In this population-based, case-control study of postmenopausal women including 726 incident ischemic strokes, 213 incident hemorrhagic strokes, and 2525 controls, current use of estrogen with or without progestin, assessed from computerized pharmacy data, was not associated with ischemic stroke or hemorrhagic stroke overall. However, Lemaitre et al observed 2-fold higher risks of ischemic stroke and hemorrhagic stroke during the first 6 months of hormone use (ischemic stroke: odds ratio, 2.16 [95% confidence interval, 1.04-4.49]; hemorrhagic stroke: odds ratio, 2.20 [95% confidence interval, 0.83-5.81]). Risk of ischemic stroke also increased with estrogen dose (P = .03). The transitory increase in risk of stroke associated with initiation of hormone replacement therapy merits further investigation.
To assess whether prolonging warfarin prophylaxis beyond the hospital stay improves the outcome of patients who underwent hip arthroplasty, 360 patients who had received warfarin prophylaxis after total hip replacement were randomized to stop the drug treatment at the time of hospital discharge or to continue it for 4 more weeks. Extending thromboprophylaxis considerably reduced the incidence of late venous thromboembolic complications without enhancing the hemorrhagic risk.
The hemodynamic abnormalities that can cause pulmonary arterial hypertension are increased pulmonary vascular resistance, pulmonary venous pressure and pulmonary blood flow, or a combination of these hemodynamic abnormalities.
Highly active antiretroviral treatment (HAART) has markedly reduced morbidity and mortality attributable to human immunodeficiency virus (HIV) type 1 infection. However, when, in the natural course of HIV infection, to initiate treatment to produce optimal clinical benefit remains undefined. In addition, these regimens have significant adverse effects and are expensive. In this analysis of 1054 women enrolled in a cohort study and followed for up to 5 years, those initiating HAART with CD4+ cell counts of 200 to 350/µL did not have faster progression to clinical disease than those initiating with CD4+ cell counts greater than 350/µL. However, individuals initiating treatment with CD4+ cell counts less than 200/µL had significantly higher rates of poor outcomes, even after adjustment for lead time bias. These results support current guidelines that treatment may be delayed until the CD4+ cell count is less than 350/µL, but should be started before the CD4+ cell count reaches 200/µL.
Kaplan-Meier estimates of percentages remaining free of acquired immunodeficiency syndrome (AIDS) among participants AIDS free at initiation of HAART, by CD4+ cell count and HIV type 1 RNA at initiation. RH indicates relative hazard; CI, confidence interval.
In This Issue of Archives of Internal Medicine. Arch Intern Med. 2002;162(17):1924. doi:10.1001/archinte.162.17.1924