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Nonsteroidal anti-inflammatory drugs use and risk of Parkinson disease: A dose-response meta-analysis.

ABSTRACT: Previous studies have indicated that nonsteroidal anti-inflammatory drugs (NSAIDs) use is associated with Parkinson disease risk, but presented controversial results.Medline, Embase, Web of Science, and the Cochrane Database were searched update to November 2017. Key data were extracted from eligible studies. A dose-response meta-analysis was conducted for synthesizing data from eligible studies.Fifteen eligible studies were included in this meta-analysis. NSAIDs use was not associated with Parkinson disease risk [relevant risk (RR): 0.06; 95% confidence interval (95% CI), 0.91-1.02]. Subgroup analysis showed that aspirin use (RR: 1.14; 95% CI, 0.98-1.30) or ibuprofen use (RR: 1.01; 95% CI, 0.88-1.17) was not associated with Parkinson disease risk; however, the use of non-aspirin NSAIDs was significantly associated with Parkinson disease risk (RR:0.91; 95% CI, 0.84-0.99). Furthermore, NSAIDs use was not associated with the risk of Parkinson disease in female (RR: 0.99; 95% CI, 0.83-1.17) and male (RR: 1.01; 95% CI, 0.88-1.16). In addition, a dose-response showed per 1 number of prescription incremental increase in NSAIDs use was not associated with the risk of Parkinson disease (RR: 0.96; 95% CI, 0.91-1.02), per 1 year of duration of NSAIDs use incremental increase was not associated with the risk of Parkinson disease (RR: 0.98; 95% CI, 0.92-1.03), and per 1 dosage of NSAIDs use incremental increase was not associated with the risk of Parkinson disease (RR: 0.98; 95% CI, 0.95-1.02).NSAIDs use was not associated with the risk of Parkinson disease. The potency and the cumulative NSAIDs use did not play critical roles.

SUBMITTER: Ren L

PROVIDER: S-EPMC6155958 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background & aimsNonsteroidal anti-inflammatory drugs (NSAIDs) have been suggested to protect against esophageal adenocarcinoma (EAC). This study examined the effect of NSAIDs on the risk of developing Barrett's esophagus (BE), the precursor lesion to EAC.MethodsWe conducted a case-control study among eligible patients scheduled for either elective esophagogastroduodenoscopy (EGD) or recruited from primary care clinics to undergo a study EGD. We compared 323 patients with BE (296 nondysplastic and 27 dysplastic) with 2 separate control groups: 1347 patients from the elective EGD group (endoscopy controls) and 502 patients from the primary care group (primary care controls) with no endoscopic or histopathologic BE. Use of aspirin products and 23 nonaspirin NSAIDs was ascertained from detailed, self-reported questionnaires. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariable logistic regression models.ResultsThere were no significant differences in self-reported NSAID use between all BE cases and all controls (58.2% vs 54.6%; P = .33); this was seen for aspirin products (43.0% vs 37.4%; P = .08) and nonaspirin NSAIDs (7.7% vs 8.9%; P = .46). These findings persisted in the multivariable model for any NSAIDs (adjusted OR, 0.89; 95% CI, 0.75-1.28), aspirin (adjusted OR, 1.16; 95% CI, 0.90-1.51), and nonaspirin NSAIDs (adjusted OR, 0.88; 95% CI, 0.55-1.39). Use of a combination of aspirin and nonaspirin NSAIDs was reported in 7.4% of cases and 8.3% of controls, and a nonsignificant inverse association with BE was seen (adjusted OR, 0.70; 95% CI, 0.44-1.11). There was no significant association between BE and daily NSAID use (adjusted OR, 1.03; 95% CI, 0.78-1.37). Similar findings were observed for comparisons involving nondysplastic or dysplastic BE cases, and endoscopy or primary care control groups separately or combined.ConclusionsThe use of NSAIDs was not associated with a reduced risk of BE. It is likely that the protective mechanism of NSAIDs on EAC occurs subsequent to the development of BE.

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Nonsteroidal anti-inflammatory drugs use and risk of Parkinson disease: A dose-response meta-analysis.

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