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Oral Contraceptives and Thromboembolic Disease

W. H.W. Inman, MB BChir; M. P. Vessey
JAMA. 1972;220(3):417. doi:10.1001/jama.1972.03200030074026.
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To the Editor.—  Drill and Calhoun make a number of criticisms of the paper by Inman et al.1 In that study, data for products containing ethinyl estradiol and those for products containing mestranol were analyzed separately, and a relationship between dose and thromboembolic risk was found for both estrogens individually. The fact that no statistically significant difference in risk could be demonstrated between products containing equal doses of the two estrogens, despite the belief that ethinyl estradiol is a more potent inhibitor of ovulation than mestranol, was not unexpected since comparisons between the two estrogens were based on very small numbers and an appreciable difference between them could easily have been missed. Apart from this, we see no reason why the potency of an estrogen as measured by its ability to inhibit ovulation should necessarily be correlated with its thrombogenicity. The statistical criticisms of the study by Inman et


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