Background and aims Curcumin has anti‐inflammatory properties. The aim of this study was to evaluate the effect of curcumin on improvement of the disease activity in ulcerative colitis (UC). Methods In this randomized double‐blind clinical trial, 70 patients with mild‐to‐moderate UC were randomly assigned to curcumin (1,500 mg/day) or placebo intake for 8 weeks. Disease clinical activity, quality of life, serum levels of tumor necrosis factor alpha (TNF‐α), high‐sensitivity C‐reactive protein (hs‐CRP), erythrocyte sedimentation rate (ESR) values, and complete blood count were measured. Results Changes in Simple Clinical Colitis Activity Index score were significantly higher in the curcumin than the placebo group (–5.9 ± 2.08 vs. –2.1 ± 2.6; p = .001). The scores of Inflammatory Bowel Disease Questionnaire‐9 and quality of life were significantly higher in the intervention group compared to the control group (p = .006). Furthermore, the curcumin supplementation reduced the serum hs‐CRP concentration (–6.3 ± 13.6 vs. 3.7 ± 11.6 μg/ml; p = .01) and ESR levels significantly (–1.6 ± 2.7 vs. –0.09 ± 2.4 mm/hr; p = .02) in comparison with the control group. No significant changes were observed in the TNF‐α levels of both groups. Conclusions Consumption of the curcumin supplement, along with drug therapy, is associated with significant improvement of the clinical outcomes, quality of life, hs‐CRP, and ESR in patients with mild‐to‐moderate UC.

sonographic findings and elevated serum transaminases randomly divided into 2 groups. The intervention group (A) treated with L-Carnitine 750mg TDS while the control group (B) received placebo. After 3 months intervention the level of liver transaminases and sonographic degree of fatty liver compared between 2 groups. RESULT: After three months of intervention, in group A the level of AST decreased from 122.7 ± 13.6 to 96.3 ± 7 while in group B raised from 125 ± 14 to 126 ± 11 (p < 0.001). The level of ALT in group A declined from 124.5 ± 11.3 to 82.1 ± 5.2 and in placebo group decreased from 120 ± 10.8 to 115.1 ± 6.3 (p < 0.001) In comparison of average level of AST and ALT between 2 groups, we found a meaningful decline in the serum level of liver transaminases in group A (p < 0.001) while there were no significant reduction in serum level of Cholesterol, TG and FBS (p > 0.05) and also the sonographic degree of fatty liver didn't change among 2 groups. CONCLUSION: It seems that L-Carnitine is effective in treatment of NAFLD among diabetic patients and could be a potential therapeutic approach in such patients. We recommend these findings to further be verified in future studies (www.irct.ir: IRCT2014020316348N2).

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We conclude that the prevalence of celiac disease is high in patients with ISS and it is important to test all children with ISS for celiac disease by measuring serologic markers and performing an intestinal biopsy.

Background The aim of this study was to evaluate the antimicrobial resistance and genetic basis for metronidazole (Mtz) and clarithromycin (Cla) resistance in strains of Helicobacter pylori , isolated from patients with gastroduodenal disorders. Patients and methods A total of 157 H . pylori isolates (from 22 gastric cancer, 38 peptic ulcer disease, and 97 non-ulcer dyspepsia patients) were analyzed for drug susceptibility to Mtz and Cla, by gradient diffusion test (E-test, MAST). The PCR and sequence analysis of the rdxA and frxA for Mtz-resistant strains and the 23S rRNA for Cla-resistant strains were used to determine the genetic basis of drug resistance in H. pylori strains. Increased expression of TolC homologous genes ( hefA ) that upregulates efflux pump activity was determined in multidrug-resistant (MDR) strain of H. pylori by real-time PCR technique. Results Among 157 H . pylori isolates, 32 (20.4%) strains were resistant to at least one of the antimicrobial agents. The highest resistance rate was attributed to Mtz (n=69, 43.94%). Among the resistant strains of H. pylori , 15 cases (9.55%) were detected as MDR. Mutations in the rdxA (85.5%) and A2143G point mutations (63.1%) in the 23S rRNA were the most common cause of resistance to Mtz and Cla in strains of H. pylori , respectively. In MDR strains, the rdxA mutation and A2143G-point mutation in the 23S rRNA were the most abundant mutations responsible for drug resistance. The relative expression of hefA in MDR strains (mean 3.706) was higher than the susceptible strains (mean 1.07). Conclusion Mutational inactivation and efflux pump overexpression are two mechanisms that increase the resistance to H. pylori antimicrobial agents and the rate of MDR strains. In Iran, the mutations of rdxA and frxA in Mtz-resistant strains and A2143G and A2142G of the 23S rRNA in Cla-resistant strains were significant. The screening for these mutations could help to prevent antibiotic resistance, and to determine the most effective anti- H. pylori drugs.