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• W2014423877 abstract "It is the aim of this article to review and appraise available data on treatments for alopecia areata (AA) according to the demands of evidence based medicine. Studies evaluating the efficacy of a treatment for AA should include appropriate controls, use cosmetically acceptable hair regrowth as a parameter for treatment success, include patients with AA totalis, universalis or extensive patchy AA, and exclude patients suffering from AA for less than 3 months. Moreover, the treatment must be safe over a prolonged period of time. Among the various therapeutic approaches presently available for AA, only treatment with contact sensitizers such as diphenylcyclopropenone or squaric acid dibutylester has been shown to be effective in studies that fulfill these criteria.Improved future treatments may be immunosup-pressive or immunomodulatory targeting of the autoimmune pathogenesis of AA, or they may otherwise protect hair follicles from the injurious effects of inflammation. Such possible future therapeutic approaches include the incorporation of immunomodulatory agents into liposomes as an improved vehicle; inhibition of apoptosis mediated by the Fas-FasL system; inhibition of the lymphocyte homing receptor CD44v10; induction of tolerance. It is the aim of this article to review and appraise available data on treatments for alopecia areata (AA) according to the demands of evidence based medicine. Studies evaluating the efficacy of a treatment for AA should include appropriate controls, use cosmetically acceptable hair regrowth as a parameter for treatment success, include patients with AA totalis, universalis or extensive patchy AA, and exclude patients suffering from AA for less than 3 months. Moreover, the treatment must be safe over a prolonged period of time. Among the various therapeutic approaches presently available for AA, only treatment with contact sensitizers such as diphenylcyclopropenone or squaric acid dibutylester has been shown to be effective in studies that fulfill these criteria. Improved future treatments may be immunosup-pressive or immunomodulatory targeting of the autoimmune pathogenesis of AA, or they may otherwise protect hair follicles from the injurious effects of inflammation. Such possible future therapeutic approaches include the incorporation of immunomodulatory agents into liposomes as an improved vehicle; inhibition of apoptosis mediated by the Fas-FasL system; inhibition of the lymphocyte homing receptor CD44v10; induction of tolerance. alopecia areata diphenylcyclopropenone squaric acid dibutylester Dundee experimental bald rat experimental autoimmune encephalomyelitis Alopecia areata (AA) is characterized by patchy or sometimes total loss of scalp or body hair with waxing and waning of bald areas. Although acute phases of hair loss are followed by spontaneous hair regrowth in most patients, the disorder may persist for many years or even for life when severe. But even in these cases hair loss is potentially reversible, because the disease usually does not result in destruction of hair follicles or scarring. Therefore, every patient suffering from AA has the right to be treated according to the rules of evidence based medicine (EBM) (Epstein, 2001Epstein E. Evidence-based treatment of alopecia areata.J Am Acad Dermatol. 2001; 45: 640-642Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar), which is the process of systematically finding, appraising, and using contemporaneous research findings as the basis for clinical decisions (Rosenberg and Donald, 1995Rosenberg W. Donald A. Evidence based medicine: An approach to clinical problem-solving.BMJ. 1995; 310: 1122-1126Crossref PubMed Scopus (853) Google Scholar). It is the aim of this review to assess critically the published studies dealing with various therapies for AA and to determine which are most effective and safe. There are about 600 publications, not to mention anecdotal reports, about treatment of AA published in the last 30 years. But “the practice of evidence based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research” (Sackett, 1996Sackett D.L. Evidence based medicine. What it is and what it isn’t.BMJ. 1996; 312: 71-72Crossref PubMed Google Scholar). Therefore, we define four