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Fixed drug eruption. Expression of epidermal keratinocyte intercellular adhesion molecule-1 (ICAM-1)

T Shiohara1, B J Nickoloff, Y Sagawa

  • 1Department of Dermatology, Kyorin University School of Medicine, Tokyo, Japan.

Archives of Dermatology
|October 1, 1989
PubMed

Insights

Localized misregulated expression of intercellular adhesion molecule-1 (ICAM-1) by keratinocytes may explain why fixed drug eruptions reappear in the same skin sites. This finding offers insight into the pathogenesis of this condition.

Area of Science:

  • Dermatology
  • Immunohistology
  • Pathogenesis of Skin Diseases

Background:

  • The pathogenic mechanism behind the specific localization of fixed drug eruption (FDE) lesions remains unclear.
  • Understanding FDE pathogenesis is crucial for managing recurrent drug reactions.

Purpose of the Study:

  • To investigate the role of intercellular adhesion molecule-1 (ICAM-1) and HLA-DR expression in the site-specificity of FDE.
  • To elucidate the immunohistological features of FDE lesions at the keratinocyte level.

Main Methods:

  • Skin biopsy specimens from four FDE patients were analyzed immunohistologically.
  • Monoclonal antibodies against ICAM-1, lymphocyte function-associated antigen-1, and HLA-DR were utilized.
  • Expression patterns were studied at various time points post-drug exposure.

Main Results:

  • ICAM-1 expression by keratinocytes was strictly localized to involved epidermis in FDE lesions.
  • HLA-DR expression was observed in both involved and uninvolved epidermis.
  • Persistent ICAM-1 expression on basal keratinocytes, even after HLA-DR down-modulation, was noted in FDE.

Conclusions:

  • Localized, misregulated ICAM-1 expression by keratinocytes is a potential factor in the site-specificity of FDE.
  • The distinct expression patterns of ICAM-1 and HLA-DR in FDE keratinocytes differentiate it from normal skin responses.

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