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Post-transfusion purpura

From Wikipedia, the free encyclopedia

Purpura spots

Post-transfusion purpura (PTP) is a delayed adverse reaction to a blood transfusion or platelet transfusion that occurs when the body has produced alloantibodies to the allogeneic transfused platelets' antigens. These alloantibodies destroy the patient's platelets leading to thrombocytopenia, a rapid decline in platelet count.[1] PTP usually presents 5–12 days after transfusion, and is a potentially fatal condition in rare cases. Approximately 85% of cases occur in women.[2]

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Transcription

Mechanism

PTP is rare, but usually occurs in women who have had multiple pregnancies or in people who have undergone previous transfusions. The precise mechanism leading to PTP is unknown, but it most commonly occurs in individuals whose platelets lack the HPA-1a antigen (old name: PLA1). The patient develops antibodies to the HPA-1a antigen leading to platelet destruction. In some cases, HPA-5b has also been implicated. It is unclear why alloantibodies attack the patient's own, as well as any transfused allogeneic random donor platelets. Probable explanation for this is that the recipient's platelets acquire the phenotype of donor's platelet by binding of the soluble antigens from the donor onto the recipient's platelet.[3]

Treatment

Symptoms are usually sudden in onset and self-limiting, most often resolving within 2 weeks.[2] IVIG therapy is the primary treatment.[4] Additionally, PTP is an American Society for Apheresis Category III indication for plasmapheresis.[5][6]

See also

References

  1. ^ Washington University School of Medicine; Cooper, Daniel E.; J Krainik, Andrew; J Lubner, Sam; EL Reno, Hilary (2007), The Washington Manual of Medical Therapeutics (Spiral Manual Series), Lippincott Williams Wilkins, p. 519, ISBN 978-0-7817-8125-1{{citation}}: CS1 maint: multiple names: authors list (link)
  2. ^ a b Savage, William J. (June 2016). "Transfusion Reactions". Hematology/Oncology Clinics of North America. 30 (3): 619–634. doi:10.1016/j.hoc.2016.01.012. ISSN 1558-1977. PMID 27113000.
  3. ^ Gresele, Paolo; Page, Clive P.; Fuster, Valentin; Vermylen, Jos (2002), Platelets in Thrombotic and Non-thrombotic Disorders: Pathophysiology, Pharmacology and Therapeutics (1st ed.), Cambridge University Press, p. 551, ISBN 978-0-521-80261-1
  4. ^ Hillyer, Christopher D.; Hillyer, Krista; Strobl, Frank; Jefferies, Leigh C.; Silberstein, Leslie E. (2001), Handbook of Transfusion Medicine (1st ed.), Academic Press, p. 328, ISBN 978-0-12-348775-9
  5. ^ Schwartz, Joseph; Padmanabhan, Anand; Aqui, Nicole; Balogun, Rasheed A.; Connelly-Smith, Laura; Delaney, Meghan; Dunbar, Nancy M.; Witt, Volker; Wu, Yanyun (June 2016). "Guidelines on the Use of Therapeutic Apheresis in Clinical Practice-Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Seventh Special Issue". Journal of Clinical Apheresis. 31 (3): 149–162. doi:10.1002/jca.21470. ISSN 1098-1101. PMID 27322218.
  6. ^ Hoffbrand, A. V.; P.A.H. Moss; J.E. Pettit (2006). <i>Essential Haematology: 5th Edition</i>. Blackwell Publishing. ISBN 978-1-4051-3649-5.
This page was last edited on 19 May 2024, at 15:55
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