In a study in the United States, Sweden, and Hungary, 335 cases of gastric bleeding without predisposing factors were compared with 670 control subjects, and 239 cases of duodenal bleeding were compared with 489 control subjects. For aspirin taken at least every other day during the week before the onset of bleeding (regular use), the relative risk of gastric bleeding was 4.4 (95% confidence interval [CI], 2.9 to 6.7); for occasional use, it was 3.3 (95% CI, 2.1 to 5.0). For ibuprofen, the corresponding estimates were 1.0 (95% CI, 0.4 to 2.6) and 1.1 (95% CI, 0.5 to 2.4). For naproxen, the estimate for regular use was 4.0 (95% CI, 1.5 to 11). The estimates for any use of piroxicam (crude estimate), indomethacin, and diclofenac during the week before onset were 18 (95% CI, 4.1 to 83), 1.6 (95% CI, 0.4 to 5.9), and 0.9 (95% CI, 0.2 to 4.2), respectively. The corresponding relative risks of duodenal bleeding were 7.1 (95% CI, 4.2 to 12) and 2.2 (95% CI, 1.3 to 3.7) for the regular and occasional use of aspirin, 2.4 (95% CI, 0.5 to 11) and 0.8 (95% CI, 0.3 to 2.0) for ibuprofen, 12 (95% CI, 2.8 to 54) and 9.9 (95% CI, 2.3 to 44) for naproxen, 17 (95% CI, 3.6 to 79) for any use of piroxicam (crude estimate), and 1.7 (95% CI, 0.2 to 14) for any use of indomethacin. There was a significant trend in the risk of gastric bleeding with increasing dose of regular aspirin use (p = 0.002). The relative risk estimates for the regular use of 325 mg or less were significantly elevated for both gastric and duodenal bleeding at 3.1 and 6.4, respectively.
Rheumatoid arthritis (RA) is a heterogeneous disease, consisting of distinct subsets with partly distinct aetiologies and risk factors. Such risk factors are environmental, including lifestyle mediated and genetic, and these factors must always be considered in the context of stochastic (i.e. chance) factors. As RA is a disease where immune reactions often precede symptoms, and where symptoms that do not involve joint inflammation such as joint pain, bone loss, and fatigue may precede arthritis, and where severe symptoms and comorbidities may follow after the first episode of joint inflammation, we also have to consider risk factors during these different phases of disease development. This chapter focuses on environmental, including lifestyle, factors, and on when and how during disease development such factors are active. The chapter also describes pathogenic mechanisms that may be triggered by such risk factors. Particular emphasis is on recognition of modifiable environmental/lifestyle factors as such knowledge can be used in primary as well as secondary prevention and also to improve effects of current pharmacological treatments.
BackgroundPrevious studies on the influence of exposure to organic solvents on multiple sclerosis (MS) risk have yielded inconclusive results. AimTo investigate the relationship between exposure to organic solvents and MS risk, and the potential interaction between organic solvents and MS HLA risk genes. MethodsWe analysed data from a Swedish population-based case-control study with incident cases of MS (2042 cases, 2947 controls). Subjects with different genotypes, smoking habits, and organic solvents exposure were compared with regard to occurrence of MS, by calculating odds ratios (OR) with 95% confidence intervals (CI) employing logistic regression. A potential interaction between exposure to organic solvents and the HLA MS risk genes was evaluated by calculating attributable proportion due to interaction (AP).ResultsOverall, exposure to organic solvents increased the risk of MS (OR 1.5, 95% CI: 1.2–1.8, p = 0.0004). A significant three way interaction between exposure to organic solvents, carriage of HLA-DRB1*15 and absence of HLA-A*02 was observed with regard to MS risk (AP 0.6, 95% CI: 0.3–0.8). Among HLA-DRB1*15 positive subject without the protective HLA-0*02 allele, there was also a significant interaction between organic solvents and smoking (AP 0.7, 95% CI: 0.4–1.0), whereas no significant interaction was observed among those with low genetic risk.Subjects exposed to smoking and organic solvents carrying HLA-DRB1*15 and lacking HLA-A*02 had a 30-fold increased risk of developing MS compared with non-exposed subjects without the genetic risk factors (OR 30.3, 95% CI: 11.7–78.3). ConclusionsAmong subjects with a genetic susceptibility, it seems like different sources of lung irritation contribute to the development of MS. We hypothesise that different sources of lung irritation may contribute to elicit an immune reaction against modified self-proteins or against potentially auto-aggressive cells resident in the lungs, and subsequently lead to MS in people with a genetic susceptibility to MS.
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