criteria that help to identify publications that are the best available evidence:Because AA is characterized by episodes of hair loss and regrowth and the spontaneous course of the disease cannot be predicted, any treatment study has to distinguish between spontaneous remission and therapeutic response. This is possible in a double-blind, placebo controlled study, which must include a large number of patients to yield statistically significant results. In topical approaches, however, the strictest criterion to exclude spontaneous remission is to treat every patient on one half of the scalp only. Only patients with substantially better hair growth on the treated side are allowed to be regarded as successfully treated. In patchy AA a large patch has to be treated unilaterally, because treatment of one patch with another patch as control does not exclude spontaneous hair regrowth. Half-side treatment can even be performed in a double-blind form by treating one side with the drug and the other with a placebo.Hair regrowth in the treated area has to be substantial and cosmetically acceptable, because ‘some regrowth’ is not of practical benefit to the patient.The prognosis of AA is influenced by several factors, in particular by the type and extent of AA (Weise et al., 1996Weise K. Kretzschmar L. John S.M. Hamm H. Topical immunotherapy in alopecia areata: Anamnestic and clinical criteria of prognostic significance.Dermatology. 1996; 192: 129-133Crossref PubMed Scopus (66) Google Scholar;Wiseman et al., 2001Wiseman M.C. Shapiro J. MacDonald N. Lui H. Predictive model for immunotherapy of alopecia areata with diphencyprone.Arch Dermatol. 2001; 137: 1063-1068PubMed Google Scholar) with a worse prognosis for patients with AA totalis or universalis or with extensive patchy AA as compared to limited patchy AA. According to the rules of EBM, we cannot accept the auxiliary hypothesis of a dichotomy between mild AA that can be ‘successfully’ treated with various doubtful approaches, such as topical corticosteroids, minoxidil or anthralin, and severe AA that cannot be treated with these drugs. Rather there is convincing evidence that these topical approaches do not exert any inhibitory effect on a possible spontaneous regrowth. Hence, studies evaluating a treatment for AA should preferably include patients with AA totalis, AA universalis and extensive patchy AA (>25% scalp hair loss).The duration of the disease also has an influence on its prognosis. Because hair regrowth is more likely in AA of short duration, patients to be included in a study should have had AA for more than 3 months.Any treatment has to be suitable for long-term therapy, because AA is a disease that can persist for many years or even for life. Hence, all therapeutic approaches showing severe side-effects in the long run are inappropriate. In summary, a study according to the demands of EBM should fulfill the following criteria:Controlled study (placebo controlled with statistically significant results, or unilateral treatment)Majority of patients with AA totalis, AA universalis or extensive patchy AA (>25% hair loss)Duration of disease for more than 3 monthsCosmetically acceptable hair regrowthNo serious side-effects Among their various anti-inflammatory effects that are beyond the scope of this article, corticosteroids are known to exert a strong inhibitory effect on the activation of T lymphocytes. In consideration of the TH-1 mediated immune attack on the hair follicle in AA, corticosteroids are potentially good candidates for the treatment of this disease. Topical, intralesional, and systemic corticosteroids have been used to treat AA, with different rates of success and side-effects. Topical treatment with corticosteroid creams, ointments or lotions are frequently used for AA. However, only two placebo-controlled studies reported a treatment response (Pascher et al., 1970Pascher F. Kurtin S. Andrade R. Assay of 0.2% fluocinolone acetonide cream for alopecia areata and totalis.Dermatologica. 1970; 141: 193-202Crossref PubMed Scopus (61) Google Scholar;Leyden and Kligman, 1972Leyden J.J. Kligman A.M. Treatment of alopcia areata with steroid solution.Arch Derm. 1972; 106: 924Crossref PubMed Scopus (27) Google Scholar), but both studies do not fulfill the other criteria for evidence based treatment of AA. Furthermore, both studies were performed in the 1970s and they have not been confirmed by others over the last 30 years (Weitgasser, 1968Weitgasser H. Erfahrungen mit einer Triamcinolon-Tinktur bei entzündlichen Dermatosen.Z Hautkr. 