Diagnostic yield of routine duodenal biopsies in iron deficiency anaemia: a study from Western Anatolia.

OBJECTIVE: The role of routine endoscopic duodenal biopsies obtained during the evaluation of iron deficiency anaemia is being increasingly emphasized, but insufficiently applied. Diagnostic yield of this practice, mainly identification of coeliac disease, differs in different populations and geographic regions. The aim of this study is to assess the usefulness of routine duodenal biopsies during upper endoscopy in patients presenting with iron deficiency anaemia in Western Anatolia. METHODS: Routine duodenal biopsies were evaluated over a 12-month period in 100 consecutive adult patients with iron deficiency anaemia undergoing upper endoscopy. All potential bleeding lesions were identified and gastric as well as duodenal biopsies were taken for histopathologic investigation. RESULTS: A bleeding lesion is identified in 44% of cases. Duodenal biopsy gives an additional 5% diagnostic yield and revealed three patients with coeliac disease and two patients with giardiasis. One of the patients diagnosed with coeliac disease had a second bleeding lesion at the upper endoscopic examination. Appearance of the duodenal mucosa was normal in all patients including those with diagnostic duodenal biopsy. CONCLUSIONS: Routine duodenal sampling during the upper endoscopic examination gives an additional 5% diagnostic benefit and this practice should be included in the diagnostic work-up of patients with iron deficiency anaemia. As one of the patients who was found to have coeliac disease had a second bleeding lesion that may otherwise explain iron deficiency anaemia, finding a source for bleeding at the upper endoscopy should not preclude duodenal biopsy. Moreover, performing duodenal biopsy is still necessary even though the endoscopic appearance of the mucosa is normal. Aside from coeliac disease, Giardia infestation could be identified as a contributory factor for iron deficiency anaemia, in endemic regions.

Relationship between non-steroidal anti-inflammatory drug use and Helicobacter pylori infection in bleeding or uncomplicated peptic ulcers: A case-control study.

BACKGROUND AND AIMS: Non-steroidal anti-inflammatory drug (NSAID) use has been closely associated with an increased risk of bleeding peptic ulcers, while the prevalence of Helicobacter pylori infection has been reported to be lower in bleeding ulcers than in non-bleeding ones. However, whether an interaction exists between NSAID use and H. pylori infection has not clearly been elucidated yet. The aims of this study were to determine the frequency of NSAID use and H. pylori infection, to predict risk factors in bleeding peptic ulcers and to determine whether NSAID use and H. pylori infection interact with each other. METHODS: Ninety-six patients with bleeding ulcer were included in the study. The control group consisted of 106 patients with non-bleeding ulcer. Data were analyzed by using the chi-squared test, Fisher's exact test and logistic regression analysis with or without interaction term (H. pylori by NSAID). RESULTS: Non-steroidal anti-inflammatory drug use was significantly more common in patients with bleeding ulcers than in controls (79.2 vs 38.7%, unadjusted odds ratio (OR): 6.02, 95% confidence interval (CI): 3.21-11.29). The frequency of the H. pylori infection was significantly lower in patients with bleeding ulcers than in controls (66.7 vs 89.6%, unadjusted OR: 0.23, 95% CI: 0.10-0.49). In the logistic regression analysis with the interaction term, male sex (adjusted OR: 3.70, 95% CI: 1.65-8.29), multiplicity of ulcers (adjusted OR: 4.10, 95% CI: 1.02-16.45) and NSAID use (adjusted OR: 33.87, 95% CI: 4.36-262.97) were independent risk factors for bleeding ulcers. There was a negative interaction between H. pylori and NSAID use (adjusted OR: 0.09, 95% CI: 0.01-0.83). CONCLUSIONS: The negative interaction between the two variables suggests that the presence of H. pylori is associated with a lower risk of bleeding in ulcer patients taking NSAIDs.

The role of serum leptin levels in chronic hepatitis C with steatosis.

BACKGROUND/AIMS: Leptin has recently been suggested to play a role in the pathogenesis of hepatic steatosis and steatohepatitis in the absence of viral infection. The aim of this study was to evaluate whether leptin levels are associated with hepatic steatosis in chronic hepatitis C. METHODOLOGY: Thirty-one patients (22 female, 9 male, mean age: 51 +/- 9) with histologically proven chronic hepatitis C were included in this prospective, controlled, observational, clinical study with blind outcome assessment. Patients with and without steatosis in liver biopsy served as each others' controls. RESULTS: Chronic hepatitis C patients with (n=23) and without steatosis (n=8) were similar with respect to their serum glucose, lipid and leptin levels (p>0.05). Serum leptin levels were correlated with both patient factors, such as obesity and with liver enzymes, such as ALT, AST only in patients with steatosis. Chronic hepatitis C patients with or without steatosis had similar leptin levels of 6.3 +/- 2.5 and 4.9 +/- 2.5, respectively. CONCLUSION: Leptin levels were well correlated with antropometrical parameters in chronic hepatitis C patients. Leptin levels were associated with evidence of impaired hepatic function in patients with chronic HCV related steatosis. Serum leptin may be a prognostic marker for patients with chronic HCV infection with steatosis.

Effect of ursodeoxycholic acid on hepatic steatosis in rats.

Ursodeoxycholic acid (UDCA) has been shown to have hepatoprotective effects in various liver diseases. This drug has also been found to be effective in patients with nonalcoholic steatohepatitis, improving hepatic steatosis (HS) significantly. The aim of this study was to evaluate whether UDCA has an effect on both preventing and regressing HS in rats. To induce fatty liver, a choline-deficient diet (CDD) was used. For the rats assigned to receive UDCA, a 1.5% UDCA solution was administered at a dose of 25 mg/kg/day using an oral feeding tube. Assessment of HS was based on the quantification of percentage of hepatocytes containing lipid vacuoles. Forty-three male Wistar rats were randomly divided into two protocols. In protocol I, 7 rats were fed a standard diet (SD) plus UDCA for 30 days (control group). In protocol II, 19 rats were fed CDD and 17 rats were fed CDD plus UDCA for 30 days. At the end of this period, after performing liver biopsies, either SD or SD plus UDCA was started in both CDD-fed rats and CDD plus UDCA-fed rats for 30 days in a random order without the knowledge of the degrees of steatosis developed. At the end of this period, liver biopsies were repeated in order to evaluate whether UDCA has an effect on the regression of HS. In protocol I, there were no specific findings on the histological examination of the livers at 30 days. In protocol II, the percentage of HS in CDD plus UDCA-fed rats was significantly lower than CDD-fed rats at the end of the same period (percentage of steatosis, mean +/- SD: 12.2 +/- 29.6 to 23.2 +/- 34.1 respectively, P = 0.0201); after starting either SD or SD plus UDCA, steatosis was almost completely regressed at 30 days in all rats that developed that steatogenic changes. UDCA seems to prevent HS in rats; addition of UDCA to SD does not cause a further contribution in regressing HS.