References: Hair growth and hair loss
Dermatologica. 1987;175 Suppl 2:29-35.
Immunohistochemical characterization of the cellular infiltrate in severe alopecia areata before and after minoxidil treatment.
Fiedler VC, Buys CM.
Department of Dermatology, University of Illinois College of Medicine at Chicago.
The mechanism of minoxidil-induced hair regrowth in alopecia areata (AA) is unknown. In vitro studies suggest that pharmacologic tissue levels of minoxidil may have both epithelial and T cell effects. Response in 36 of 47 patients with severe AA to topical minoxidil 5% b.i.d. was characterized by a return toward normal of hair follicle diameter, depth and structure, and an apparent shift in T cell populations from the skin into the peripheral blood. Nonresponders showed none of these changes. Biopsies from 34 patients subsequently treated with oral minoxidil 5 mg q. 12 h showed no further changes in perifollicular total T, helper-inducer T or suppressor-cytotoxic T cell counts; they did, however, demonstrate significant decreases in perifollicular Langerhans cell and activated T cell counts, and nearly significant decreases in perifollicular monocyte counts. It is possible that minoxidil may be altering a presumed follicular chemoattractive stimulus to a variety of cell types. Decreases in activated T cell counts suggest the possibility of direct immunomodulatory effects of minoxidil on T cells which might contribute to a hair regrowth response in AA.
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Hautarzt. 1988 Jan;39(1):5-11.
[Autoimmunity in alopecia areata. An assessment in 100 patients]
[Article in German]
Lutz G, Bauer R.
Universitats-Hautklinik und Poliklinik, Rheinischen Friedrich-Wilhelms-Universitat Bonn.
The sera of 100 patients with varying degrees of alopecia areata were examined for the presence of circulating autoantibodies against nuclear, mitochondrial, reticulin-fibril, smooth muscle, parietal cell, thyroglobulin, and microsomal components. Furthermore, in all cases we measured the percentage of total T-lymphocytes, T-helper, and T-suppressor cells. Other diseases were also considered that could cause such antibodies. In addition, the assumption was examined as to whether or not the loss of suppressor cells correlates with the presence of autoantibodies. The incidence of autoantibodies mentioned was not found to be statistically higher in our study; most of the autoantibodies could be explained by other accompanying diseases. Only in the T-suppressor cells was there a significant decrease. Patients with autoantibodies showed no more deficit in T-suppressor cells than patients without autoantibodies.
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Arch Dermatol. 1988 Jun;124(6):897-902.
Efficiency of acitretin in the treatment of cutaneous lupus erythematosus.
Ruzicka T, Meurer M, Bieber T.
Department of Dermatology, University of Munich, West Germany.
Acitretin (etretin [Ro-10-1670]) is the major metabolite of etretinate with a much shorter elimination half-life. The drug was used in the treatment of 20 patients who had cutaneous lupus erythematosus. All patients responded to treatment, but in five, the result was unsatisfactory. In 15 patients, an excellent (total clearing) or good response (marked reduction of all lesions) was seen. In seven of them, acitretin was superior to previous therapy with antimalarials and/or systemic corticosteroids. In particular, five of six patients with subacute cutaneous lupus erythematosus showed complete clearing of their lesions, usually within two to four weeks. Side effects were the same as with etretinate. It is concluded that acitretin is a highly effective and well-tolerated drug in the treatment of cutaneous lupus erythematosus.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2967674&dopt=Abstract
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