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Coeliac disease (CD) is an autoimmune disorder which leads to chronic inflammation of the gut. Untreated CD is associated with upper gastrointestinal malignancies, Small-bowel lymphoma and adenocarcinoma are recognized complications of untreated coeliac disease (CD). We report the case of a 43-year-old male suffering from CD who was treated with a gluten-free diet one year, presenting with complaints of intractable nausea and vomiting. After several studies, He underwent push enteroscopy, which identified one large mass lesion in the third part of duodenum. However, histopathological examination showed adenocarcinoma. Subsequently, a duodenal segment resection was performed. After surgery, the patient recovered well and left our hospital in good condition. Clinicians should take into small bowel adenocarcinoma is rare but associated with CD particularly in CD patients with worrying symptoms such as nausea and vomiting unresponsiveness to treatment and these patients should be screened for long term complications like malignancy. [ABSTRACT FROM AUTHOR]

Aim: The aim of this study was to assess the prevalence of celiac disease (CD) in dyspeptic patients. Background: Although severe mucosal abnormality with villous atrophy (lesions Marsh III) is the histology gold standard for the diagnosis of CD, non-specific microenteropathy (Marsh I-II) with positive serology is also common Patients with dyspepsia, specific CD antibodies and microenteropathy, could have CD. Patients and methods: From November 2007 to October 2008, 407 randomly chosen patients who underwent diagnostic upper gastrointestinal endoscopy for dyspeptic symptoms (193 male, 214 women; mean age 36.1 years) were studied. Small bowel biopsies were performed in all of them. Histologic characteristics in duodenal biopsy specimens for CD were evaluated according to the modified Marsh Classification. All the patients were also tested for serum total immunoglobulin A and anti-transglutaminase (tTG) antibodies. Those with IgA deficiency were tested for IgG tTG. Results: Duodenal histology showed Marsh I-IIIc lesions in 6.4% cases. 4 patients (0.98%) were IgA deficient and none of them were positive for IgG tTG. Serology showed positive results for tTGA in 8% of the patients and 2.5% of them had abnormal histology (Marsh I-IIIc) compatible with CD. Conclusion: The results of this study showed that milder enteropathy (Marsh 0-II) have a low specificity for CD. The prevalence of CD among dyspeptic individuals is significantly (2.5%) higher than in the general population (1%) and CD should be investigated in these patients. [ABSTRACT FROM AUTHOR]

Background Given that obesity and insulin resistance play key roles in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and the connection between leptin and these metabolic diseases, the association between NAFLD and a leptin receptor gene (LEPR) polymorphism was examined. Methods In this genetic case-control association study, 144 biopsy-proven NAFLD patients and 144 controls were genotyped for the LEPR gene Gln223Arg (rs1137101) polymorphism using the polymerase chain reaction–restriction fragment length polymorphism method. Results The distributions of genotypes and alleles of Gln223Arg variant were in accordance with the Hardy-Weinberg equilibrium in the study groups (P >.05). Multivariate logistic regression analysis showed that the LEPR Gln223Arg Arg/Arg genotype was an independent risk factor for NAFLD; the Arg/Arg genotype, compared with the Gln/Gln genotype, was associated with a 2.09-fold increased risk for NAFLD (P =.036, odds ratio = 2.09 [95% CI = 1.31-5.95]). Conclusions We found that the LEPR Gln223Arg Arg/Arg genotype was independently associated with a more than 2-fold rise in biopsy-proven NAFLD risk. Our findings, however, need to be corroborated by further studies. [ABSTRACT FROM AUTHOR]

Objective Nonalcoholic fatty liver disease (NAFLD), which is an emerging global chronic liver disease, has a close association with insulin resistance. We aimed to determine whether the Gly1057Asp (rs1805097) polymorphism of the insulin receptor substrate 2 (IRS2) gene is associated with NAFLD. Methods Using the polymerase chain reaction-restriction fragment length polymorphism method, 135 patients with biopsy-proven NAFLD and 135 controls underwent IRS2 genotype analysis. Results Genotype and allele distributions of the IRS2 gene Gly1057Asp variant conformed to the Hardy-Weinberg equilibrium in both the case and control groups (P >.05). The Asp/Asp genotype of IRS2 gene Gly1057Asp polymorphism compared with Gly/Gly genotype was associated with a 2.1-fold increased risk for NAFLD after adjustment for confounding factors (P =.029; odds ratio = 2.10, 95% CI = 1.23-3.97). Conclusion Our findings revealed for the first time that the Gly1057Asp Asp/Asp genotype of the IRS2 gene is a marker of increased NAFLD susceptibility; however, studies in other populations are required to confirm the results. [ABSTRACT FROM AUTHOR]

