Biomedical subjects

Nicolle M Gatto

Publications and source records attributed to Nicolle M Gatto.

3 recordsLinked to original sources

PubMed2005

Distributional interaction: Interpretational problems when using incidence odds ratios to assess interaction.

It is well known that the incidence odds ratio approximates the risk ratio when the disease of interest is rare, but increasingly overestimates the risk ratio as the disease becomes more common. However when assessing interaction, incidence odds ratios may not approximate risk ratios even when the disease is rare. We use the term "distributional interaction" to refer to interaction that appears when using incidence odds ratios that does not appear, or appears to a lesser degree, when using risk ratios. The interpretational problems that arise from this discrepancy can have important implications in epidemiologic research. Therefore, quantification of the relationship between the interaction odds ratio and the interaction risk ratio is warranted. In this paper, we provide a formula to quantify the differences between incidence odds ratios and risk ratios when they are used to estimate effect modification on a multiplicative scale. Using this formula, we examine the conditions under which these two estimates diverge. Furthermore, we expand this discussion to the implications of using incidence odds ratios to assess effect modification on an additive scale. Finally, we illustrate how distributional interaction arises and the problems that it causes using an example from the literature. Whenever the risk of the outcome variable is non-negligible, distributional interaction is possible. This is true even when the disease is rare (e.g., disease risk is less than 5%). Therefore, when assessing interaction on either an additive or multiplicative scale, caution should be taken in interpreting interaction estimates based on incidence odds ratios.

Journal Article↗

PubMed2004

Further development of the case-only design for assessing gene-environment interaction: evaluation of and adjustment for bias.

BACKGROUND: The case-only study for investigating gene-environment interactions provides increased statistical efficiency over case-control analyses. This design has been criticized for being susceptible to bias arising from non-independence between the genetic and environmental factors in the population. Given that independence is critical to the validity of case-only estimates of interaction, researchers frequently use controls to evaluate whether the independence assumption is tenable, as advised in the literature. Our work investigates to what extent this approach is appropriate and how non-independence can be accounted for in case-only analyses. METHODS: We provide a formula in epidemiological terms that illustrates the relationship between the gene-environment association measured among controls and the gene-environment association in the source population. Using this formula, we conducted sensitivity analyses to describe the circumstances in which controls can be used as proxy for the source population when evaluating gene-environment independence. Lastly, we generated hypothetical cohort data to examine whether multivariable modelling approaches can be used to control for non-independence. RESULTS: Our sensitivity analyses show that controls should not be used to evaluate gene-environment independence in the population, even when the baseline risk of disease is low (i.e. 1%), and the interaction and independent effects are moderate (i.e. risk ratio = 2). When the factors are associated, it is possible to remove bias arising from non-independence using standard statistical multivariable techniques in case-only analyses. CONCLUSIONS: Even when the disease risk is low, evaluation of gene-environment independence in controls does not provide a consistent test for bias in the case-only study. Given that control for non-independence is possible when the source of the non-independence can be conceptualized, the case-only design may still be a useful epidemiological tool for examining gene-environment interactions.

Bias↗

PubMed2003

Risk of perforation after colonoscopy and sigmoidoscopy: a population-based study.

BACKGROUND: Although the risk of bowel perforation is often cited as a major factor in the choice between colonoscopy and sigmoidoscopy for colorectal screening, good estimates of the absolute and relative risks of perforation are lacking. METHODS: We used a large population-based cohort that consisted of a random sample of 5% of Medicare beneficiaries living in regions of the United States covered by the Surveillance, Epidemiology, and End Results (SEER) Program registries to determine rates of perforation in people aged 65 years and older. We identified individuals who were cancer-free and had undergone colonoscopy or sigmoidoscopy between 1991 and 1998, calculated both the incidence and risk of perforation within 7 days of the procedure, and explored the impact on incidence and risk of perforation of age, race/ethnicity, sex, comorbidities, and indication for the procedure. We also estimated the risk of death after perforation. Risks were calculated with odds ratios (ORs) and 95% confidence intervals (CIs). All statistical tests were two-sided. RESULTS: There were 77 perforations after 39 286 colonoscopies (incidence = 1.96/1000 procedures) and 31 perforations after 35 298 sigmoidoscopies (incidence = 0.88/1000 procedures). After adjustment, the OR for perforation from colonoscopy relative to perforation from sigmoidoscopy was 1.8 (95% CI = 1.2 to 2.8). Risk of perforation from either procedure increased in association with increasing age (P(trend)<.001 for both procedures) and the presence of two or more comorbidities (P(trend)<.001 for colonoscopy and P(trend) =.03 for sigmoidoscopy). Compared with those who were endoscopied and did not have a perforation, the risk of death was statistically significantly increased for those who had a perforation after either colonoscopy (OR = 9.0, 95% CI = 3.0 to 27.3) or sigmoidoscopy (OR = 8.8, 95% CI = 1.6 to 48.5). The risk of perforation after colonoscopy, especially for screening procedures, declined during the 8-year study period. CONCLUSIONS: The risk of perforation after colonoscopy is approximately double that after sigmoidoscopy, but this difference appears to be decreasing. These observations should be useful to clinicians making screening and diagnostic decisions for individual patients and to policy officials setting guidelines for colorectal cancer screening programs.

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