Association between liver fibrosis and glucose intolerance in HCV-infected patients by measuring insulin sensitivity and B-cell function

HCV mainly affects the liver, but also several tissues outside the liver have been reported to be involved, resulting in a wide spectrum of extrahepatic manifestations. Several clinical studies have suggested a possible link between chronic hepatitis caused by hepatitis C [HCV] and the development of diabetes mellitus. We investigated the association between liver fibrosis and glucose intolerance in HCV-infected patients by measuring insulin sensitivity and beta-cell function. Untreated 38 chronic HCV-infected nondiabetic patients were recruited into this study [anti-HCV+]. Eighteen patients with chronic hepatitis other than HCV infection served as the control group [anti-HCV-]. We evaluated insulin sensitivity and beta-cell function of all patients in a fasting state [homeostasis model assessment of insulin resistance [HOMA-R] and homeostasis model assessment of beta-cell function [HOMA-beta]] and after an oral load of 75g glucose [whole -body insulin sensitivity index [WBISI] and delta-insulin/ delta-glucose 30]. For all included patients; histopathological changes in liver biopsies were evaluated. Severe fibrosis was a main factor associated with insulin resistance. There were significant differences in both HOMA-R [P< 0.01] and WBISI [P<0.05] between patients with mild fibrosis [N=17] and those with severe fibrosis [N=21]. Although HOMA-beta was increased significantly in the subjects with severe fibrosis compared with those with mild fibrosis [P<0.05], delta-insulin/ delta-glucose 30 showed no significant difference in stage of liver fibrosis. Last results suggest an uncertain association between liver fibrosis and beta cell function. Our findings suggest that the development of liver fibrosis is associated with insulin resistance in HCV-infected patients

Helicobacter pylori infection with iron deficiency anemia and subnormal growth at adolescence

It is thought that helicobacter pylori infection may influence growth rate in children. The aim of this study was to determine whether helicobacter pylori infection can contribute to growth deficit, especially in adolescent children who need large amount of iron for growth. A structured questionnaire was sent to the parents of 265 healthy children aged 10 to 15 years [mean 12.9] to obtain demographic information in the parents and the environment of the 265 questionnaires sent out, 187 [70.6%, 85 girls and 102 boys] were returned. After collecting blood samples from participants, hemoglobin, serum iron, total iron binding capacity, serum ferritin, the children were tested for H. pyloti infection by CI 3-urea breath test then,for positive one, upper gastrointestinal endoscope was done to see the antrum and biopsy specimens were obtained from the antrum from which rapid urease test was done. The effects of risk factors such as H.pylori infection, iron deficiency anemia, sex, socio economic status, type of house and crowding index on growth were analyzed during multiple regression analysis of 32 H.pylori positive children, 9 [28.1%] were below 25 centile values for height, compared with 32 of 156 [20.5] H.pylori negative children. The prevalence rate of H.plylori infection was 15.8%[27 of 171]] in children without iron deficiency anemia and 31.3% [5 of 16] in those affected. The relative risk of short stature was 2.2 [95% confidence interval [CI], 1.0 to 4.8] for iron deficiency anemia, and 1.4 [95% CI, 0.8 to 2.4] for H. pylori infection. The mean height was significantly lower in the group having both H.pylori infection and iron deficiency anemia. Therefore, H.pylori infection accompanied by iron deficiency anemia, rather than H.pylori infection per se, might delay pubertal growth