1968; 43: 505-508Google Scholar;Verbov, 1973Verbov J. Steroid solution treatment of alopecia areata.Arch Derm. 1973; 108: 135Crossref PubMed Scopus (2) Google Scholar;Lehnert, 1974Lehnert W. Zur Lokalbehandlung schwerer Formen der Alopecia areata mit Kortikosteroidsalbe.Dermatol Monatsschr. 1974; 160: 396-398PubMed Google Scholar;Montes, 1977Montes L.F. Topical halcinonide in alopecia areata and in alopecia totalis.J Cut Pathol. 1977; 4: 47-50Crossref PubMed Scopus (22) Google Scholar). Only one placebo-controlled study with an appropriate number of patients has been performed to date, but the rate of treatment success was not statistically significant (Charuwichitratana et al., 2000Charuwichitratana S. Wattanakrai P. Tanrattanakorn S. Randomized double-blind placebo-controlled trial in the treatment of alopecia areata with 0.25% desoximetasone cream.Arch Dermatol. 2000; 136: 1276-1277Crossref PubMed Scopus (52) Google Scholar). The failure of topical corticosteroids is most likely due to the insufficient penetration of topically applied drugs from ointments, creams or lotions into the hair bulb. Improving penetration by occlusion has been tried without success (Lehnert, 1974Lehnert W. Zur Lokalbehandlung schwerer Formen der Alopecia areata mit Kortikosteroidsalbe.Dermatol Monatsschr. 1974; 160: 396-398PubMed Google Scholar). Considering the lack of treatment response and the side-effects of topically applied corticosteroids, we conclude that topical corticosteroids are not an effective method of treating AA. Intralesional injection of corticosteroid crystal suspensions, primarily triamcinolone acetonide, has been used to treat AA for more than 40 years (Kalkoff and Macher, 1958Kalkoff K.W. Macher E. Über das Nachwachsen der Haare bei der Alopecia areata und maligna nach intracutaner Hydrocortisoninjektion.Hautarzt. 1958; 9: 441-451PubMed Google Scholar). Several studies reported hair regrowth at the site of injection in the majority of cases (Kalkoff and Macher, 1958Kalkoff K.W. Macher E. Über das Nachwachsen der Haare bei der Alopecia areata und maligna nach intracutaner Hydrocortisoninjektion.Hautarzt. 1958; 9: 441-451PubMed Google Scholar;Orentreich et al., 1960Orentreich N. Sturm H.M. Weidman A.I. Pelzig A. Local Injection of steroids and hair regrowth in alopecias.Arch Dermatol. 1960; 82: 894-902Crossref PubMed Scopus (31) Google Scholar,Fülöp and Vajda, 1971Fülöp E. Vajda Z. Experimentelle Untersuchungen über die therapeutische und schädigende Wirkung der intrafokalen Steroidbehandlung.Dermatol Monatsschr. 1971; 157: 269-277PubMed Google Scholar;Porter and Burton, 1971Porter D. Burton J.L. A comparison of intra-lesional triamcinolone hexacetonide and triamcinolone acetonide in alopecia areata.Br J Dermatol. 1971; 85: 272Crossref PubMed Scopus (66) Google Scholar;Abell and Munro, 1973Abell E. Munro D.D. Intralesional treatment of alopecia areata with triamcinolone acetonide by jet injector.Br J Dermatol. 1973; 88: 55-59Crossref PubMed Scopus (75) Google Scholar;Frentz, 1977Frentz G. Topical treatment of extended alopecia.Dermatologica. 1977; 155: 147-154Crossref PubMed Google Scholar). Most of these studies tried to exclude spontaneous hair regrowth by comparing the injected sites of the scalp with uninjected areas, especially in alopecia totalis. However, in practice, it is impossible to treat the whole scalp by intralesional injections of corticosteroids and so this treatment is only indicated in patchy AA with longstanding bald areas. Apart from the painful procedure of injection, permanent atrophy can occur after injection. Taken together, intralesional injection of corticosteroids is a reasonable treatment in exceptional, selected cases of longstanding small patches of AA, but has potentially serious side-effects. AA has been treated with systemic corticosteroids since 1952 (Dillaha and Rothman, 1952Dillaha C.J. Rothman S. Therapeutic experiments in alopecia areata with orally administered cortisone.J Am Med Ass. 1952; 150: 546-550Crossref PubMed Scopus (32) Google Scholar). Whereas, initially, oral