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Prevention of relapse in patients with acquired thrombotic thrombocytopenic purpura undergoing elective surgery: a case series.

07:00 EST 10th January 2019 | BioPortfolio

Summary of "Prevention of relapse in patients with acquired thrombotic thrombocytopenic purpura undergoing elective surgery: a case series."

Severe ADAMTS13 deficiency has been recognized as the main risk factor for recurrence of thrombotic thrombocytopenic purpura (TTP). Several conditions including surgery may influence the levels of ultra large Von Willebrand factor and ADAMTS13, acting as a trigger for an acute TTP event.

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This article was published in the following journal.

Name: Journal of thrombosis and haemostasis : JTH
ISSN: 1538-7836
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Medical and Biotech [MESH] Definitions

An acquired, congenital, or familial disorder caused by PLATELET AGGREGATION with THROMBOSIS in terminal arterioles and capillaries. Clinical features include THROMBOCYTOPENIA; HEMOLYTIC ANEMIA; AZOTEMIA; FEVER; and thrombotic microangiopathy. The classical form also includes neurological symptoms and end-organ damage, such as RENAL FAILURE.

Diseases that result in THROMBOSIS in MICROVASCULATURE. The two most prominent diseases are PURPURA, THROMBOTIC THROMBOCYTOPENIC; and HEMOLYTIC-UREMIC SYNDROME. Multiple etiological factors include VASCULAR ENDOTHELIAL CELL damage due to SHIGA TOXIN; FACTOR H deficiency; and aberrant VON WILLEBRAND FACTOR formation.

Any form of purpura in which the PLATELET COUNT is decreased. Many forms are thought to be caused by immunological mechanisms.

An ADAMTS protease that contains eight thrombospondin (TS) motifs. It cleaves VON WILLEBRAND FACTOR to control vWF-mediated THROMBOSIS. Mutations in the ADAMTS13 gene have been identified in familial cases of PURPURA, THROMBOTIC THROMBOCYTOPENIC and defects in ADAMTS13 activity are associated with MYOCARDIAL INFARCTION; BRAIN ISCHEMIA; PRE-ECLAMPSIA; and MALARIA.

A systemic non-thrombocytopenic purpura caused by HYPERSENSITIVITY VASCULITIS and deposition of IGA-containing IMMUNE COMPLEXES within the blood vessels throughout the body, including those in the kidney (KIDNEY GLOMERULUS). Clinical symptoms include URTICARIA; ERYTHEMA; ARTHRITIS; GASTROINTESTINAL HEMORRHAGE; and renal involvement. Most cases are seen in children after acute upper respiratory infections.

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