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Using the results of an analysis of available scientific evidence and a survey of current practice in Canada, as well as expert opinion, these guidelines attempt to consider current partner notification practice in Canada and recommend an approach to determining practice which is flexible enough to address local circumstances. Priority areas for future research were also identified.

To estimate the rate of underreporting of AIDS (acquired immune deficiency syndrome) to the Federal Centre for AIDS (FCA), in 1988 the initials, date of birth and place of residence of 66 patients with AIDS known to the Toronto Sexual Contact Study (TSCS), 65 patients with AIDS known to the Vancouver Lymphadenopathy-AIDS Study (VLAS) and other participants in both studies who did not have AIDS were sent to the Bureau of Epidemiology and Surveillance, FCA. The FCA conducted a manual record linkage to link these data to the national registry of reported cases. The rate of underreporting was 12% (8/65) for the VLAS and 18% (12/66) for the TSCS. The specific diagnosis was not related to the rate of underreporting. For the TSCS the rate of underreporting had increased from 0% in 1983-84 to 44% in 1987-88 (p = 0.001). Differences in the observed rates of underreporting between the two studies are likely the result of differences in the reporting responsibilities of physicians involved in the studies.

Recent epidemiologic studies report a significant association between alcohol consumption and elevations in both systolic (SBP) and diastolic (DBP) blood pressures. To test this hypothesis, we conducted a multivariate analysis of physical examination and other data on 721 men and 697 women aged 20 or more collected during the Canada Health Survey in 1978-1979. SBP and DBP were considered as separate dependent variables in multiple regression models with the following independent variables: age, alcohol consumption (measured as a 7-day recall history and as an average frequency of consumption), serum cholesterol, plasma glucose, physical activity, Quetelet index, parental history of hypertension, cigarette consumption, income, education, and exogenous hormonal use in women. In both weighted and unweighted multiple regression analyses, we could not demonstrate for either sex, a significant association between alcohol consumption (as recorded and following quadratic and logarithmic transformations) and either SBP or DBP. For both sexes, only age and Quetelet index were highly significantly (P less than 0.0001) and consistently associated with both SBP and DBP. No other independent variables were consistently associated, for either sex, with SBP and DBP. Further, the dose-response patterns noted by other investigators suggesting either a positive and linear relationship or a curvilinear relationship were not found in either our univariate or multivariate analyses. Rather, the alcohol-blood pressure curves showed no consistent patterns of any kind in either sex. These findings do not support recent claims that alcohol consumption is a determinant of elevations in either SBP or DBP.