alopecia
Psychological effects of androgenetic alopecia on women: comparisons with balding men and with female control subjects.

Cash TF, Price VH, Savin RC.

Department of Psychology, Old Dominion University, Norfolk, VA 23529-0267.

BACKGROUND: Several studies have examined the psychological impact of androgenetic alopecia on men but scientific evidence is absent regarding its effects on women. OBJECTIVE: Our purpose was to determine the psychosocial sequelae of androgenetic alopecia in women and, comparatively, in men. METHODS: Subjects were newly referred patients with androgenetic alopecia (96 women and 60 men) and 56 female control patients. Subjects completed standardized questionnaires to assess their psychological reactions to their respective conditions and to measure body image, personality, and adjustment. RESULTS: Androgenetic alopecia clearly was a stressful experience for both sexes, but substantially more distressing for women. Relative to control subjects, women with androgenetic alopecia possessed a more negative body image and a pattern of less adaptive functioning. Specific correlates of the adversity of patients' hair-loss experiences were identified. CONCLUSION: The results confirm the psychologically detrimental effects of androgenetic alopecia, especially on women. The implications for patient care are discussed.

Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8408792&dopt=Abstract alopecia, hair loss



alopecia
Severe alopecia areata treated with systemic corticosteroids.

Alabdulkareem AS, Abahussein AA, Okoro A.

Department of Dermatology, King Fahd Hospital of the University, Dammam, Saudi Arabia.

BACKGROUND: Treatment of severe alopecia areata is difficult, and most efforts to successfully treat this condition have been disappointing. Systemic corticosteroids have been demonstrated as an effective treatment of severe alopecia areata. METHODS: Eighteen patients with alopecia areata (extensive patchy and totalis universalis types) were treated with systemic corticosteroids. RESULTS: Satisfactory hair regrowth was achieved in seven patients (38.9%). Hair fall subsequently occurred in all of these patients on discontinuation or tapering of corticosteroid therapy. CONCLUSIONS: Systemic corticosteroid therapy does not prevent the spread or relapse of severe alopecia areata and, when complete regrowth is obtained, it is rarely maintained off therapy.

Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9732014&dopt=Abstract alopecia, hair loss



alopecia
Cloning, genomic organization, alternative transcripts and mutational analysis of the gene responsible for autosomal recessive universal congenital alopecia.

Cichon S, Anker M, Vogt IR, Rohleder H, Putzstuck M, Hillmer A, Farooq SA, Al-Dhafri KS, Ahmad M, Haque S, Rietschel M, Propping P, Kruse R, Nothen MM.

Institute of Human Genetics, University of Bonn, Wilhelmstrasse 31, 53111 Bonn, Germany.

Complete or partial congenital absence of hair (congenital alopecia) may occur isolated or with associated defects. The majority of families with isolated congenital alopecia has been reported to follow an autosomal recessive mode of inheritance (MIM 203655). We have previously mapped the gene for autosomal recessive congenital alopecia in a large inbred Pakistani family in which affected persons show complete absence of hair development (universal congenital alopecia) to a 15 cM region on chromosome 8p21-22. Here we report the cloning and characterization of the human homologue of the mouse hairless gene and show that it is located in the critical region on chromosome 8p21-22. Determining the exon-intron structure allowed detailed mutational analysis of DNA samples of patients with universal congenital alopecia. We detected a homozygous missense mutation in the Pakistani family and a homozygous splice donor mutation in a family from Oman. In addition, we show that the human hairless gene undergoes alternative splicing and that at least two isoforms generated by alternative usage of exon 17 are found in human tissues. Interestingly, the isoform containing exon 17 is the predominantly expressed isoform in all tissues but skin, where exclusive expression of the shorter isoform was observed. We speculate that this tissue-specific difference in the proportion of hairless transcripts lacking exon 17 sequences could contribute to the tissue-specific disease phenotype observed in individuals with isolated congenital alopecia.

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alopecia
Quantification of hair follicle parameters using computer image analysis: a comparison of androgenetic alopecia with normal scalp biopsies.

Lee MS, Kossard S, Wilkinson B, Doyle JA.

Skin & Cancer Foundation Australia, Darlinghurst, New South Wales, Australia.

