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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.
Tissue Antigens 2002 Dec;60(6):489-95
Role of the Autoimmune Regulator (AIRE) gene in alopecia areata: Strong association of a potentially functional AIRE polymorphism with alopecia universalis.
On screening the AIRE coding sequence, we identified 20 variants. Two of these at positions, G961C and T1029C, give rise to amino acid changes, S278R and V301A, located in the DNA-binding segment (SAND) and PHD1 zinc finger motif, respectively. We found no difference in the frequency of the AIRE T1029C polymorphism between the control and patient groups. We genotyped 202 alopecia areata patients and 175 matched Caucasian controls for the AIRE G961C alleles. The frequency of the rare allele (961G) was 0.08 in the controls and there was a significant increase to 0.13 in alopecia areata overall and 0.20 in severe disease (alopecia universalis). We found no association between the AIRE G961G variant and mild (patchy) alopecia areata or alopecia totalis. However, the AIRE 961G allele is a potent risk factor (> 3) for the severest form of alopecia areata, and for disease of early age at onset (at 30 years). The change from serine to arginine in the SAND domain of AIRE protein may have a significant effect on AIRE DNA-binding activity. Moreover, our results could provide a rational explanation of the unusually high frequency of AA in APECED patients, supporting the concept of AA as an autoimmune disease.
Eur J Dermatol 2002 Jan-Feb;12(1):32-7
Finasteride improves male pattern hair loss in a randomized study in identical twins.
OBJECTIVES: This study compared the efficacy of finasteride with placebo in the treatment of male pattern hair loss (androgenetic alopecia) in nine pairs of male identical twins. METHODS: In this randomized, double-blind, placebo-controlled, single-center study, one twin from each identical twin pair received finasteride 1 mg/day for one year while the other received placebo. Hair growth was evaluated from standardized clinical photographs, hair counts and patient self-assessment questionnaires. Serum dihydrotestosterone and testosterone levels were analyzed and adverse events recorded. RESULTS: Finasteride significantly improved hair growth at one year compared to placebo (p < 0.05) based on analysis of photographs of the vertex and superior-frontal scalp. These results were consistent with the hair count change measured in the finasteride group, which was superior (p < 0.05) to the change measured in the placebo group. Patient self-assessment demonstrated that treatment with finasteride, in comparison to placebo, led to improvements in scalp hair growth and patients' satisfaction with appearance of hair. No drug-related adverse events were reported during the study. CONCLUSION: Through the use of identical twins, this study provides further evidence that finasteride significantly reduces hair loss progression and restores hair growth in men with male pattern hair loss.
Dermatol Clin 2001 Oct;19(4):711-26, ix
Hair and systemic disease.
Hair loss (alopecia) occurs as a manifestation of numerous systemic diseases, but usually can be categorized into one of five general groups: telogen effluvium, anagen arrest, follicular destruction, hair miniaturization, and hair shaft defects. An excess of hair also can be evidence of internal disease, and there are two general categories of increased hair density: hypertrichosis and hirsutism. The basic categories of hair disease and the systemic conditions associated with them are discussed. The history, physical examination, and histopathologic data usually are sufficient to categorize the form of hair disorder and may provide a clue to the nature of the underlying systemic disease.
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