Persistent erythema with niacin is not attributable to aspirin resistance
详细信息    查看全文
文摘

Background

Niacin is suboptimally used in patients because it causes flushing and erythema. These side effects have been attributed to release of the vasodilating prostaglandin D2, generated in a reaction catalyzed by cyclooxygenase-1. Aspirin reduces but does not completely eliminate these side effects. Because some patients are resistant to its antiplatelet effects, we hypothesized that patients with persistent niacin-induced erythema might be aspirin resistant.

Methods

Platelet function studies (via the use of a whole-blood platelet function aggregometer [VerifyNow; Accumetrics, San Diego, CA] with end points of aspirin reaction unit [ARUs] and P2Y12 reaction units [PRUs]) were performed on 32 healthy, drug-free subjects before and after 324 mg of aspirin. A niacin skin test with the use of topical methylnicotinate was also performed before and after the administration of aspirin. Reponses to methyl nicotinate were assessed by a reaction score and by counting the time to first visible redness (TTR).

Results

All subjects had an expected decrease in arachidonic acid induced platelet response (ARU 642.8 ± 47.20 before to 431.5 ± 41.1 after aspirin, P < .0001) without a significant change in the PRU. The reaction score and TTR were prolonged by aspirin at methylnicotinate concentrations ≥0.001 M. Although no subject had aspirin resistance (defined as ARU >550), there was considerable variability in skin responses with erythema elicited in all subjects at the greatest concentrations. There was no difference in the ARU for subjects with TTR values above and below the mean, indicating that aspirin resistance does not explain the variation in skin responses to a topical niacin derivative.

Conclusion

Aspirin resistance is unlikely to be a significant contributor to the persistent erythema and flushing in niacin-treated patients.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700