Steatosis is a relatively common finding in CHB and metabolic host factors rather than viral factors responsible for the presence of steatosis in these patients.

ObjectiveThe very low-density lipoprotein receptor (VLDLR) plays an important role in the development of hepatic steatosis. In this study, we investigated the role of Peroxisome Proliferator-Activated Receptor (PPAR)β/δ and fibroblast growth factor 21 (FGF21) in hepatic VLDLR regulation.MethodsStudies were conducted in wild-type and Pparβ/δ-null mice, primary mouse hepatocytes, human Huh-7 hepatocytes, and liver biopsies from control subjects and patients with moderate and severe hepatic steatosis.ResultsIncreased VLDLR levels were observed in liver of Pparβ/δ-null mice and in Pparβ/δ-knocked down mouse primary hepatocytes through mechanisms involving the heme-regulated eukaryotic translation initiation factor 2α (eIF2α) kinase (HRI), activating transcription factor (ATF) 4 and the oxidative stress-induced nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathways. Moreover, by using a neutralizing antibody against FGF21, Fgf21-null mice and by treating mice with recombinant FGF21, we show that FGF21 may protect against hepatic steatosis by attenuating endoplasmic reticulum (ER) stress-induced VLDLR upregulation. Finally, in liver biopsies from patients with moderate and severe hepatic steatosis, we observed an increase in VLDLR levels that was accompanied by a reduction in PPARβ/δ mRNA abundance and DNA-binding activity compared with control subjects.ConclusionsOverall, these findings provide new mechanisms by which PPARβ/δ and FGF21 regulate VLDLR levels and influence hepatic steatosis development.

Eosinophilic esophagitis should be considered in the differential diagnosis of any cases with refractory reflux who complain of chronic unexplained dysphagia, with history of recurrent food impaction, and atopy or abnormal endoscopic features.

Background: we assessed the prevalence, the related symptoms, and the endoscopic and histologic gastric features of celiac disease (CD) in patients with Helicobacter pylori (Hp).Methods: 450 dyspeptic patients were studied. Biopsies of gastric antrum and duodenum, CD serology, and total IgA were obtained. Histological findings were scored with the Marsh-Rostami criteria.Results: 411 (91.3%) patients were Hp positive. Duodenal histology was normal in 385 (85.6%) patients, 124 (27.5%) had duodenitis and 28 (6.2%) showed duodenal abnormalities (Marsh I-IIIc). Twenty three/28 (82.1%) patients with malabsorption pattern were also Hp positive. Serological analysis: 12 of 31 (38.7%) positive patients had abnormal histology (Marsh I,-IIIc). Nine out 450 patients were IgA deficient; none of them was serologically positive for CD.Conclusion: although a high prevalence of Hp infection was found in this study, the relationship between Hp infection and CD was similar to that reported in other geographic areas. disease and Hp infection association in Iran. Rev Esp Enferm Dig 2009; 101: 850-854.

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