Maladies inflammatoires cryptogéniques de l'intestin de novo après transplantation hépatique: rapport de quatre nouveaux cas et revue de la littérature [De novo inflammatory bowel diseases after liver transplantation: description of four new cases and a review of the literature]

Inflammatory bowel diseases are a result of an aberrant mucosal immune response to gut microflora. Several groups have reported newly diagnosed inflammatory bowel diseases following solid organ transplantation and subsequent immunosuppressive therapy. We describe four cases of newly diagnosed inflammatory bowel diseases following liver transplantation in a pool of 120 transplanted patients. These patients had no prior history of inflammatory bowel diseases or primary sclerosing cholangitis and were immunosuppressed. Two patients were transplanted for a hepatitis C related cirrhosis, one for alcoholic cirrhosis and one patient for autoimmune cirrhosis. Three patients were diagnosed with ulcerative colitis and one with Crohn's disease. These four patients were on a cyclosporin monotherapy when their inflammatory bowel diseases were diagnosed. These data suggest that cyclosporin monotherapy following solid organ transplantation does not prevent development of inflammatory bowel diseases.

Actualités en gastroentérologie et hépatologie [Highlights in gastroenterology and hepatology 2013].

This review highlights recent advances in gastroenterology and hepatology, including new insights into the diagnosis, pathogenesis and the treatment of ulcerative colitis, of achalasia, of irritable bowel syndrome, of chronic hepatitis B and of eosinophilic esophagitis. These new developments will be summarized and discussed critically, with a particular emphasis on their potential implications for current and future clinical practice. The recent advances on treatment of chronic hepatitis C will be published in another summary this year.

Pathogenesis of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common malignant tumours worldwide. The major aetiologies and risk factors for the development of HCC are well defined and some of the multiple steps involved in hepatocarcinogenesis have been elucidated in recent years. However, no clear picture of how and in what sequence these factors interact at the molecular level has emerged yet. Malignant transformation of hepatocytes may occur as a consequence of various aetiologies, such as chronic viral hepatitis, alcohol, and metabolic disorders, in the context of increased cellular turnover induced by chronic liver injury, regeneration and cirrhosis. Activation of cellular oncogenes, inactivation of tumour suppressor genes, genomic instability, including DNA mismatch repair defects and impaired chromosomal segregation, overexpression of growth and angiogenic factors, and telomerase activation may contribute to the development of HCC. Overall, HCCs are genetically very heterogeneous tumours. New technologies, including gene expression profiling and proteomic analyses, should allow us to further elucidate the molecular events underlying HCC development and identify novel diagnostic markers as well as therapeutic targets.

Durability and outcome of initial antiretroviral treatments received during 2000--2005 by patients in the Swiss HIV Cohort Study.

BACKGROUND: Little is known about time trends, predictors, and consequences of changes made to antiretroviral therapy (ART) regimens early after patients initially start treatment. METHODS: We compared the incidence of, reasons for, and predictors of treatment change within 1 year after starting combination ART (cART), as well as virological and immunological outcomes at 1 year, among 1866 patients from the Swiss HIV Cohort Study who initiated cART during 2000--2001, 2002--2003, or 2004--2005. RESULTS: The durability of initial regimens did not improve over time (P = .15): 48.8% of 625 patients during 2000--2001, 43.8% of 607 during 2002--2003, and 44.3% of 634 during 2004--2005 changed cART within 1 year; reasons for change included intolerance (51.1% of all patients), patient wish (15.4%), physician decision (14.8%), and virological failure (7.1%). An increased probability of treatment change was associated with larger CD4+ cell counts, larger human immunodeficiency virus type 1 (HIV-1) RNA loads, and receipt of regimens that contained stavudine or indinavir/ritonavir, but a decreased probability was associated with receipt of regimens that contained tenofovir. Treatment discontinuation was associated with larger CD4+ cell counts, current use of injection drugs, and receipt of regimens that contained nevirapine. One-year outcomes improved between 2000--2001 and 2004--2005: 84.5% and 92.7% of patients, respectively, reached HIV-1 RNA loads of <50 copies/mL and achieved median increases in CD4+ cell counts of 157.5 and 197.5 cells/microL, respectively (P < .001 for all comparisons). CONCLUSIONS: Virological and immunological outcomes of initial treatments improved between 2000--2001 and 2004--2005, irrespective of uniformly high rates of early changes in treatment across the 3 study intervals.

Two Cases of Interferon-Alpha-Induced Sarcoidosis Koebnerized along Venous Drainage Lines: New Pathogenic Insights and Review of the Literature of Interferon-Induced Sarcoidosis.

Sarcoidosis is a systemic granulomatous disorder of unknown origin commonly affecting the lung, the lymphoid system and the skin. We report here two cases of cutaneous sarcoidosis in two former intravenous drug users following interferon (IFN)-α and ribavirin therapy for chronic hepatitis C. Both patients developed skin sarcoidosis along venous drainage lines of both forearms, coinciding with the areas of prior drug injections. The unique distribution of the skin lesions suggests that tissue damage induced by repeated percutaneous drug injections represents a trigger for the local skin manifestation of sarcoidosis. Interestingly, skin damage was recently found to induce the local expression IFN-α, a well-known trigger of sarcoidosis in predisposed individuals. Here we review the literature on sarcoidosis elicited in the context of IFN-α therapy and propose a new link between the endogenous expression of IFN-α and the induction of disease manifestations in injured skin. © 2013 S. Karger AG, Basel.