Regarding the central role of insulin resistance in NAFLD, we explored whether insulin-like growth factor 1 (IGF1) and insulin-like growth factor-binding protein 3 (IGFBP3) gene variants were associated with NAFLD susceptibility. IGF1 (rs6214) and IGFBP3 (rs3110697) gene variants were genotyped in 154 cases with biopsy-proven NAFLD and 156 controls using PCR-RFLP method. The IGF1 rs6214 "AA + AG" genotype compared with the "GG" genotype appeared to be a marker of decreased NAFLD susceptibility (p =.006; OR = 0.47, 95%CI = 0.28–0.80). Furthermore, the IGF1 rs6214 "A" allele was underrepresented in the cases than controls (p =.024; OR = 0.61, 95%CI = 0.40–0.94). However, we observed no significant difference in genotype or allele frequencies between the cases and controls for IGFBP3 gene. To our knowledge, these findings suggest, for the first time, that the IGF1 rs6214 "A" allele and "AA + AG" genotype have protective effects for NAFLD susceptibility. Nonetheless, further studies are needed to validate our findings. [ABSTRACT FROM AUTHOR]

Objective Nonalcoholic fatty liver disease (NAFLD) is an emerging global chronic liver disease encompassing a wide spectrum of disorders ranging from simple steatosis to nonalcoholic steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Considering the strong association between NAFLD and insulin resistance, and the vital role of insulin-like growth factor 1 (IGF1) in IR, we hypothesized that IGF1 gene polymorphism might be associated with NAFLD. Methods A total of 302 subjects, including 149 patients with biopsy-proven NAFLD and 153 controls, were enrolled in this case-control study. All the subjects were genotyped for the rs5742612 polymorphism of the IGF1 gene using the polymerase chain reaction-restriction fragment length polymorphism method. Results The distribution of IGF1 rs5742612 genotypes and alleles differed significantly between the cases with NAFLD and controls. The IGF1 rs5742612 CC genotype compared with the TT genotype or the TT+TC genotype occurred more frequently in the cases than the controls and the differences remained significant after adjustment for confounding factors such as age and body mass index (P  = .011, OR = 2.71, 95%CI = 1.16-5.85; and P  = .032, OR = 2.29, 95% CI = 1.10-5.24, respectively). Conclusion For the first time, this study uncovered that the IGF1 rs5742612 CC genotype compared with the TT genotype or the TT+TC genotype had a 2.71-fold or 2.29-fold increased risk for NAFLD, respectively. [ABSTRACT FROM AUTHOR]

Ghrelin and its receptors are present in the stomach, suggesting that the ghrelin axis plays an essential role in gastrointestinal complications. This investigation aimed to explore the effects of H. pylori infection and gastritis on serum ghrelin and ghrelin axis gene expression. In this study, we enrolled 68 adult ambulatory people referred for upper gastrointestinal endoscopy. The individuals were classified into three groups based on H. pylori infection and gastritis. Total serum ghrelin and tissue gene expression were tested with ELISA and quantitative RT-PCR, respectively. Serum ghrelin and mRNA expression were significantly lower in H. pylori -positive with gastritis subjects compared with both H. pylori -negative with and without gastritis. Growth hormone secretagogue receptor1a mRNA expression was not different between groups while GHSR1b expression was significantly higher in patients with H. pylori infection and gastritis. We propose the ghrelin axis intermediaries, such as GHSR1b, as a potential clinical target for gastric disorders. • H. pylori cause gastritis and have been identified as a class 1 carcinogen. • The study of the ghrelin axis in subjects at risk of gastric cancer can be helpful. • Serum levels and gastric expression of ghrelin were reduced in H. pylori infection. • GHSR1b gastric expression was increased in H. pylori -positive subjects. [ABSTRACT FROM AUTHOR]