corticosteroids were used daily or every other day for several months, this continuous use of corticosteroids is obsolete today. Doses that are required to maintain hair regrowth in AA are between 30 and 150 mg daily, giving rise to unacceptable side-effects such as hypertension, diabetes, immunosuppression, osteoporosis and proneness to thrombosis. Since 1975 several authors have performed pulsed administration of corticosteroids in single doses, given once monthly in order to reduce the side-effects of corticosteroids to an acceptable level, but all studies which noted hair regrowth, were uncontrolled and the majority of patients had patchy AA (Perriard-Wolfensberger et al., 1993Perriard-Wolfensberger J. Pasche-Koo F. Mainetti C. Laborthe M.P. Salomon D. Saurat J. Pulse of methylprednisolone in alopecia areata.Dermatology. 1993; 187: 282-285Crossref PubMed Scopus (53) Google Scholar;Sharma, 1996Sharma V.K. Pulsed administration of corticosteroids in the treatment of alopecia areata.Int J Dermatol. 1996; 35: 133-136Crossref PubMed Scopus (81) Google Scholar;Friedli et al., 1998Friedli A. Labarthe M.P. Engelhardt E. Feldman R. Salomon D. Saurat J.H. Pulse methyprednisolone therapy for severe alopecia areata. An open prospective study of 45 patients.J Am Acad Dermatol. 1998; 39: 597-602Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar;Sharma and Muralidhar, 1998Sharma V.K. Muralidhar S. Treatment of widespread alopecia areata in young patients with monthly oral corticosteroid pulse.Pediatr Dermatol. 1998; 15: 313-317Crossref PubMed Scopus (46) Google Scholar;Seiter et al., 2001Seiter S. Ugurel S. Tilgen W. Reinhold U. High-Dose pulse corticosteroid therapy in the treatment of severe alopecia areata.Dermatology. 2001; 202: 230-234Crossref PubMed Scopus (56) Google Scholar). Moreover, other studies reported treatment failure after corticosteroid pulse therapy (Burton and Shuster, 1975Burton J.L. Shuster S. Large doses of glucocorticoid in the treatment of alopecia areata.Acta Derm Venereol (Stockh). 1975; 55: 493-496PubMed Google Scholar;Schulz et al., 1996Schulz A. Hamm H. Weiglein U. Axt M. Bröcker E.B. Dexamethasone pulse therapy in severe long-standing alopecia areata: a treatment failure.Eur J Dermatol. 1996; 6: 26-29Google Scholar). Controlled studies should be conducted to prove the efficacy and long-term value of this treatment. Especially the efficacy in interrupting acute phases of rapid hair loss by pulsed administration of oral corticosteroids should be investigated. Based on the data presently available, pulsed administration of corticosteroids for AA cannot be recommended. Several studies have examined treatment of AA with PUVA using either oral 8-methoxypsoralen (8-MOP) with ultraviolet A radiation (UVA) on the scalp or the whole body, or topical application of 8-MOP and UVA radiation on the scalp, including one study with topical application of psoralen via the PUVA-turban (Claudy and Gagnaire, 1983Claudy A.L. Gagnaire D. PUVA treatment of alopecia areata.Arch Dermatol. 1983; 119: 975-978Crossref PubMed Scopus (62) Google Scholar;Larkö and Swanbeck, 1983Larkö O. Swanbeck G. PUVA treatment for alopecia totalis.Acta Derm Venereol (Stockh). 1983; 63: 546-549PubMed Google Scholar;Lassus et al., 1984Lassus A. Eskelinen A. Johansson E. Treatment of alopecia areata with three different PUVA modalities.Photodermatology. 1984; 1: 141-144PubMed Google Scholar;Mitchell and Douglass, 1985Mitchell A.J. Douglass M.C. Topical photochemotherapy for alopecia areata.J Am Acad Dermatol. 1985; 12: 644-649Abstract Full Text PDF PubMed Scopus (55) Google Scholar;Healy and Rogers, 1993Healy E. Rogers S. PUVA treatment for alopecia areata. Does it work? A retrospective review of 102 cases.Br J Dermatol. 1993; 129: 42-44Crossref PubMed Scopus (75) Google Scholar;Taylor and Hawk, 1995Taylor C.R. Hawk J.L.M. PUVA treatment of alopecia areata partialis, totalis and universalis: Audit of 10 years’ experience at St John's Institute of Dermatology.Br J Dermatol. 1995; 133: 914-918Crossref PubMed Scopus (96) Google Scholar;Behrens-Williams et al., 2001Behrens-Williams S. Leiter U. Schiener R. Weidmann M. Peter R.U. Kerscher M. The PUVA-turban as a new option of applying a dilute psoralen solution selectively to the scalp of patients with alopecia areata.J Am Acad Dermatol. 