Computer image analysis enables large numbers of hairs to be measured in an automated fashion. In this study, we examined horizontal scalp biopsies from 10 patients with a histological diagnosis of androgenetic alopecia and 10 normal control subjects. The density of hair follicles and the ratio of terminal to vellus hairs were determined. Hair shaft, hair canal and hair follicle diameter, inner root sheath width and outer root sheath area were measured using the Chromatic Colour Image Analysis program. This study showed a statistically significant progressive decrease in size of hair canal diameters from normal terminal hairs (85.93 +/- 10.07 microns) through to androgenetic alopecia terminal (68.83 +/- 13.60 microns) and vellus hairs (28.67 +/- 5.60 microns). This pattern is also seen with hair follicle diameters; normal terminal (268.41 +/- 24.88 microns), androgenetic alopecia terminal (236.34 +/- 17.23 microns), and vellus hairs (130.88 +/- 19.96 microns). Outer root sheath areas, hair shaft diameters and ratio of terminal to vellus hairs were significantly larger in normal (18,500 +/- 4222 microns 2; 82.71 +/- 13.79 microns; 36:1; respectively) compared with androgenetic alopecia scalp biopsies (8403 +/- 3322 microns 2; 61.11 +/- 14.42 microns; 3:1; respectively), whereas inner root sheath width and density did not vary significantly. Computer image analysis can be adapted for use in clinical trials where large numbers and objectivity are critical in determining the efficacy of hair growth promoters.

Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7487740&dopt=Abstract alopecia, hair loss



alopecia
Antismooth muscle and antiparietal cell antibodies in Indians with alopecia areata.

Kumar B, Sharma VK, Sehgal S.

Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

BACKGROUND: Alopecia areata is suspected to be an autoimmune disease. We studied 104 consecutive patients with alopecia areata for the presence of autoantibodies and associated autoimmune diseases. METHODS: A detailed history and examination was carried out in all patients to look for associated atopy, diabetes mellitus, hypertension, rheumatoid arthritis, vitiligo, lupus erythematosus, and thyroid disorders, etc. in the patients or their family members. Venous blood for estimation of fasting and postprandial blood glucose was collected in 30 patients, especially in those with family history of diabetes mellitus. Antimitochondrial (AMA), antismooth muscle (SMA), antinuclear antibodies (ANA), antiparietal cell antibody (PCA), and antibody against thyroid microsome (TMA) were detected employing indirect immunofluorescence on a composite section of rat liver, stomach, kidney, and human thyroid. Skin biopsy was processed for direct immunofluorescence by a conventional technique. RESULTS: Disseminated discoid lupus erythematosus, lichen planus, urticaria, psoriasis, and seronegative spondylarthritis were associated with alopecia areata in one case each. Antismooth-muscle-antibodies and PCA were found in 36 (34.6%) and 44 (42.3%) patients respectively, followed by TMA in 8 (7.7%), AMA in 6 (5.7%), antithyroglobulin antibodies in 3 (2.8%), and ANA in 2 (1.9%) patients. The incidence of SMA was higher in men with alopecia areata (P < 0.001). Direct immunofluorescence carried out in 24 patients did not reveal significant findings, except for occasional immunoglobulin deposits around hair follicles and blood vessels. CONCLUSION: Alopecia areata in India is associated more often with antismooth muscle and antiparietal cell antibodies.

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alopecia
HLA class II antigen associations help to define two types of alopecia areata.

Colombe BW, Price VH, Khoury EL, Garovoy MR, Lou CD.

Department of Surgery, University of California, San Francisco, USA.

BACKGROUND: Multiple HLA class I and class II antigen associations have been described for alopecia areata (AA). As in other immune-mediated diseases, the HLA antigens associated with AA could influence the patient's ability to respond to immune challenge from both self- and non-self-antigens and may offer clues to the cause and prognosis of and potential therapy for the disease. OBJECTIVE: Our purpose was to determine which HLA class II antigens are associated with two forms of long-standing AA, which we define to be long-standing patchy AA and long-standing alopecia totalis (AT) and alopecia universalis (AU). We also examined other factors such as age at onset of disease and familial and patient histories of autoimmune disease for correlation with the two groupings. METHODS: Patients were typed for HLA class I and class II antigens by serologic methods and were typed by molecular methods for the subtypes of the HLA class II antigens. RESULTS: HLA-DR11 (DRB1*1104) and HLA-DQ7 (DQB1*0301) were found to be highly significantly increased in frequency in patients with long-standing AT/AU (group III) but not in patients with long-standing patchy AA (group II); both patient groups showed increased frequencies of HLA-DQ3 (DQB1*03). Group III patients were unique in their early age at onset of disease. Familial incidence of AA was 37% in patients who had their first patch by 30 years of age and 7.1% with the first patch after 30 years of age. CONCLUSION: The data support the differential association of two well-defined clinical forms of AA, namely long-standing AT/AU and long-standing patchy AA, with specific HLA antigens and age at onset; they also suggest that the broad antigen HLA-DQ3, DQB1*03, is a likely candidate for general susceptibility to AA. Our findings also suggest a bimodal pattern of disease with an early-onset form associated with greater severity, long duration, and family history of the disease and a late-onset form characterized by milder severity, shorter duration, and low family incidence.

Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7593774&dopt=Abstract alopecia, hair loss