Background & Aims: Nonalcoholic fatty liver disease (NAFLD) is a growing problem and the commonest cause of chronic liver disease throughout the world. Given the strong association between NAFLD and insulin resistance and obesity, as well as the central role of ghrelin in these metabolic disorders, we explored whether ghrelin (GHRL) and ghrelin receptor (GHSR) gene polymorphisms were associated with susceptibility to NAFLD. Methods: In this case-control retrospective study which was conducted between April 2010 and July 2013, GHRL (rs696217 or Leu72Met) and GHSR (rs2922126) gene polymorphisms were genotyped in 153 cases with biopsy-proven NAFLD and 157 controls using the polymerase chain reaction - restriction fragment length polymorphism method. Results: The GHRL rs696217 "GT+TT" genotype or "GT" genotype compared with the "GG" genotype occurred less frequently in the patients with NAFLD than the controls and the differences remained significant after adjustment for confounding factors such as age and body mass index (p=0.018; OR=0.35, 95%CI: 0.14-0.84 and p=0.046; OR=0.40, 95%CI: 0.16-0.98, respectively). Furthermore, the GHRL rs696217 'T' allele compared with 'G' allele was significantly underrepresented in the cases (p=0.007; OR=0.33, 95%CI: 0.15-0.76). Nevertheless, no significant difference was found for GHSR rs2922126 gene polymorphism. Conclusions: Our findings suggested, for the first time, that the GHRL rs696217 or Leu72Met "GT+TT" genotype and "GT" genotype compared with "GG" genotype, as well as the "T" or Met72 allele compared with "G" or Leu72 allele had a protective effect for NAFLD susceptibility. However, other studies are required to confirm these findings. [ABSTRACT FROM AUTHOR]

Background: Vitamin D and insulin play an important role in susceptibility to polycystic ovary syndrome (PCOS), and therefore vitamin D receptor (VDR), parathyroid hormone (PTH), and insulin receptor (INSR) gene variants might be involved in the pathogenesis of PCOS. Objective: The present study was designed to investigate the possible associations between polymorphisms in VDR, PTH, and INSR genes and the risk of PCOS. Materials and Methods: VDR, PTH, and INSR gene variants were genotyped in 35 women with PCOS and 35 controls using Polymerase chain reaction - Restriction fragment length polymorphism method. Furthermore, serum levels of glucose and insulin were measured in all participants. Results: No significant differences were observed for the VDR FokI, VDR Tru9I, VDR TaqI, PTH DraII, INSR NsiI, and INSR PmlI gene polymorphisms between the women with PCOS and controls. However, after adjustment for confounding factors, the VDR BsmI "Bb" genotype and the VDR ApaI "Aa" genotype were significantly under transmitted to the patients (p= 0.016; OR= 0.250; 95% CI= 0.081-0.769, and p= 0.017; OR= 0.260; 95% CI= 0.086-0.788, respectively). Furthermore, in the women with PCOS, insulin levels were lower in the participants with the INSR NsiI "NN" genotype compared with those with the "Nn + nn" genotypes (P= 0.045). Conclusion: The results showed an association between the VDR gene BsmI and ApaI polymorphisms and PCOS risk. These data also indicated that the INSR "NN" genotype was a marker of decreased insulin in women with PCOS. Our findings, however, do not lend support to the hypothesis that PTH gene DraII variant plays a role in susceptibility to PCOS. [ABSTRACT FROM AUTHOR]

Aim: The purpose of the present study was to evaluate the number and proportion of various causes of upper gastrointestinal bleeding and actual numbers of non-NSAID, non-Helicobacter pylori (H.pylori) peptic ulcers seen in endoscopy of these patients. Background: The number and the proportion of patients with non- H.pylori, non-NSAIDs peptic ulcer disease leading to upper gastrointestinal bleeding is believed to be increasing after eradication therapy for H.pylori. Patients and methods: Medical records of patients referred to the emergency room of Taleghani hospital from 2010 with a clinical diagnosis of upper gastrointestinal bleeding (hematemesis, coffee ground vomiting and melena) were included in this study. Patients with hematochezia with evidence of a source of bleeding from upper gastrointestinal tract in endoscopy were also included in this study. Results: In this study, peptic ulcer disease (all kinds of ulcers) was seen in 61 patients which were about 44.85% of abnormalities seen on endoscopy of patients. Among these 61 ulcers, 44 were duodenal ulcer, 22 gastric ulcer (5 patients had the both duodenal and gastric ulcers). Multiple biopsies were taken and be sent to laboratory for Rapid Urease Test and pathological examination. About 65.53% of patients had ulcers associated with H.pylori, 9.83% had peptic ulcer disease associated with NSAIDs and 11.47% of patients had ulcers associated with both H.pylori and consumption of NSAIDs. 13.11% of patients had non-NSAIDs non- H.pylori peptic ulcer disease. Conclusion: The results of this study supports the results of other studies that suggest the incidence of H.pylori infection related with duodenal ulcer is common, and that non-H pylori and non-NSAIDs duodenal ulcer is also common. [ABSTRACT FROM AUTHOR]