2001; 44: 248-252Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar). Some studies seemed to have good results (Claudy and Gagnaire, 1983Claudy A.L. Gagnaire D. PUVA treatment of alopecia areata.Arch Dermatol. 1983; 119: 975-978Crossref PubMed Scopus (62) Google Scholar;Lassus et al., 1984Lassus A. Eskelinen A. Johansson E. Treatment of alopecia areata with three different PUVA modalities.Photodermatology. 1984; 1: 141-144PubMed Google Scholar;Healy and Rogers, 1993Healy E. Rogers S. PUVA treatment for alopecia areata. Does it work? A retrospective review of 102 cases.Br J Dermatol. 1993; 129: 42-44Crossref PubMed Scopus (75) Google Scholar;Taylor and Hawk, 1995Taylor C.R. Hawk J.L.M. PUVA treatment of alopecia areata partialis, totalis and universalis: Audit of 10 years’ experience at St John's Institute of Dermatology.Br J Dermatol. 1995; 133: 914-918Crossref PubMed Scopus (96) Google Scholar;Behrens-Williams et al., 2001Behrens-Williams S. Leiter U. Schiener R. Weidmann M. Peter R.U. Kerscher M. The PUVA-turban as a new option of applying a dilute psoralen solution selectively to the scalp of patients with alopecia areata.J Am Acad Dermatol. 2001; 44: 248-252Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar), but there were no controls in any of the studies. Moreover, there were a large number of recurrences (between 30% and 50% of successfully treated patients) after initial hair regrowth, which strongly decreased the efficacy of PUVA treatment for AA (Claudy and Gagnaire, 1983Claudy A.L. Gagnaire D. PUVA treatment of alopecia areata.Arch Dermatol. 1983; 119: 975-978Crossref PubMed Scopus (62) Google Scholar;Lassus et al., 1984Lassus A. Eskelinen A. Johansson E. Treatment of alopecia areata with three different PUVA modalities.Photodermatology. 1984; 1: 141-144PubMed Google Scholar;Healy and Rogers, 1993Healy E. Rogers S. PUVA treatment for alopecia areata. Does it work? A retrospective review of 102 cases.Br J Dermatol. 1993; 129: 42-44Crossref PubMed Scopus (75) Google Scholar;Taylor and Hawk, 1995Taylor C.R. Hawk J.L.M. PUVA treatment of alopecia areata partialis, totalis and universalis: Audit of 10 years’ experience at St John's Institute of Dermatology.Br J Dermatol. 1995; 133: 914-918Crossref PubMed Scopus (96) Google Scholar). The high number of recurrences is most likely due to the fact that regrown hair inhibits UVA radiation from reaching the skin. Technical improvements such as a comb that emits UVA radiation have been tried, but so far no results have been reported. Unfortunately, continuous hair regrowth after an initial response has to be actively maintained for several years in most cases. Because of an increased risk for skin malignancies after long-term therapy, PUVA cannot be recommended for AA, even if technical improvements such as a UVA-comb should ultimately prove to be effective. AA has been treated with contact sensitizers for more than 20 years. Dinitrochlorobenzene (DNCB) was the first to be used (Happle and Echternacht, 1977Happle R. Echternacht K. Induction of hair growth in alopecia areata with D.N.C.B.Lancet. 1977; 2: 1002-1003Abstract PubMed Scopus (85) Google Scholar), but because it has been shown to be mutagenic in the Ames test, it can no longer be recommended (Happle, 1979Happle R. Hinweis zur DNCB-Therapie bei Alopecia areata.Hautarzt. 1979; 30: 556PubMed Google Scholar,Happle, 1985Happle R. The potential hazards of dinitrochlorobenzene.Arch Dermatol. 1985; 121: 330-331Crossref PubMed Scopus (20) Google Scholar). Today diphenylcyclopropenone (DCP) or squaric acid dibutylester (SADBE), which are not mutagenic in the Ames test, are widely used in Europe and in Canada. Treatment with contact sensitizers is preceded by sensitization of the patient with 2% DCP solution on a small area of the scalp. Two weeks later, treatment is initiated by applying a 0.001% DCP solution, followed by weekly applications of increasing concentrations until a mild eczematous reaction is obtained. In this way, an appropriate eliciting concentration of DCP is identified for each patient. This concentration is then applied once a week to induce a mild eczematous reaction characterized by itching and erythema, without blistering or oozing. SADBE is used in those patients who become tolerant to DCP. It is