more than cutaneous disease.
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