Lyme disease.

Lyme disease is the most common tick-borne disease in the United States, and the number of reported cases has increased steadily since 1992. Coinfection of ticks with Borrelia burgdorferi and Ehrlichia phagocytophila did not appear to affect the transmission of the other agent. Serologic evidence of exposure to Babesia microti did not significantly impact the clinical course of Lyme disease. Two clinical studies indicated that the long-term outcome of Lyme disease is good. Results are pending of chronic Lyme disease studies funded by the US National Institutes of Health. A better understanding of the pathogenesis of Lyme disease provided clues about possible mechanisms for persistent symptoms. Use of the current method of diagnosis by the two-step approach has proven to be reliable, but new methods are under investigation. Treatment guidelines were published recently. OspA vaccination of children aged 2 to 5 years was shown to be safe and immunogenic.

Comparison of the effects of ketoprofen on platelet function in the presence and absence of aspirin.

PURPOSE: Although aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) exert inhibitory effects on platelets in vitro and in vivo, there are insufficient data to substantiate the use of NSAIDs alone as antiplatelet drugs in patients already taking aspirin. We therefore sought to determine whether aspirin, added to NSAID therapy, further suppresses platelet function. SUBJECTS AND METHODS: We enrolled 25 healthy adult volunteers who were administered ketoprofen (extended-release capsules, 200 mg daily) for 1 week, followed by ketoprofen (200 mg daily) and aspirin (325 mg daily) or ketoprofen (200 mg daily) alone during the second week. Platelet aggregation, stimulated by epinephrine and arachidonic acid, and cyclooxygenase activity, measured by thromboxane B(2), were measured at baseline, on day 8, and on day 15. RESULTS: On day 8, all subjects demonstrated abnormal platelet aggregation (>50% inhibition), which persisted at day 15 in both the aspirin and no aspirin groups. One week of ketoprofen treatment reduced thromboxane B(2) levels by 84% in the aspirin group and by 85% in the no aspirin group (P = 0.8), without any further inhibition measured on day 15. CONCLUSION: Extended-release ketoprofen significantly inhibited platelet aggregation and thromboxane B(2) production in healthy volunteers. Addition of aspirin had no additional effect. Trials are warranted to determine whether these in vitro effects result in clinical antiplatelet activity in patients who require chronic treatment with NSAIDs, thereby avoiding the toxicity of NSAID/aspirin combination therapy.