applied in the same way and shows similar rates of response. Initial hair regrowth is usually visible after 8–12 weeks. Treatment must be continued once weekly until complete hair regrowth is obtained. Treatment intervals are then decreased, and, eventually treatment may be discontinued. However, if relapse occurs, treatment can be restarted immediately to stop further progression of AA and to induce renewed hair growth. At the Department of Dermatology, University of Marburg, treatment is always applied initially to half of the scalp and the other half is left untreated to exclude spontaneous hair regrowth coincident with treatment initiation. Treatment is continued on both sides only after the treated side has shown a response that is better than that of the untreated side. Mild eczematous reactions and enlargement of retroauricular lymph nodes are desired reactions and inherent to treatment. These are usually well tolerated if patients are informed that they are desired for the therapeutic effect. Undesired side-effects are noted in 2–5% of patients (Hoffmann and Happle, 1996Hoffmann R. Happle R. Topical immunotherapy in alopecai areata: What; how; and why?.Dermatol Clin. 1996; 14: 739-744Abstract Full Text Full Text PDF PubMed Scopus (43) Google Scholar). Vesicular or bullous reactions sometimes occur at the beginning of treatment before appropriate individual concentrations have been determined. Dissemination of allergic contact dermatitis, urticarial or erythema multiforme-like reactions may also occur (Perret et al., 1990Perret C.M. Steijlen P.M. Happle R. Erythema multiforme-like eruptions. A rare side effect of topical immunotherapy with diphenylcyclopropenone.Dermatologica. 1990; 180: 5-7Crossref PubMed Scopus (51) Google Scholar), but these can be treated successfully with topical corticosteroids. Pigmentary disturbances such as postinflammatory hyperpigmentation with spotty hypopigmentation (‘dyschromia in confetti’) have been observed, especially in patients with dark skin, but these have resolved within 1 years after discontinuing treatment in most instances (van der Steen and Happle, 1992van der Steen P. Happle R. Dyschromia in confetti as a side effect of topical immunotherapy with diphenylcyclopropenone.Arch Dermatol. 1992; 128: 518-520Crossref PubMed Scopus (33) Google Scholar;Hoffmann and Happle, 1996Hoffmann R. Happle R. Topical immunotherapy in alopecai areata: What; how; and why?.Dermatol Clin. 1996; 14: 739-744Abstract Full Text Full Text PDF PubMed Scopus (43) Google Scholar). Apart from these acute and subacute side-effects, no long-term side-effects have been reported after 18 years of DCP (21 years of SADBE) treatment worldwide of about 10000 patients, including children. However, it should be borne in mind that DCP and SADBE are not approved therapeutic substances. More than 25 studies have been performed to test the efficacy of treating AA with contact sensitizers. The most significant controlled studies are listed in Table 1. In contrast to corticosteroid and PUVA treatment studies, the majority of studies with contact sensitizers were controlled, with most using an untreated side of the scalp as a control. When comparing response rates for various modalities, one should bear in mind that spontaneous regrowth is excluded in these controlled, within-patient studies, but not in the uncontrolled ones. Response rates of treatment with contact sensitizers varies from 29% to 78% (see Table). The differences may be explained in part by the different extent and duration of AA prior to treatment for the patients in each study, and in part by differences in methods of treatment. However, the median response rate of all studies is 51%, rendering contact sensitizers an effective therapeutic tool for AA according to the demands of EBM. ULT, unilateral treatment, untreated side serves as control. How contact sensitizers act in treating AA is still not fully understood, but recent studies have contributed useful information. This has been discussed in detail elsewhere (Freyschmidt-Paul et al., 2001Freyschmidt-Paul P. Hoffmann R. Levine E. Sundberg J.P. Happle R. McElwee K.J. Current and potential agents for the treatment of alopecia areata.Curr Pharm Des. 2001; 7: 213-230Crossref PubMed Scopus (43) Google Scholar;Happle et al., 