BackgroundThe development of ascites in cirrhotic patients generally heralds a deterioration in their clinical status. A differential gene expression profile between alcohol- and hepatitis C virus (HCV)-related cirrhosis has been described from liver biopsies, especially those associated with innate immune responses. The aim of this work was to identify functional differences in the inflammatory profile of monocyte-derived macrophages from ascites in cirrhotic patients of different etiologies in an attempt to extrapolate studies from liver biopsies to immune cells in ascites. To this end 45 patients with cirrhosis and non-infected ascites, distributed according to disease etiology, HCV (n = 15) or alcohol (n = 30) were studied. Cytokines and the cell content in ascites were assessed by ELISA and flow cytometry, respectively. Cytokines and ERK phosphorylation in peritoneal monocyte-derived macrophages isolated and stimulated in vitro were also determined.ResultsA different pattern of leukocyte migration to the peritoneal cavity and differences in the primed status of macrophages in cirrhosis were observed depending on the viral or alcoholic etiology. Whereas no differences in peripheral blood cell subpopulations could be observed, T lymphocyte, monocyte and polymorphonuclear cell populations in ascites were more abundant in the HCV than the alcohol etiology. HCV-related cirrhosis etiology was associated with a decreased inflammatory profile in ascites compared with the alcoholic etiology. Higher levels of IL-10 and lower levels of IL-6 and IL-12 were observed in ascitic fluid from the HCV group. Isolated peritoneal monocyte-derived macrophages maintained their primed status in vitro throughout the 24 h culture period. The level of ERK1/2 phosphorylation was higher in ALC peritoneal macrophages at baseline than in HCV patients, although the addition of LPS induced a greater increase in ERK1/2 phosphorylation in HCV than in ALC patients.ConclusionsThe macrophage inflammatory status is higher in ascites of alcohol-related cirrhotic patients than in HCV-related patients, which could be related with differences in bacterial translocation episodes or regulatory T cell populations. These findings should contribute to identifying potential prognostic and/or therapeutic targets for chronic liver diseases of different etiology.

Hepatoportal sclerosis (HPS) is characterized by presinusoidal intrahepatic portal hypertension associated with splenomegaly and anemia in patients with non-cirrhotic liver. Liver biopsy is essential, especially to rule out other processes. Being a disease of unknown etiology, the majority of cases have been described in eastern countries. However, it may be an underdiagnosed disease in the West. Symptoms are related to portal hypertension and the clinical spectrum is wide, ranging from anemia with normal liver function tests to bleeding due to esophageal varices. Treatment is directed to the complications and the prognosis is better than in patients with cirrhosis. We report three cases of HPS presenting at different clinical stages and the findings of liver biopsies, the clinical outcomes and a review of scientific literature.

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Scleroderma is a disease characterized by multiorgan fibrosis due to connective tissue proliferation and vasculitis of small vessels. Sclerodermia can be localized or systemic, and the latter can compromise skin in a limited or diffuse type. Digestive tract involvement is common in the systemic form (82%) and is often characterized by dysphagia and gastroesophageal reflux disease. CASE REPORTA 50 year old male, with no relevant family history, who was diagnosed of subclinical hypothyroidism and early scleroderma has been follow-up by Rheumatology and Dermatology. Due to the finding of necrosis in his finger pads since the previous year examinations were initiated. Capillaroscopy was consistent, ANA were positive (1/640) and anticentromere antibody, RNP and Scl-70 were negative. Therefore, treatment was started with bosentan and aspirin.The patient was referred to the Emergency ward of our hospital because of melena and epistaxis. At admission, hemoglobin level was 8.5 mg/dL, with normal platelet count, normal coagulation and an ESR of 48 mm/h. Examination revealed multiple telangiectasias on his fingertips (Fig. 1), in oral mucosa and perioral region. Gastroscopy was performed which showed multiple small vascular appearance lesions (less than 5 mm) in esophageal, gastric and duodenal mucosa, with no signs of recent bleeding or clots (Fig. 2). In colonoscopy, multiple telangiectases were visualized from the anus to the cecum (Fig. 3). Neither melena nor decrease in hematocrit was presented during admission and he was discharged with supplemental oral iron and folic acid.

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