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  • Title: Lichen planus associated with hepatitis C virus: no viral transcripts are found in the lichen planus, and effective therapy for hepatitis C virus does not clear lichen planus.
    Author: Harden D, Skelton H, Smith KJ.
    Journal: J Am Acad Dermatol; 2003 Nov; 49(5):847-52. PubMed ID: 14576663.
    Abstract:
    BACKGROUND: Although hepatitis C virus (HCV) was not discovered until 1989, it was recognized for many years that a viral agent was responsible for many cases of posttransfusion or parenterally transmitted hepatitis. Acute HCV is often relatively mild; however, 70% to 80% of patients with HCV go on to develop chronic liver disease during a prolonged period of up to 40 years, and up to 50% of them may remain relatively asymptomatic during that time. A number of associated cutaneous findings have been reported in up to 15% of these patients including lichen planus-like eruptions (LP). OBJECTIVE: We sought to determine whether viral transcripts were present within the skin of patients with HCV and LP, and if systemic virologic response to interferon alfa and ribavirin correlated with response of the LP. Materials and methods A total of 4 men and 1 woman all presented with cutaneous eruptions of LP, and 1 had oral LP lesions. Cutaneous biopsies were performed on all patients. All patients were found to have chronic HCV. In addition to pathologic examination, immunohistochemical stains for lymphoid markers and reverse-transcriptase polymerase chain reaction for HCV was performed on the biopsy specimens. All patients were treated with interferon alfa and ribavirin. RESULTS: In LP there were scattered eosinophils seen in biopsy specimens of 4 of the 5 patients. The lymphoid infiltrate contained predominantly CD3(+) T cells and scattered KP-1(+) mononuclear cells, without CD20(+) B cells. Approximately one fourth of the T cells failed to mark with CD4. Although all patients were seropositive for HCV RNA at the time of biopsy, we were unable to detect HCV RNA by reverse-transcription polymerase chain reaction in any of the patients. The patients' LP showed an inconsistent response to therapy. CONCLUSION: The virus was not found in the LP lesion using reverse-transcription polymerase chain reaction for HCV. Thus, LP appears to be related to the pattern of immune dysregulation induced by HCV, probably in a host with an underlying susceptibility for autoimmune disease. The combination of interferon alfa and ribavirin may be effective in clearing the virus, but viral response did not correlate with clearing of LP.
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