1986Happle R. Klein H.M. Macher E. Topical immunotherapy changes the composition of the peribulbar infiltrate in alopecia areata.Arch Dermatol Res. 1986; 278: 214-218Crossref PubMed Scopus (70) Google Scholar). Briefly, the specific interaction of CD8+/CD4+ T lymphocytes with dendritic cells and MHC class I/MHC class II positive hair follicle keratinocytes leading to AA may be interrupted by treatment with a contact sensitizer, by introducing tolerogenic cytokines T-cells or cytokines. While treatment of AA using allergic contact dermatitis has proven to be effective, treatment of AA with an irritant contact dermatitis has never been shown to be successful in a controlled study. In a half-side controlled study, using 0.1% anthralin to produce a mild irritant contact dermatitis, no differences between treated and untreated sides were observed (Nelson and Spielvogel, 1985Nelson D.A. Spielvogel R.L. Anthralin therapy for alopecia areata.Int J Dermatol. 1985; 24: 606-607Crossref PubMed Scopus (35) Google Scholar). Therefore, anthralin cannot be recommended for treatment of AA. Because the antihypertensive agent minoxidil causes hypertrichosis as a side-effect, Weiss et al attempted to use it as a treatment for various forms of hair loss, including alopecia areata (Weiss et al., 1984Weiss V.C. West D.P. Fu T.S. Robinson L.A. Cook B. Cohen R.L. Chambers D.A. Alopecia areata treated with topical minoxidil.Arch Dermatol. 1984; 120: 457-463Crossref PubMed Scopus (85) Google Scholar). But none of the studies that have claimed success with minoxidil fulfillled the criteria of evidence based treatment (Weiss et al., 1984Weiss V.C. West D.P. Fu T.S. Robinson L.A. Cook B. Cohen R.L. Chambers D.A. Alopecia areata treated with topical minoxidil.Arch Dermatol. 1984; 120: 457-463Crossref PubMed Scopus (85) Google Scholar;Fiedler-Weiss et al., 1986Fiedler-Weiss V.C. West D.P. Buys C.M. Rumsfield J.A. Topical minoxidil dose–response effect in alopecia areata.Arch Dermatol. 1986; 122: 180-182Crossref PubMed Scopus (52) Google Scholar;Price, 1987aPrice V.H. Double-blind, placebo-controlled evaluation of topical minoxidil in extensive alopecia areata.J Am Acad Dermatol. 1987; 16: 730-736Abstract Full Text PDF PubMed Scopus (84) Google Scholar,Price, 1987bPrice V.H. Topical minoxidil (3%) in extensive alopecia areata, including long-term efficacy.J Am Acad Dermatol. 1987; 16: 737-744Abstract Full Text PDF PubMed Scopus (48) Google Scholar;Ranchoff et al., 1989Ranchoff R.E. Bergfeld W.F. Steck W.D. Subichin S.J. Extensive alopecia areata. Results of treatment with 3% topical minoxidil.Cleve Clin J Med. 1989; 56: 149-154Crossref PubMed Scopus (30) Google Scholar). Six other placebo-controlled studies performed by various groups failed to show statistically significant differences between the placebo and minoxidil (White and Friedmann, 1985White S.I. Friedmann P.S. Topical minoxidil lacks efficacy in alopecia areata.Arch Dermatol. 1985; 121: 591Crossref PubMed Scopus (13) Google Scholar;Frentz, 1984Frentz G. Topical minoxidil for extended areate alopecia.Acta Derm Venereol. 1984; 65: 172-175Google Scholar;Maitland et al., 1984Maitland J.M. Alridge R.D. Main R.A. White M.I. Ormerod A.D. Topical minoxidil in the treatment of alopecia areata.Br Med J. 1984; 288: 794Crossref PubMed Scopus (13) Google Scholar;Vanderveen et al., 1984Vanderveen E.E. Ellis C.N. Kang S. Case P. Headington J.T. Voorhees J.J. Swanson N.A. Topical minoxidil for hair regrowth.J Am Acad Dermatol. 1984; 11: 416-421Abstract Full Text PDF PubMed Scopus (70) Google Scholar;Vestey and Savin, 1986Vestey J.P. Savin J.A. A trial of 1% minoxidil used topically for severe alopecia areata.Acta Derm Venereol (Stockh). 1986; 66: 179-180PubMed Google Scholar;Fransway and Muller, 1988Fransway A.F. Muller S.A. 3 percent topical minoxidil compared with placebo for the treatment of chronic severe alopecia areata.Cutis. 1988; 41: 431-435PubMed Google Scholar). In three of these studies cosmetically ac" @default.
• W2014423877 created "2016-06-24" @default.
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• W2014423877 date "2003-06-01" @default.
• W2014423877 modified "2023-10-09" @default.
• W2014423877 title "Alopecia Areata: Treatment of Today and Tomorrow" @default.
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