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עמוד בית
Sun, 19.05.24

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October 2006
M. Shtalrid, L. Shvidel, E. Vorst, E.E. Weinmann, A. Berrebi and E. Sigler
 Background: Post-transfusion purpura is a rare syndrome characterized by severe thrombocytopenia and bleeding caused by alloimunization to human platelet specific antigens following a blood component transfusion. The suggested incidence is 1:50,000–100,000 transfusions, most often occurring in multiparous women. The diagnosis is not easy because these patients, who are often critically ill or post-surgery, have alternative explanations for thrombocytopenia such as infection, drugs, etc.

Objectives: To describe patients with initially misdiagnosed PTP[1] and to emphasize the diagnostic pitfalls of this disorder.

Patients and Results: During a period of 11 years we have diagnosed six patients with PTP, four women and two men. The incidence of PTP was approximately 1:24,000 blood components transfused. We present the detailed clinical course of three of the six patients in whom the diagnosis was particularly challenging. The patients were initially misdiagnosed as having heparin-induced thrombocytopenia, systemic lupus erythematosus complicated by autoimmune thrombocytopenia, and disseminated intravascular coagulation. A history of recent blood transfusion raised the suspicion of PTP and the diagnosis was confirmed by appropriate laboratory workup.

Conclusions: PTP seems to be more frequent than previously described. The diagnosis should be considered in the evaluation of life threatening thrombocytopenia in both men and women with a recent history of blood transfusion.


 





[1] PTP = post-transfusion purpura


November 2002
June 2002
Nurit Rosenberg, PhD, Ariella Zivelin, PhD, Angela Chetrit, PhD, Rima Dardik, PhD, Nurit Kornbrot, MSc, Dov Freimark, MD and Aida Inbal, MD

Background: Platelet adhesion and aggregation are mediated by specific platelet membrane glycoproteins GPIa/IIa, GPIba, and GPIIb/IIIa, and are essential steps in thrombus formation and development of acute myocardial infarction.

Objective: To evaluate the risks exerted by each of the following polymorphisms: HPA-1a/b in GPIIIa; 807C/T in GPIa; and HPA-2a/b, VNTR and Kozak C/T in GPIba in young males with AMI[1]..

Methods: We conducted a case-control study of 100 young males with first AMI before the age of 53 and 119 healthy controls of similar age. All subjects were tested for the above polymorphisms.

Results: The allele frequencies of each of the platelet polymorphism were not significantly different between the young men with AMI and the controls. Smoking alone was associated with a 9.97-fold risk, and the presence of at least one metabolic risk factor resulted in a 2.57-fold risk of AMI.

Conclusion: These results indicate that platelet glycoproteins polymorphisms are not an independent risk factor for AMI.






[1] AMI = acute myocardial infarction


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