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[II型肝素诱导的血小板减少症:再次暴露于肝素]

[Heparin-induced thrombocytopenia type II: reexposure to heparin].

作者信息

Matthies B, Bürger T, Koch B, Böck M

机构信息

Klinik für Chirurgie, Universität Magdeburg.

出版信息

Dtsch Med Wochenschr. 1999 Oct 29;124(43):1267-70. doi: 10.1055/s-2007-1024530.

DOI:10.1055/s-2007-1024530
PMID:10587713
Abstract

HISTORY AND ADMISSION FINDINGS

At the age of 55 years a now 70-year-old man had his aortic valve replaced by a prosthetic (Björk-Shiley) valve, and 11 years later a VDD pacemaker had been implanted. 18 months before the latest admission he had been hospitalized for treatment of staphylococcal endocarditis involving the aortic prothesis. At that time thrombocytopenia developed during heparin administration, diagnosed clinically and with the heparin-induced platelet activity (HIPA) test as type II heparin induced thrombocytopenia. His latest admission was for the diagnosis and treatment of peripheral arterial disease of the right leg (Fontaine stage IIb).

INVESTIGATIONS

Right popliteal and pedal pulses were not palpable. He was able to walk pain-free for only 70 m. Doppler sonography demonstrated an arm-leg index on the right of 0.7. Angiography revealed marked stenosis in the right superficial femoral artery and a filiform stenosis in the right popliteal artery.

TREATMENT AND COURSE

Both stenoses were relieved by percutaneous transluminal balloon angioplasty, in the course of which 5000 IU heparin were administered as a bolus intraarterially. Postoperative anticoagulation was maintained for 2 days with recombinant hirudin. There was no evidence of platelet reduction or heparin-induced antibodies despite the renewed infusion of heparin.

CONCLUSION

Single re-administration of heparin in a patient who had developed a type II heparin-induced thrombocytopenia several years before does not necessarily lead to a booster of antibodies and thus to a reduction of platelets in the peripheral blood. It is a moot point whether the course in this case was an exception or the rule.

摘要

病史及入院检查结果

一名现年70岁的男性在55岁时接受了人工(Björk-Shiley)主动脉瓣置换术,11年后植入了VDD起搏器。在最近一次入院前18个月,他因涉及主动脉人工瓣膜的葡萄球菌性心内膜炎住院治疗。当时,在肝素治疗期间出现了血小板减少症,经临床诊断及肝素诱导的血小板活性(HIPA)试验诊断为II型肝素诱导的血小板减少症。他最近一次入院是为了诊断和治疗右腿外周动脉疾病(Fontaine IIb期)。

检查

右侧腘动脉和足背动脉搏动未触及。他仅能无痛行走70米。多普勒超声检查显示右侧手臂-腿部指数为0.7。血管造影显示右侧股浅动脉明显狭窄,右侧腘动脉呈丝状狭窄。

治疗及病程

通过经皮腔内球囊血管成形术缓解了两处狭窄,在此过程中动脉内推注了5000 IU肝素。术后用重组水蛭素进行了2天的抗凝治疗。尽管再次输注肝素,但没有血小板减少或肝素诱导抗体的证据。

结论

在数年前发生过II型肝素诱导的血小板减少症的患者中,单次重新给予肝素不一定会导致抗体增强,从而导致外周血中血小板减少。这种情况是例外还是普遍规律尚无定论。

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引用本文的文献

1
Heparin "hitts" again.肝素再次“出击”。
Eur J Clin Pharmacol. 2002 Feb;57(12):917-8. doi: 10.1007/s00228-001-0403-8.
2
Perspectives on the long term management of heparin-induced thrombocytopenia.肝素诱导的血小板减少症的长期管理展望
J Thromb Thrombolysis. 2000 Nov;10 Suppl 1:69-70. doi: 10.1023/a:1027337405002.