PubMed · 9106799
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R Bellocco, M Sturkenboom, M Pagano. 1997. Misclassification in case-control studies.. https://doi.org/10.1016/s0899-9007(96)00435-2
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Novel epidemiologic study designs are often required to assess gene-environment interaction. A design using only cases, without controls, is one of several approaches that have been proposed as more efficient alternatives to the typical random sampling of cases and controls. However, it has not been pointed out that a case-only analysis estimates a different interaction parameter than does a traditional case-control analysis: The latter typically estimates departure from multiplicative population odds or rate ratios, depending on the method of control selection, while the former estimates departure from multiplicative risk ratios if genotype and environmental exposure are not associated in the population. These parameters are approximately equal if the disease risk is small at all levels of the study variables. The authors quantify the impact of allowing for higher disease risk among gene carriers, a relevant situation when the gene under study is highly penetrant. Their findings show that the cross-product ratio computed from case-only data may be substantially smaller than the odds ratio computed from case-control data and may therefore underestimate either the population odds or the rate ratio. Thus, to avoid misinterpretation of interaction parameters estimated from case-only data, the definition of multiplicative interaction should be made explicit.
We sought to evaluate the potential interactions between systemic hypertension and blood lipids on the risk of myocardial infarction (MI). Recent evidence suggests that hypertension may interact with other risk factors such as dyslipidemia in the development of coronary heart disease. However, the precise nature of that interrelation remains unclear. We selected 340 cases of first MI and an equal number of age-, sex-, and community-matched controls. Data were collected on a large number of coronary risk factors, and fasting blood samples were obtained. Logistic regression was used to calculate the odds ratio (OR) of nonfatal MI. The age- and sex-adjusted OR of MI was 1.61 (95% confidence interval [CI] 1.15 to 2.25) among treated hypertensives compared with nonhypertensives. Further adjustment for coronary risk factors did not materially alter the results (OR 1.67, 95% CI 1.16 to 2.41). To explore the interrelations among hypertension, lipids, and risk of MI, each lipoprotein parameter was individually added to the risk factor-adjusted multivariate model. The apparent risk associated with hypertension was substantially attenuated by the addition of either high-density lipoprotein cholesterol (OR 1.25, 95% CI 0.82 to 1.90) or triglycerides (OR 1.37, 95% CI 0.91 to 2.05). No significant interactions were found between hypertension and any lipoprotein parameter. These data indicate that the risk of MI associated with treated hypertension may have a lipid mechanism involving high-density lipoprotein cholesterol and/or triglycerides.
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