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Clin Exp Dermatol 2003 Jan;28(1):25-7

Postmenopausal frontal fibrosing alopecia.


Recently a new entity, postmenopausal frontal fibrosing alopecia, was added to the established subtypes of scarring alopecias affecting postmenopausal women. This condition is characterized by a progressive frontal hairline recession associated with scarring. We studied the clinical and histopathologic features in four women with this disorder. Of note, a history of bilateral oophorectomy in two of them appears to be a new association. All four cases had frontoparietal recession of the hairline and two of them also had loss of their eyebrows. None of our four patients had any mucous membrane or other skin lesions. Histological examination showed perifollicular fibrosis and lymphocytic inflammation around the isthmus and infundibular areas of the follicles. No effective treatments have emerged for this type of postmenopausal alopecia, but progression of the hair loss and scarring appears to be self-limiting. We believe that this condition is a distinct clinicopathological variant of lichen planopilaris.


J Am Acad Dermatol 2002 Nov;47(5):795

Female pattern hair loss.


In this issue of the Journal (pages 733-9), Shum et al1 describe 4 female patients with increased androgens whose central scalp hair loss responded to finasteride. This is an important observation and one that highlights why the term androgenetic or androgenic alopecia, as used to describe the hereditary pattern balding of men, should be replaced with the term female pattern hair loss when applied to women.2 It is clear that only a small but distinct subset of women with central scalp pattern hair loss, such as the patients presented in the report by Shum et al, has signs of hyperandrogenism such as acne, hirsutism, and irregular periods with or without elevation of serum androgens. Therefore these women may have hair loss resulting from a different mechanism and may respond differently to treatments targeted at androgen blockade than women with a similar type of hair loss but without evidence of hyperandrogenism. Certainly these women with hyperandrogenemia may develop, in contradistinction to those without hyperandrogenemia, a Hamilton pattern of hair loss (male pattern baldness). Many of these women may, on more careful evaluation, have polycystic ovarian syndrome.

It is not surprising that a 5-reductase inhibitor such as finasteride, which has documented efficacy in men with androgenetic alopecia3,4 and has been shown to advantageously affect hirsutism,5,6 may cause hair growth in women with female pattern hair loss and hyperandrogenism. The fact that finasteride has not previously been shown to induce hair growth in postmenopausal women with “androgenetic alopecia”7 speaks for (1) adoption of different terminology for this type of hair loss in women and (2) separate evaluation of the different subgroups of women with female pattern hair loss as recently described,2 that is, early onset with and without hyperandrogenemia and late onset/postmenopausal with and without hyperandrogenemia. We should not be too quick to rule out efficacy of a potential therapeutic agent in all women with female pattern hair loss without first testing it in all the various subsets of women.

Clearly, finasteride may be an effective treatment for women with early-onset female pattern hair loss and hyperandrogenemia, but definitive results would require a large, well-controlled trial. Such a trial would likely necessitate inclusion of a “placebo” run-in phase with an oral contraceptive, both to protect these women of child-bearing potential from getting pregnant while taking a drug known to cause genital abnormalities in male fetuses and to rule out any effect from the oral contraceptive alone on female pattern hair loss (a study that needs to be conducted in any case). Anecdotal reports, such as that presented by Shum et al,1 should ignite interest in evaluating finasteride and other 5-reductase inhibitors, either type II or combination type I/II, in women with female pattern hair loss, a group of patients whose current treatment options are extremely limited.


J Invest Dermatol 2002 Aug;119(2):392-402

Gene array profiling and immunomodulation studies define a cell-mediated immune response underlying the pathogenesis of alopecia areata in a mouse model and humans.


Alopecia areata is a suspected autoimmune hair loss disease. In a rodent model, alopecia areata can be induced in normal haired C3H/HeJ mice by transfer of skin grafts from mice with spontaneous alopecia areata. At weeks 2, 4, 6, and 10 after surgery, grafted mice were euthanized, skin collected and processed for histology, and RNA extracted. Age-matched sham-grafted mice, and mice with and without spontaneous alopecia areata, were similarly processed. For comparison, skin biopsies from alopecia areata and androgenetic alopecia affected humans were also collected. Skin mRNA processed to cDNA was analyzed using Affymetrix mouse 11K and human 6800 gene chip(R) array technology. Microarray results indicated 42 known genes upregulated or downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-mediated disease pathogenesis involving antigen presentation, costimulation, and a T helper 1 lymphocyte response. In contrast, 114 genes, many regulating immunoglobulin response, were altered late in disease development. In alopecia areata affected humans, 95 genes were significantly modulated. As confirmation of microarray analysis results, lymph node and spleen cells from alopecia areata affected mice injected into normal haired littermates transferred the alopecia areata phenotype. Alopecia areata onset could be inhibited in skin-grafted mice by modulation with B7.1- and B7.2-specific monoclonal antibodies. In addition, depletion of CD4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitted hair regrowth. The results consistently demonstrated the importance of an immune cell-mediated disease mechanism in alopecia areata pathogenesis and suggested targeting antigen-presenting cells and reactive lymphocytes may be effective in alopecia areata treatment.


Cancer Epidemiol Biomarkers Prev 2002 Jun;11(6):549-53

Androgenetic alopecia and prostate cancer: findings from an Australian case-control study.


The purpose of this study was to examine the relationship between androgenetic alopecia (AA) and prostate cancer with particular emphasis on early age at diagnosis and higher grade tumors. We conducted an age-stratified, population-based case-control study in Australia of men who were diagnosed before 70 years of age during 1994-1997 with histopathology-confirmed adenocarcinoma of the prostate, excluding well-differentiated tumors. Controls were selected from the electoral rolls, and the frequency was matched on age. After excluding subjects with missing values, the analysis was based on 1446 cases and 1390 controls of whom direct observations were made of their pattern of AA during face-to-face interviews. Our data suggest an association between prostate cancer and vertex baldness; compared with men who had no balding, the adjusted odds ratio (OR) was 1.54 (1.19-2.00). No associations were found between prostate cancer and frontal baldness or when frontal baldness was present concurrently with vertex baldness. The ORs were 0.98 (0.79-1.23) and 1.14 (0.90-1.45), respectively. The highest ORs were for high-grade disease in men 60-69 years of age: 1.80 (1.02-3.16) for frontal baldness; 2.91 (1.59-5.32) for vertex baldness; and 1.95 (1.10-3.45) for frontal and vertex baldness. This association between the pattern of AA and prostate cancer points to shared androgen pathways that are worthy of additional investigation.


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  • What is hair?
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  • Alopecia info.
  • Alopecia treatment info.
  • Alopecia treatment info.
  • Hair care info.
  • Hair loss and alopecia research articles: abstracts and source links.



    DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.





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