PubMed · 14900351
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1952. COMMUNITY requirements for developing heart programs.. https://pubmed.ncbi.nlm.nih.gov/14900351/
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In many ways, adjustment for publication bias in meta-analysis parallels adjustment for ascertainment bias in genetic studies. We investigate a previously published simulation-based method for dealing with complex ascertainment bias and show that it can be modified for use in meta-analysis when publication bias is suspected. The method involves simulating sets of pseudo-data under the assumed model using guesses for the unknown parameters. The pseudo-data are subjected to the same selection criteria as are believed to have operated on the original data. A conditional likelihood is then used to estimate the adjusted values of the unknown parameters. This method is used to re-analyse a published meta-analysis of the effect of the MTHFR gene on homocysteine levels. Simulation studies show that the pseudo-data method is unbiased; they give an indication of the number of pseudo-data values required and suggest that a two-stage adjustment produces less variable estimates. This method can be thought of as an example of the selection model approach to publication bias correction. As the selection mechanism must be assumed, it is important to investigate the sensitivity of any conclusions to this assumption.
Randomised clinical trials and observational studies have shown an increased risk of myocardial infarction, stroke, hypertension and heart failure during treatment with cyclooxygenase inhibitors. Adverse cardiovascular effects occurred mainly, but not exclusively, in patients with concomitant risk factors. Cyclooxygenase inhibitors cause complex changes in renal, vascular and cardiac prostanoid profiles thereby increasing vascular resistance and fluid retention. The incidence of cardiovascular adverse events tends to increase with the daily dose and total exposure time. A comparison of individual selective and unselective cyclooxygenase inhibitors suggests substance-specific differences, which may depend on differences in pharmacokinetic parameters or inhibitory potency and may be contributed by prostaglandin-independent effects. Diagnostic markers such as N-terminal pro brain natriuretic peptide (NT-proBNP) or high-sensitive C-reactive protein might help in the early identification of patients at risk, thus avoiding the occurrence of serious cardiovascular toxicity.
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