Programme Hospitalier Recherche Clinique, Institut Pasteur, Inserm, French Public Health Agency.

In the post-HAART era, ESLD due to HCV is a growing cause of mortality in HIV-infected patients. Increased longevity attributable to HAART, and a higher prevalence of alcohol consumption, are probably involved in this trend.

Several studies have suggested that the progression of hepatitis C virus (HCV) infection is more severe in patients infected by the human immunodeficiency virus (HIV). Two national retrospective multicenter cohort surveys were performed in France that included 17,487 HIV-infected patients during 1995 and 26,497 during 1997. The following data was evaluated: total number of deaths; number of deaths linked to AIDS, cirrhosis, or hepatocellular carcinoma (HCC); and number of deaths related to other (non-HCV--linked) causes. In 1995, the causes of death were as follows: AIDS, 1307 (7.47%); cirrhosis or HCC, 21 (0.12%); and other (non-HCV--linked) causes, 99 (0.56%). In 1997, the causes of deaths were as follows: AIDS, 459 (1.73%); cirrhosis or HCC 36 (0.13%); and other (non-HCV--linked) causes, 48 (0.18%). Comparative results between the 1995 and 1997 surveys showed a dramatic decrease in AIDS-related mortality rates (7.47% vs. 1.73%; P<.001) but not in HCV-related mortality rates (0.06% vs. 0.07%; P=.79). In France, despite the high prevalence of HCV infection in HIV-positive patients, the mortality rate in 1995 and 1997 caused by HCV-related cirrhosis or HCC was low.

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Background Large granular lymphocyte (LGL) leukemia represent ∼5–10% peripheral blood mononuclear cells. These include mainly cytotoxic T cells and natural killer (NK) cells. LGL disease has four forms: chronic or transient LGL lymphocytosis and aggressive or indolent LGL leukemia. Many autoimmune diseases have been reported associated with LGL diseases: e.g. rheumatoïd arthritis, immune thrombopenic purpura. The association between vasculitis and large granular lymphocyte (LGL) leukemia has rarely been reported or investigated. Objectives Thus, we assessed the clinical and biological phenotypes of LGL leukemia associated with vasculitis. Methods This retrospective study was conducted through the SNFMI (“Société Nationale Française de Médecine Interne”) and the “Amicale des Jeunes Internistes”. A total of 1552 internists were contacted by e-mail and asked to supply the medical characteristics of patients displaying LAV and LGL leukemia. Results We studies a series of 11 patients displaying LGL leukemia associated with vasculitis (LAV). The mean age at diagnosis of LGL leukemia was 60.3 years; there were nine women, two men. The mean follow-up period was 45 months. The main LGL lineage was T-LGL (10 patients) and only one NK-LGL was identified. Clinical and biological features of T-LGL leukemia were compared with those from the 2009 French T-LGL registry. We did not find any relevant differences except that patients with LAV were predominantly female (p <0.05). The most frequently observed vasculitis was cryoglobulinemia (n=5). Three patients presented with single-organ vasculitis, two patients had ANCA-negative microscopic polyangiitis, and one patient had giant-cell arteritis. The main clinical features involved the skin, e.g., purpura (91%), arthralgia (37%), peripheral neuritis (27%), and renal glomerulonephritis (18%). The most frequent histologic finding was leucocytoclastic vasculitis (54%). The rate of complete remission was high: i.e., 80% with corticosteroid and immunosuppressive therapy. A minority of patients had a vasculitis relapse (27%). Three patients (27%) died: one related to LGL leukemia (acute infection) and two other deaths were related to vasculitis (both with heart failure). Conclusions We conclude that vasculitis is overrepresented in the population of LGL patients, that LAV predominantly affects women, that vasculitis preferentially affects the small vessels, andthat LAV has high rate of complete response. Disclosure of Interest None Declared