During the next year, the patient was treated with diphenylcyclopropanone in concentrations of 0.0001% to 0.1% (poorly tolerated by the patient, with some response but eventual relapse) and with squaric acid in concentrations of 0.0001% to 0.001% (no response), as well as oral prednisone tapers, mycophenolate mofetil, halobetasol propionate cream, and 0.03% bimatoprost topical solution, with no improvement. She then began to experience dramatic hair loss on the sides of the scalp, with eventual progression to the loss of her eyebrows and eyelashes. She had minimal response to injections during the course of 1 year. The patient was diagnosed as having AA and was started on monthly injections of triamcinolone acetonide in concentrations of 3 to 5 mg/mL. Double-stranded DNA antibody and rheumatoid factor were negative. Antinuclear antibody was positive, with a titer of 1:80 and a homogeneous and speckled mixed pattern. Laboratory results for comprehensive metabolic panel and complete blood cell count, as well as iron, total iron-binding capacity, ferritin, vitamin D, thyrotropin, free thyroxine, and lipid panel levels were all within normal limits. Her medical history included atopic dermatitis, kidney stones, and hypothyroidism that was well-controlled on a levothyroxine sodium regimen. The appearance of alopecia coincided with emotional stressors in the patient’s life. At age 28 years, she began to notice patches of alopecia on her temporal scalp. The patient had first experienced a patch of alopecia at age 7 years that was successfully treated with triamcinolone acetonide (5 mg/mL) injections. These conclusions warrant further investigation on this subject.Ī woman in her 30s with a history of moderate atopic dermatitis was seen for evaluation of patches of alopecia on the parietal and temporal scalp. Pharmacogenetics and the inherent physiologic levels of TNF may explain why TNF inhibitors cause AA in some individuals, while treating AA in others. Observations A woman in her 30s with alopecia universalis, refractory to multiple treatment modalities, was successfully treated with adalimumab.Ĭonclusions and Relevance Tumor necrosis factor has multiple important roles in the pathogenesis of AA, and its interplay with other cytokines, specifically interferons, may be responsible for the development of AA in patients treated with TNF inhibitors. We report herein a case of alopecia universalis successfully treated with adalimumab and discuss the possible mechanism. Tumor necrosis factor (TNF) inhibitors have been largely unsuccessful in treating AA and have been reported to induce or worsen AA in patients. Importance Alopecia universalis is an uncommon form of alopecia areata (AA) involving hair loss over the entire scalp and body and is often difficult to treat.
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