Soluble P selectin levels in chronic liver disease: relationship to disease severity.

BACKGROUND/AIMS: Thrombocytopenia and platelet function abnormalities are problems commonly found in patients with chronic liver disease (CLD). Despite lack of widespread recognition as to the clinical significance of Soluble P-selectin (sP-selectin), in that increased levels of sP-selectin have been described in patients with CLD, it has been proposed as a marker of in-vivo platelet activation. The study's aim was to determine whether levels of sP-selectin in patients with CLD increase in accordance with the degree of liver failure, the likelihood of CLD patients with high sP-selectin levels being more prone to thrombosis, as well as investigating the coagulation and fibrinolytic parameters related to the sP-selectin. METHODOLOGY: This study was comprised of two groups: 40 patients with cirrhosis and portal hypertension (28 males and 12 females); and a control group of 10 healthy volunteers (6 males and 4 females). In both groups, biochemical parameters, sP-selectin, coagulation and fibrinolytic activity levels were measured and a Doppler ultrasound was performed. RESULTS: Plasma sP-selectin levels were found to be higher in the patients compared to those of the control group (p < 0.01), while at the same time significant differences were observed with respect to the stage of disease. Patients with low platelet counts were found to have higher sP-selectin levels than those with normal platelet counts (p < 0.01). Seven patients (17.5%) were seen to have portal vein thrombosis upon doppler ultrasound examination, while sP-selectin levels were significantly lower in those patients with thrombosis than those without (p < 0.05). It was our finding that sP-selectin levels inversely correlated with anti thrombin III. CONCLUSIONS: In conclusion, sP-selectin levels related to the degree of liver disease and thrombosis are seen together with low platelet and sP-selectin levels in patients with cirrhosis.

Assessment of lipid peroxidation and antioxidant capacity in non-alcoholic fatty liver disease.

BACKGROUND/AIMS: Lipid peroxidation/oxidative stress and/or endotoxin-induced cytokine release are implicated in the non-alcoholic fatty liver disease pathogenesis. Studies in the literature are experimental in nature and are based on histopathological evaluation and peripheral blood findings. In this study, we aimed to investigate the relationships between lipid peroxidation and antioxidant capacity in non-alcoholic fatty liver disease. METHODS: Twenty-six patients with an ethanol consumption of less than 20 g/day who were diagnosed ultrasonographically and histopathologically as non-alcoholic fatty liver disease and 16 healthy control subjects with normal ultrasonographical findings were included in the study. All viral and autoimmune markers in patient and control groups included in the study were negative. Non-alcoholic steatohepatitis samples obtained by fine needle aspiration were evaluated according to Brunt et al. The levels of glutathione, catalase, superoxide dismutase, and malonyldialdehyde in peripheral blood and liver biopsy samples were measured. RESULTS: Of patients with non-alcoholic fatty liver disease, 17 (65%) were detected to have mild, 7 (27%) moderate and 2 (8%) severe steatosis; portal inflammation was found in 17 patients (65%) and stage I fibrosis in 21 patients (80%). Minimal lobular inflammation was observed in all patients. In the patient group, the levels of erythrocytic glutathione, catalase, and superoxide dismutase were significantly lower but malonyldialdehyde levels were higher compared to the control group. It was revealed that hepatocytic reduced glutathione, catalase, and malonyldialdehyde levels were not correlated with peripheral blood levels, but there was a positive correlation between liver malonyldialdehyde level and liver reduced glutathione level. Plasma malonyldialdehyde level and liver glutathione had a negative correlation. CONCLUSIONS: It was discovered that lipid peroxidation and antioxidant capacity suppression due to its overuse were important in the non-alcoholic fatty liver disease pathogenesis, but antioxidant capacity was maintained well at tissue level in the early stages of the disease. Furthermore, it was identified that tissue lipid peroxidation and changes in antioxidant capacity were not reflected in the peripheral blood to the same extent.

Dual infection in chronic hepatitis C patients.

