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Drug Induced Immune-Thrombocytopenia
Author(s) -
R Hoigné
Publication year - 1982
Publication title -
acta haematologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.574
H-Index - 56
eISSN - 1421-9662
pISSN - 0001-5792
DOI - 10.1159/000206940
Subject(s) - drug , immune thrombocytopenia , medicine , immune system , immunology , pharmacology , platelet
Drug Induced Immune-Thrombocytopenia Immune-thrombocytopenia caused by drugs has fascinated hematologists, internists and other investigators for more than 30 years. A number of elaborate in vitro tests based on different principles have been developed. These methods have been derived partly from experience in bacteriology, such as platelet agglutination, lysis and complement fixation, or from the blood coagulation process and immunology such as clot retraction inhibition, platelet factor 3 immuno-injury test, 51Cr platelet lysis test, release (or inhibition of uptake) of serotonin, platelet aggregometry, serologic-nephelo-metric tests, lymphocyte transformation, etc. (The last two tests are not specifically related to the thrombocyte as the mainly involved cell of the allergic drug reaction.) Three papers in this journal (vol. 68, pp. 68, 74 and 75) deal with drug-induced thrombocytopenic purpura and add two more causative drugs, namely carbama-zepine (Tegretol®) and the beta blocking agent oxprenolol (Trasitensin®). These two agents have hardly been known to provoke this syndrome by an allergic or immunolog-ic mechanism before. One of the most important and practical problems in drug-induced thrombocytopen-ias is the identification of the responsible drug, as follows. The Possibility to Identify the Causative Drug by in vitro Tests Most of the in vitro tests are either not very sensitive or difficult to perform and therefore not yet a part of routine laboratory studies. They seem to correlate well with the clinical estimation of causality of a given drug, provided they are precisely performed, critically interpreted, and show a positive result. A negative result, however, does not exclude a suspected drug. Thus, the clinician responsible for the patient is always confronted with the question if it is not best to discontinue all the drugs taken by the patient before the appearance of acute throm-bocytopenia and to substitute chemically non-related preparations. This is especially true for drugs known to occasionally induce thrombocytopenia. 2 Hoigné

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