Post-transfusion purpura: Difference between revisions
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'''Post-transfusion purpura''' ('''PTP''') is an adverse reaction to a [[blood transfusion]] or [[platelet transfusion]] that occurs when the body produces [[alloantibodies]] to the introduced [[blood platelet|platelets']] [[antigens]]. These alloantibodies destroy the patient's platelets leading to [[thrombocytopenia]], a rapid decline in platelet count.<ref>{{Citation|author=Washington University School of Medicine; Cooper, Daniel E.; J Krainik, Andrew; J Lubner, Sam; EL Reno, Hilary | authorlink= | title=The Washington Manual of Medical Therapeutics (Spiral Manual Series) | publisher=Lippincott Williams Wilkins | location= | isbn=978-0-7817-8125-1 | page=519}}</ref> PTP usually presents 5–12 days after transfusion, and is a potentially fatal condition. | '''Post-transfusion purpura''' ('''PTP''') is an adverse reaction to a [[blood transfusion]] or [[platelet transfusion]] that occurs when the body produces [[alloantibodies]] to the introduced [[blood platelet|platelets']] [[antigens]]. These alloantibodies destroy the patient's platelets leading to [[thrombocytopenia]], a rapid decline in platelet count.<ref>{{Citation|author=Washington University School of Medicine; Cooper, Daniel E.; J Krainik, Andrew; J Lubner, Sam; EL Reno, Hilary | authorlink= | title=The Washington Manual of Medical Therapeutics (Spiral Manual Series) | publisher=Lippincott Williams Wilkins | location= | isbn=978-0-7817-8125-1 | page=519}}</ref> PTP usually presents 5–12 days after transfusion, and is a potentially fatal condition. | ||
== | ==Historical Perspective== | ||
==Classification== | |||
==Pathophysiology== | |||
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: PL<sup>A1</sup>). 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 the introduced platelets. Probable explanation for this is that the recipient's platelet acquire the phenotype of donor's platelet by binding of the soluble antigens from the donor onto the recipient's platelet.<ref>{{citation | 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: PL<sup>A1</sup>). 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 the introduced platelets. Probable explanation for this is that the recipient's platelet acquire the phenotype of donor's platelet by binding of the soluble antigens from the donor onto the recipient's platelet.<ref>{{citation | ||
| last = Gresele | | last = Gresele | ||
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| isbn = 0-521-80261-X | | isbn = 0-521-80261-X | ||
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</ref> It is usually self-limiting, but [[IVIG]] therapy is the primary treatment.<ref>{{citation | </ref> | ||
==Causes== | |||
==Differentiating {{PAGENAME}} from Other Diseases== | |||
==Epidemiology and Demographics== | |||
==Risk Factors== | |||
==Screening== | |||
==Natural History, Complications, and Prognosis== | |||
===Natural History=== | |||
===Complications=== | |||
===Prognosis=== | |||
==Diagnosis== | |||
===Diagnostic Criteria=== | |||
===History and Symptoms=== | |||
===Physical Examination=== | |||
===Laboratory Findings=== | |||
===Imaging Findings=== | |||
===Other Diagnostic Studies=== | |||
==Treatment== | |||
===Medical Therapy=== | |||
It is usually self-limiting, but [[IVIG]] therapy is the primary treatment.<ref>{{citation | |||
| last = Hillyer | | last = Hillyer | ||
| first = Christopher D. | | first = Christopher D. | ||
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}} | }} | ||
</ref> [[Plasmapheresis]] is also an option for treatment.<ref>{{cite book |last= Hoffbrand |first= A. V. |author2=P.A.H. Moss |author3=J.E. Pettit |title= [[Essential Haematology: 5th Edition]] |publisher= [[Blackwell Publishing]] |year= 2006 |isbn= 1-4051-3649-9}}</ref> | </ref> [[Plasmapheresis]] is also an option for treatment.<ref>{{cite book |last= Hoffbrand |first= A. V. |author2=P.A.H. Moss |author3=J.E. Pettit |title= [[Essential Haematology: 5th Edition]] |publisher= [[Blackwell Publishing]] |year= 2006 |isbn= 1-4051-3649-9}}</ref> | ||
===Surgery=== | |||
===Prevention=== | |||
==See also== | ==See also== | ||
* [[Blood transfusion]] | * [[Blood transfusion]] | ||
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{{Reflist|2}} | {{Reflist|2}} | ||
[[Category: | [[Category:Hematology]] | ||
Latest revision as of 20:59, 23 June 2016
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Post-transfusion purpura (PTP) is an adverse reaction to a blood transfusion or platelet transfusion that occurs when the body produces alloantibodies to the introduced 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.
Historical Perspective
Classification
Pathophysiology
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 the introduced platelets. Probable explanation for this is that the recipient's platelet acquire the phenotype of donor's platelet by binding of the soluble antigens from the donor onto the recipient's platelet.[2]
Causes
Differentiating Post-transfusion purpura from Other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Natural History
Complications
Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
It is usually self-limiting, but IVIG therapy is the primary treatment.[3] Plasmapheresis is also an option for treatment.[4]
Surgery
Prevention
See also
References
- ↑ Washington University School of Medicine; Cooper, Daniel E.; J Krainik, Andrew; J Lubner, Sam; EL Reno, Hilary, The Washington Manual of Medical Therapeutics (Spiral Manual Series), Lippincott Williams Wilkins, p. 519, ISBN 978-0-7817-8125-1
- ↑ 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 0-521-80261-X
- ↑ 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 0-12-348775-7
- ↑ Hoffbrand, A. V.; P.A.H. Moss; J.E. Pettit (2006). Essential Haematology: 5th Edition. Blackwell Publishing. ISBN 1-4051-3649-9.