UNLABELLED: Hepatitis C and B virus(HCV, HBV) dual infection may occur and even persist in the same patient. Different results have been found in clinical and laboratory studies of dually infected patients. AIM: In our study, we aimed to investigate the effect of previous or present hepatitis B virus infection to clinical course and antiviral therapy in patients with chronic hepatitis C. METHOD: Hundredthirty consecutive patients with hepatitis C, who were referred to our gastroenterology unit, were studied retrospectively. Patients who were exposed to HBV infection were named as group 1, and patients who had pure hepatitis C infection were named as group 2. Fifty patients in group 1 were compared with 80 patients in group 2. HBs Ag was positive in 12, and HBV antibodies were positive in the other 38 patients of group 1. RESULTS: Age, sex, follow-up duration, transaminase levels, liver synthesis functions, histopathological findings, Child-Pugh stages and presence of complications were not statistically different in groups 1 and 2. HBV-DNA by PCR assay was negative in all 12 HBs Ag positive patients. Hepatocelluler carcinoma(HCC) was found totally in 8 cases, 2 in group 1 and 6 in group 2, while none in HBs Ag positive patients. Antiviral therapy was administired to 39 patients, 15 in group 1 and 24 in group 2. There was no difference in regard to treatment duration and response to treatment between both groups. CONCLUSION: In our study, we have found previous or present HBV infections were observed frequently in chronic hepatitis C patients, although it's effect to clinical course and antiviral therapy is not significant.

Effects of intrarectal and intraperitoneal N(G)-nitro-L-arginine methyl ester treatment in 2,4,6-trinitrobenzenesulfonic acid induced colitis in rats.

Inflammatory bowel disease (IBD) has been associated with an increased generation of nitric oxide (NO). Different authors have shown that NO in IBD can be either harmful or protective. The aim of this study was to investigate the efficiency of intrarectal (i.r.) and intraperitoneal (i.p.) application of N(G)-nitro-L-arginine methyl ester (L-NAME), a non-specific nitric oxide synthase inhibitor, in experimental acute colitis in the rats. Acute colitis was induced in rats by 2,4,6-trinitrobenzenesulfonic acid (TNBS) and ethanol. Twenty-eight rats were divided into four groups. L-NAME (50 mg/kg/day) was administered i.p. (Group 1) and i.r. (Group 2) for 7 days following the day when colitis was induced. Group 3 rats were not given any treatment after induction of colitis. Control group rats were given saline solution i.r. instead of TNBS. The presence of hyperemia, inflammation and ulcer was evaluated to score of macroscopic morphologic damage. The severity of colitis was assessed by microscopic criteria including ulceration, mucus cell depletion, crypt abscesses, inflammatory cysts, mucosal atrophy, edema, inflammatory cell infiltration, and vascular dilatation. Rectal tissue myeloperoxidase (MPO) activity and serum-rectal tissue nitrite levels were measured. Serum and rectal tissue nitrite levels increased in Group 3 rats. Both i.p. and i.r. L-NAME treatment significantly reduced serum and rectal tissue nitrite levels, but no effect on MPO activity and histologic damage score was observed. Under the present conditions we concluded i.r. and i.p. L-NAME treatment, applied at the dosage of 50 mg/kg/day, does not have any protective effect on the colonic injury.

Type 1 gastric carcinoid tumor: another extrahepatic manifestation of hepatitis C virus infection?

A 67 year-old female with a 10-year history of cirrhosis due to hepatitis C virus who developed a gastric carcinoid tumor of the corpus is described. Carcinoid tumor was identified during her last routine gastroscopic evaluation for portal hypertension. In the case, serum parietal cell antibodies, hypergastrinemia and atrophic gastritis were also found. Chronic hepatitis C virus infection is known to induce clinical and laboratory signs of autoimmunity. But the question of whether hepatitis C virus plays a pathogenic role in the development of gastric carcinoid tumor is unknown. As far as we know, this is the first report describing gastric carcinoid tumor in hepatitis C virus induced chronic liver disease. We suggest that the possibility of the development of autoimmune atrophic gastritis and carcinoid tumors should be considered in patients with chronic hepatitis C that coexists with autoimmune diseases and has positive parietal cell antibodies.

Resolution of immune thrombocytopenic purpura after colectomy for ulcerative colitis.

A number of different hematologic abnormalities are often encountered in patients with ulcerative colitis. Among them, thrombocytopenia is observed mostly as a side effect of therapy. Immune thrombocytopenic purpura is rarely reported in patients with ulcerative colitis, and various treatment modalities have been used for these two disorders. We report a case with ulcerative colitis and immune thrombocytopenic purpura which were cured after the colectomy. This result suggests that immune thrombocytopenic purpura is the extraintestinal manifestation of ulcerative colitis.