alopecia
Decreased serum ferritin is associated with alopecia in women.

Kantor J, Kessler LJ, Brooks DG, Cotsarelis G.

Department of Dermatology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

Alopecia in women is a common problem, and conflicting observational data have failed to determine whether an association exists between alopecia and iron deficiency in women. We therefore utilized an analytical cross-sectional methodology to evaluate whether common types of alopecia in women are associated with decreased tissue iron stores, as measured by serum ferritin. We studied patients with telogen effluvium (n = 30), androgenetic alopecia (n = 52), alopecia areata (n = 17), and alopecia areata totalis/universalis (n = 7). The normal group consisted of 11 subjects without hair loss from the same referral base and source population as those patients with alopecia. We analyzed the data utilizing the unpaired Student's t test assuming unequal variances with an alpha adjustment for multiple comparisons to assess whether the mean ages, ferritin levels, and hemoglobin levels of women without hair loss differed from the means in each alopecia group. The mean age of patients and normals did not differ significantly. We found that the mean ferritin level (ng per ml [95% confidence intervals]) in patients with androgenetic alopecia (37.3 128.4, 46.1]) and alopecia areata (24.9 [17.2, 32.6]) were statistically significantly lower than in normals without hair loss (59.5 [40.8, 78.1]). The mean ferritin levels in patients with telogen effluvium (50.1 [33.9, 66.33]) and alopecia areata totalis/universalis (52.3 [23.1, 81.5]) were not significantly lower than in normals. Our findings have implications regarding therapeutics, clinical trial design, and understanding the triggers for alopecia.

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alopecia
Occurrence and severity of alopecia in patients on combination chemotherapy.

Pai GS, Vimala AM, Dinesh M.

Department of Dermatology and STD, Kasturba Medical College, Manipal Academy of Higher Education, Mangalore, Karnataka, India.

The aim of the study was to evaluate the occurrence and severity of alopecia resulting from combination chemotherapy on cancer patients. The study was conducted during the period 1994-1996 on 58 confirmed cases of malignancies attending the Kasturba Medical College Hospital, Mangalore, South India. The treatment regimens followed were standard protocols recommended for those malignancies and which are widely adopted. Specific drug combinations, their dosage and routes and schedules of administration were studied. The influence of 20 different treatment regimens, most of them in combination chemotherapy, were studied. The patients studied were not receiving any other medication which could have caused alopecia as observed in the present study. The pathophysiology of the hair, as influenced by the treatment regimens, were studied by examination of samples of the affected hairs under a Leica compound microscope. Alopecia was the most dominant side effect influencing 35 of the 58 patients undergoing the treatment (60%). The severity of alopecia was assessed by grouping them in four distinct grades. Specific drugs and their combinations causing varying degrees of severity were identified. The initiation of hair loss in different treatment regimens were analysed. It is seen that alopecia is an early manifestation of cutaneous side effects of cancer chemotherapy. In a majority of patients, the manifestation initiated after the first or the second cycle of administration of the rapeutic regimen, indicating a time interval of 1 to 8 weeks after the start of chemotherapy. Single agent drugs, when used alone or in combination with immunomodulator drugs seem to cause much less side effects, including alopecia, when compared to multiple drug regimens. Microscopic examination of the affected hair showed trichorrhexis, fragmentation, decrease in diameter and depigmentation of the hair shaft.

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alopecia
Steroid sulfatase in the human hair follicle concentrates in the dermal papilla.

Hoffmann R, Rot A, Niiyama S, Billich A.

Philipp University, Department of Dermatology, Marburg, Germany. rolf.hoffmann mailer.uni-marburg.de

5 alpha-dihydrotestosterone is known to play a crucial part in the regulation of hair growth and in the development of androgenetic alopecia. 5 alpha-dihydrotestosterone is formed locally within the hair follicle from the systemic precursor testosterone by cutaneous steroid 5 alpha-reductase. Moreover, adrenal steroids such as dehydroepiandrosterone are converted to 5 alpha-dihydrotestosterone by isolated hair follicles, which may provide an additional source of intrafollicular 5 alpha-dihydrotestosterone levels. Elevated urinary dehydroepiandrosterone and serum dehydroepiandrosterone sulfate have been reported to be present in balding young men. These reports suggest that dehydroepiandrosterone sulfate may act as an important endocrine factor in the development of androgenetic alopecia. Hence the question arises whether the dehydroepiandrosterone sulfate can be metabolized within the hair follicles to yield dehydroepiandrosterone by the microsomal enzyme steroid sulfatase, and where steroid sulfatase might be localized. We therefore performed immunostaining for steroid sulfatase on human scalp biopsies as well as analysis of steroid sulfatase enzyme activity in defined compartments of human beard and occipital hair follicles ex vivo. Using both methods steroid sulfatase was primarily detected in the dermal papilla. Steroid sulfatase activity was inhibited by estrone-3-O-sulfamate, a specific inhibitor of steroid sulfatase, in a concentration-dependent way. Furthermore, we show that dermal papillae are able to utilize dehydroepiandrosterone sulfate to produce 5 alpha-dihydrotestosterone, which lends further support to the hypothesis that dehydroepiandrosterone sulfate contributes to androgenetic alopecia and that steroid sulfatase inhibitors could be novel drugs to treat androgen-dependent disorders of the hair follicle such as androgenetic alopecia or hirsutism.

