+NO 3 in serum and urine in patients with type 1 diabetes, as identified by linear regression models. The present study concludes that NO metabolism is impaired by type 1 diabetes and diabetic nephropathy.

Chronic hyperglycemia leads to DNA damage in diabetes and might be associated with nitrosative stress. In this study, we aimed at assessing the level of DNA strand breaks in leukocytes, serum nitrite, and nitrate in patients with type 1 diabetes and healthy controls and associations of these parameters with diabetes-related outcomes in a prospective study. The level of DNA damage was determined in 71 patients with type 1 diabetes and 57 healthy controls by comet assay, and scored with arbitrary units (AU). The chemiluminescence method was used to measure nitrite and nitrate. Clinical information and data on consumption of alcohol, physical activity and smoking were collected. Progression of complications in patients with diabetes was assessed after a follow-up time of 4-5 years. We observed a higher level of DNA damage in leukocytes of patients with type 1 diabetes compared to healthy subjects (type 1 diabetes AU 50 (36-74.5); control AU 30 (24.1-43), p<0.001). According to regression analysis type 1 diabetes leads to a two-fold increase in DNA damage. In the group of type 1 diabetes, DNA damage correlated positively with total cholesterol R=0.262, p=0.028; and negatively with serum glucose level R=-0.284; p=0.018 and serum nitrite R=-0.335; p=0.008. DNA damage was not significantly associated with HbA1c, diabetes duration, complications, and lifestyle factors. However, DNA damage above 57 AU was associated with statistically significantly lower serum nitrite and 1.52 higher risk of progression of complications of diabetes over the follow-up period. The latter result was not statistically significant due to insufficient study power (relative risk 1.52 (95% CI 0.68, 3.42, p=0.31). Our results confirm that type 1 diabetes is associated with a higher level of DNA strand breaks in leukocytes as compared to the reference group and demonstrate the negative association between DNA damage and serum nitrite concentration.

Background and Aims: Studies suggest that the prevalence of celiac disease (CD) is increased in individuals with functional gastrointestinal disorders (FGIDs), in particular, irritable bowel syndrome (IBS); however, the evidence is conflicting. We aimed to analyze the prevalence of CD in patients with FGIDs in Latvia. Methods: This retrospective study included patients with FGIDs, referred for a gastroenterologist consultation in a secondary gastroenterology practice unit. Patients were divided into three groups – patients only with IBS (IBS group), patients only with functional dyspepsia (FD) (FD group), patients with mixed symptoms IBS and FD (Mixed group). Patient levels of tissue transglutaminase IgA (tTG-IgA) and/or antiendomysial IgA group antibodies (EMA-IgA) were evaluated. Four duodenal biopsies were obtained and reported according to Marsh classification. Patients diagnosed or being referred for confirmation of CD were excluded from the study. Results: Overall, 1,833 FGIDs patients were enrolled. Celiac serology was available for 1,570 patients, duodenal histology for 582 patients, both histology and serology for 319 patients. In total, celiac seropositivity was present in 1.78% (28/1570) (3.18% in IBS group, 0.90% in FD group and 1.11% of cases in the mixed group). Fifteen patients had histopathological changes (2.58%; 15/582). Three IBS patients (2.36%) were both serology and biopsy positive. None of the FD patients had CD. Conclusion: Prevalence of biopsy-proven CD in patients from Latvia with FGIDs was low. Routine screening for CD could be considered only among patients with IBS.

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