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J Invest Dermatol 2002 Dec;119(6):1237-43
Loss of cell adhesion in Dsg3bal-Pas mice with homozygous deletion mutation (2079del14) in the desmoglein 3 gene.
Pemphigus encompasses a group of autoimmune blistering diseases with circulating pathogenic autoantibodies recognizing several proteins, including the desmosomal cadherin, desmoglein 3. Targeted disruption of the Dsg3 gene by homologous recombination (Dsg3tm1stan) in mouse results in fragility of the skin and oral mucous membranes, analogous to the human disease. In addition, the Dsg3tm1stan mice develop phenotypic runting and hair loss, identical to that of the mouse mutant, Dsg3bal-2J. The Dsg3bal-2J mice are homozygous for a 1 bp insertion (2275insT) in the Dsg3 gene resulting in a nonfunctional Dsg3 mRNA. In this study, we characterized an allelic mutation, Dsg3bal-Pas, with clinical features similar to those in Dsg3bal-2J. We have identified a 14 bp deletion in exon 13 of the Dsg3 gene resulting in a frameshift and premature termination codon 7 bp downstream from the site of the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating virtually all of the intracellular domain. We demonstrate that, although a Dsg3 mRNA transcript was detectable in Dsg3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal epithelium of homozygous Dsg3bal-Pas compared with that of +/Dsg3bal-Pas mice. No significant changes in the expression of desmogleins 1 and 2 were detected. To elucidate a potential mechanism causing loss of cell adhesion in the Dsg3bal-Pas mice, we generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes. The myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein was found predominantly in the cytoplasm possibly due to increased proteolytic degradation. Cell surface staining was also detected but was jagged, not linear along the cell-cell border like that observed for the full-length desmoglein 3. The expression of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining of other desmosomal proteins, including desmoglein 1 and 2, plakophilin 2, and plakoglobin. In addition, the cells expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell morphology and exhibited striking extensive filopodia. Collectively, these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in disadhesion of keratinocytes manifested with blistering phenotype.
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 Dermatol 2002 Apr;29(4):197-201
Ultrastructural study of acquired pili torti-like hair defects accompanying pseudopelade.
Acquired structural hair defects are caused by various physical and chemical manipulations. Plucked hairs and hair follicle biopsy specimens of pili torti-like hairs that arose from pseudopelade scalp were studied. In scanning electron microscopy, the hair shafts had a segmental pili torti-like appearance, accompanied by oblique or longitudinal grooves and ridges. In light microscopy, the hair follicles showed an asymmetric hair bulb and inner root sheath, and a shortened keratogenous zone within sclerosing fibrous connective tissue. In transmission electron microscopy, the numbers and thickness of the hair cuticle cells were different on the opposite sides of the hair shaft. The hair cuticle was irregularly shaped and formed asymmetric waves. The tonofilaments in the hair cortex ran almost parallel to the hair axis. From these findings, it was clear that the grooves and ridges were produced by the deformed hair cuticle and cortex, whose shapes were modulated by the asymmetric inner root sheath. This asymmetry most likely resulted from a dysfunctional dermal papilla, which was affected by fibrosis. The pili torti-like appearance appeared to be caused by the grooves and ridges that ran obliquely on the hair shaft surface.
Eur J Dermatol. 2003 Mar-Apr;13(2):150-60.
Efficacy and tolerability of finasteride 1 mg in men aged 41 to 60 years with male pattern hair loss.
A 24-month double-blind, randomized, placebo-controlled, parallel-group, multicenter study of 424 men was conducted to determine the efficacy and tolerability of finasteride 1 mg on hair growth/loss in men aged 41 to 60 years with mild-to-moderate, predominantly vertex male pattern hair loss. Efficacy was evaluated by review of global photographs of the vertex scalp taken at baseline and at Months 6, 12, 18, and 24 and by patient self-assessments and investigator clinical assessments of change from baseline in hair growth/loss collected at Months 6, 12, 18, and 24. Safety analyses included assessment of clinical and laboratory adverse experiences, including sexual adverse experiences. Analysis of global photographic assessment data showed significant improvement in hair growth for men in the finasteride group compared with those taking placebo beginning at Month 6 (p < 0.001) and maintained through Month 24 (p < 0.001). Results of the patient self-assessment and investigator assessments were consistent with those from the global photographic assessment. Finasteride 1 mg improved scalp hair growth in men aged 41 to 60 years with predominantly vertex male pattern hair loss compared with results seen with placebo. Improvement was evident by 6 months of treatment and continued through 24 months. Treatment with finasteride 1 mg was generally well tolerated.
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