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alopecia
Melanocyte-associated T cell epitopes can function as autoantigens for transfer of alopecia areata to human scalp explants on Prkdc(scid) mice.

Gilhar A, Landau M, Assy B, Shalaginov R, Serafimovich S, Kalish RS.

Skin Research Laboratories, Flieman Medical Center and Rappaport Faculty of Medicine, Technion Institute of Technology, Haifa, Israel.

Alopecia areata is a tissue restricted autoimmune condition affecting the hair follicle, resulting in hair loss. The goal of this study was to test the hypothesis that the autoantigen of alopecia areata is melanocyte associated. Potential autoantigens were tested in the human scalp explant/Prkd(scid) CB-17 mouse transfer system. Scalp T cells from lesional (bald) alopecia areata scalp were cultured with antigen-presenting cells, and antigen, along with interleukin-2. The T cells were then injected into autologous lesional scalp grafts on SCID mice, and hair regrowth was measured. Hair follicle homogenate was used as an autoantigen control. T cells cultured with melanoma homogenate induced statistically significant reduction in hair growth (p <0.01 by ANOVA). HLA-A2-restricted melanocyte peptide epitopes were then tested with lesional scalp T cells from HLA-A2-positive alopecia areata patients. Melanocyte-peptide-activated T cells significantly reduced the number of hairs regrowing in two experiments with six patients (p <0.001 by ANOVA). Injected scalp grafts showed histologic and immunochemical changes of alopecia areata. The most consistent peptide autoantigens were the Gp100-derived G9-209 and G9-280 peptides, as well as MART-1 (27-35). Melanocyte peptide epitopes can function as autoantigens for alopecia areata. Multiple peptides were recognized, suggesting epitope spreading.

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alopecia
Changes in populations of HLA-DR+CD3+ cells and CD57-CD16+ cells in alopecia areata after corticosteroid therapy.

Imai R, Takamori K, Ogawa H.

Department of Dermatology, Juntendo University School of Medicine, Tokyo, Japan.

We investigated the populations of activated T (HLA-DR+CD3+) cells and natural killer (CD57-CD16+) cells in the peripheral blood of patients with various types of alopecia areata (AA) and noted any changes that occurred in the said populations after administration of local and systemic corticosteroid therapy. In type 2 (severe multiple AA and alopecia totalis) and type 3 (alopecia universalis), the mean percentages of HLA-DR+CD3+ cells and CD57-CD16+ cells were significantly higher when compared with those of the normal controls. The percentages of both subsets in type 1 (mild AA) and the normal controls were consistent. Twenty-four patients in types 2 and 3 had received corticosteroid treatment, and all patients experienced new hair growth. With the changes in disease activity, the populations of HLA-DR+CD3+ cells in these patients after corticosteroid therapy significantly decreased when compared with those recorded prior to treatment. Subsequent to treatment, the mean percentages of CD57-CD16+ cells decreased to levels that were not significant relative to that of the normal controls. These findings indicate that HLA-DR+CD3+ and CD57-CD16+ cells in the peripheral blood of patients with AA may be correlated with the disease activity of AA.

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alopecia
Cytokeratin expression in alopecia areata hair follicles.

Van Baar HM, Van Vlijmen IM, Ramaekers FC, Van Muijen GN, Troyanovsky SM, Perret CM, Van de Kerkhof PC, Schalkwijk J.

Department of Dermatology, University Hospital Nijmegen, The Netherlands.

Alopecia areata is a human hair disease of unknown etiology. Immunological mechanisms, alterations in the extracellular matrix and follicular growth abnormalities have been suggested as a possible cause. Here we compare the expression of cytokeratins in normal hair follicles to that of alopecia areata using immunohistology with monoclonal antibodies. A number of cytokeratins were specifically expressed in defined anatomical parts of the follicle; however, no gross qualitative or quantitative differences were found between normal and diseased scalp. Interestingly, the expression of cytokeratin 16, which is modulated by conditions that affect the rate of keratinocyte proliferation, was found to be unchanged in the outer root sheet of alopecia areata follicles. This is in contrast with earlier observations of a decrease in the expression of the proliferation-associated, Ki-67 nuclear antigen.

Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7511864&dopt=Abstract alopecia, hair loss