Stem cell apoptosis in HIV-1 alopecia
Background: Diffuse alopecia occurs in almost 7% of HIV‐1‐infected patients. Telogen effluvium is the main pathogenic mechanism involved. Apoptotic keratinocytes in the outer root sheath at bulge level was described as the most characteristic histopathologic finding of this kind of hair loss. Metho...
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Published in: | Journal of cutaneous pathology Vol. 33; no. 10; pp. 667 - 671 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
Oxford, UK
Blackwell Publishing Ltd
01-10-2006
Blackwell |
Subjects: | |
Online Access: | Get full text |
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Summary: | Background: Diffuse alopecia occurs in almost 7% of HIV‐1‐infected patients. Telogen effluvium is the main pathogenic mechanism involved. Apoptotic keratinocytes in the outer root sheath at bulge level was described as the most characteristic histopathologic finding of this kind of hair loss.
Methods: A case–control study was conducted to investigate the occurrence of apoptosis of follicular stem cells at the bulge in diffuse alopecia of HIV‐1 infection. We applied a double‐staining procedure to transverse scalp sections from 15 HIV‐1‐infected patients and 12 controls, with the monoclonal antibody anticytokeratin 19 as stem cell marker and TUNEL technique to identify apoptosis.
Results: Eighty percent of cases and 25% of controls presented at least one double‐stained follicle. The proportion of positive follicles per section was 48% (±7%) for cases and 26% (±13%) for controls.
Conclusion: Our study demonstrated that diffuse alopecia related to HIV‐1 infection represents a hair cycle disturbance and that part of the follicular stem cell population become apoptotic in a higher proportion than normal subjects. We found no cytotoxic folliculitis. Owing to its cell‐cycle interaction and caspase‐induction capacities, we propose HIV‐1 viral protein R as a possible follicular stem cell apoptosis inductor. |
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Bibliography: | istex:60925F6FAEE8B84FA01E32161B81C793C8EADFCF ArticleID:CUP517 ark:/67375/WNG-53LZD5N0-R ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0303-6987 1600-0560 |
DOI: | 10.1111/j.1600-0560.2006.00517.x |