Background & AimsDiet contributes to colorectal cancer development and may be potentially modified. We wanted to identify the biological mechanisms underlying colorectal carcinogenesis by assessment of diet-gene interactions.MethodsThe polymorphisms IL10 C-592A (rs1800872), C-rs3024505-T, IL1b C-3737T (rs4848306), G-1464C (rs1143623), T-31C (rs1143627) and PTGS2 (encoding COX-2) A-1195G (rs689466), G-765C (rs20417), and T8473C (rs5275) were assessed in relation to risk of colorectal cancer (CRC) and interaction with diet (red meat, fish, fibre, cereals, fruit and vegetables) and lifestyle (non-steroid-anti-inflammatory drug use and smoking status) was assessed in a nested case-cohort study of nine hundred and seventy CRC cases and 1789 randomly selected participants from a prospective study of 57,053 persons.Results IL1b C-3737T, G-1464C and PTGS2 T8473C variant genotypes were associated with risk of CRC compared to the homozygous wildtype genotype (IRR=0.81, 95%CI: 0.68-0.97, p=0.02, and IRR=1.22, 95%CI: 1.04-1.44, p=0.02, IRR=0.75, 95%CI: 0.57-0.99, p=0.04, respectively). Interactions were found between diet and IL10 rs3024505 (P-value for interaction (Pint); meat=0.04, fish=0.007, fibre=0.0008, vegetables=0.0005), C-592A (Pint; fibre=0.025), IL1b C-3737T (Pint; vegetables=0.030, NSAID use=0.040) and PTGS2 genotypes G-765C (Pint; meat=0.006, fibre=0.0003, fruit 0.004), and T8473C (Pint; meat 0.049, fruit=0.03) and A-1195G (Pint; meat 0.038, fibre 0.040, fruit=0.059, vegetables=0.025, and current smoking=0.046).ConclusionsGenetically determined low COX-2 and high IL-1β activity were associated with increased risk of CRC in this northern Caucasian cohort. Furthermore, interactions were found between IL10, IL1b, and PTGS2 and diet and lifestyle factors in relation to CRC. The present study demonstrates that gene-environment interactions may identify genes and environmental factors involved in colorectal carcinogenesis.

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This study gives insight into health-related quality of life and objective findings in persons with chronic rhinosinusitis recruited from the general population.

These findings support the hypothesis that hospital accreditation leads to improvements in patient care.

BackgroundHealth-related quality of life (HRQoL) is known to be impaired in patients who develop post-thrombotic syndrome (PTS) following deep vein thrombosis (DVT). However, there is limited knowledge of the long-term HRQoL after DVT compared to controls without DVT. The objectives of this study were to evaluate long-term HRQoL following DVT and to compare that with age and sex matched control group and to population norms as well as to investigate possible predictors for reduced HRQoL.MethodsHRQoL was evaluated in 254 patients with confirmed DVT using the generic EQ-5D and the diseases specific VEINES-QOL/Sym questionnaire, whereas PTS was assessed by the Villalta scale. Patients were asked to give the EQ-5D questionnaire to two friends of same age- (±5 years) and sex (buddy controls).ResultsPatients scored significantly lower on all dimensions of EQ-5D compared to controls. EQ-5D index value was lower in patients compared with buddy controls; mean 0.79 (SD 0.17; IQR 0.72–1.00) versus 0.9 (SD 0.12; IQR 0.80–1.00), p < 0.001. EQ-5D index value was also significantly lower than age- and sex-adjusted population norms (p < 0.001). PTS and obesity (BMI >30/m2) were significantly associated with impaired HRQoL assessed by EQ-5D index value (odds ratio [OR] 11.0: 95 % confidence interval [CI] 4.6–29.7; and 2.3: 95 % CI 1.1–4.8, respectively) and VEINES-QOL (OR 28.2: 95 % CI 10.6–75.0; and OR 4.1: 95 % CI 1.7–9.7, respectively).ConclusionLong-term HRQoL was significantly impaired in DVT patients compared with buddy controls and population norms. PTS and obesity were independently associated with impaired HRQoL.