Although cases of lichen planus (LP) associated with hepatitis C virus (HCV) infection have been described, the association between the two diseases has not been established because the geographic origin of patients could be an important factor in HCV prevalence in patients with LP. The serum samples of 78 consecutive patients with cutaneous and/or mucous LP and 82 control patients were analysed for the presence of antibodies to HCV by enzyme-immunoassay and for the presence of antigens of HCV by two-stage polymerase chain reaction (PCR). The clinical features of patients with LP associated with HCV infection were compared with patients with LP without HCV infection. Sixteen of the 78 (20%) patients had anti-HCV antibodies. In 13 of these 16 cases (81%), HCV-RNA was detected by PCR in serum samples. In the 82 control patients, anti-HCV antibodies was observed in two (2.4%) patients. We have found a statistically significant association (P < 0.05) between erosive LP and HCV infection. We conclude that the high prevalence of HCV-RNA in patients with LP provides some evidence for the role of HCV in the pathogenesis of LP. Our results suggest an association between erosive LP and HCV infection.

Interferon-alpha therapy has been shown to be active in the treatment of mycosis fungoides although the individual response to this therapy is unpredictable and dependent on essentially unknown factors. In an effort to better understand the molecular mechanisms of interferon-alpha resistance we have developed an interferon-alpha resistant variant from a sensitive cutaneous T-cell lymphoma cell line. We have performed expression analysis to detect genes differentially expressed between both variants using a cDNA microarray including 6386 cancer-implicated genes. The experiments showed that resistance to interferon-alpha is consistently associated with changes in the expression of a set of 39 genes, involved in signal transduction, apoptosis, transcription regulation, and cell growth. Additional studies performed confirm that STAT1 and STAT3 expression and interferon-alpha induction and activation are not altered between both variants. The gene MAL, highly overexpressed by resistant cells, was also found to be expressed by tumoral cells in a series of cutaneous T-cell lymphoma patients treated with interferon-alpha and/or photochemotherapy. MAL expression was associated with longer time to complete remission. Time-course experiments of the sensitive and resistant cells showed a differential expression of a subset of genes involved in interferon-response (1 to 4 hours), cell growth and apoptosis (24 to 48 hours.), and signal transduction.

Objective: To describe a series of 41 patients with fresh lesions of Sweet syndrome in which the histopathologic study demonstrated an inflammatory infiltrate mostly composed of histiocytoid mononuclear cells. Design: Histopathologic, immunohistochemical, and cytogenetic studies of the inflammatory infiltrate in a case series of histiocytoid Sweet syndrome. Setting: University departments of dermatology and a private laboratory of dermatopathology. Methods: Conventional histopathologic study as well as immunohistochemical investigations were performed using the alkaline phosphatase antialkaline phosphatase technique with a large panel of antibodies. In some cases, fluorescent in situ hybridization studies were performed to investigate the presence of the bcr/abl gene fusion. Results: Immunohistochemical studies demonstrated that most cells of the infiltrate showed immunoreactivity for CD15, CD43, CD45, CD68, MAC-386, HAM56, and ly-sozyme, which is consistent with a monocytichistiocytic immunoprofile. However, intense myeloperoxidase reactivity was detected in most of the cells with histiocytic appearance, which raised the possibility of specific cutaneous involvement by myelogenous leukemia. Nevertheless, cytologic peripheral blood examinations, fluorescent in situ hybridization studies to investigate the bcr/abl gene fusion, and follow-up of the patients, taken all together, ruled out this possibility. Conclusions: This case series demonstrates that some fresh cutaneous lesions of Sweet syndrome are histopathologically characterized by an infiltrate mostly composed of cells that may be misinterpreted as histiocytes, when in fact they are immature myeloid cells. We named this histopathologic variant histiocytoid Sweet syndrome, which should not be mistaken with leukemia cutis or other inflammatory dermatoses that are histopathologically characterized by histiocytes interstitially arranged between collagen bundles of the dermis.

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The cold agglutinin syndrome is a haemolytic disorder that can cause skin lesions, mainly on the acral areas, with acrocyanosis being the most frequent manifestation. Cutaneous necrosis due to cold agglutinins is very rare. Reactive angioendotheliomatosis (RAE) is an uncommon condition that exclusively affects the skin, characterized by a hyperplasia of endothelial cells and pericytes that can result in the formation of glomeruloid structures. The association of cold agglutinin syndrome with glomeruloid RAE has not been previously described. We report a 70-year-old man diagnosed as having a B-cell low-grade non-Hodgkin's lymphoma. He had two episodes of cutaneous necrosis in acral areas which were related to exposure to cold and due to IgM anti-I(T) cold agglutinins. Biopsy specimens showed vessel proliferations composed of dilated vascular spaces in the dermis and subcutis. Some vessel lumina were partially occluded by eosinophilic thrombi of fibrin and erythrocytes. Numerous closely packed capillaries were observed within pre-existing dilated vessels. This intravascular proliferation of capillaries displayed a glomeruloid pattern. We emphasize the possible presence of a cold agglutinin syndrome in patients with skin necrosis and findings of RAE with a glomeruloid pattern. Cold agglutinaemia may cause these distinctive histological changes.