Drug-Induced Platelet Destruction

Hackett, Thomas P.; Kelton, John G.; Powers, Peter

doi:10.1055/s-2007-1005047

Cited by 100 publications

(44 citation statements)

References 76 publications

(101 reference statements)

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“…In 1982 Hackett et al proposed the following criteria: (1) Thrombocytopenia developed while the patient is taking the drug, resolved once the drug is stopped and did not recur while the patient was off the drug; (2) other causes of thrombocytopenia were excluded; (3) the thrombocytopenia recurred upon re-administration of the drug; and (4) an in vitro test for drug-dependent platelet antibodies was positive [48]. A positive re-challenge or positive laboratory test was sufficient to confirm the diagnosis.…”

Section: Clinical Criteria For Ditpmentioning

confidence: 99%

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Arnold

Nazi

Warkentin

et al. 2013

Transfusion Medicine Reviews

152

144

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Drug-induced immune thrombocytopenia (DITP) is a challenging clinical problem that is underrecognized, difficult to diagnose and associated with severe bleeding complications. DITP may be caused by classic drug-dependent platelet antibodies (eg, quinine); haptens (eg, penicillin); fibandependent antibodies (eg, tirofiban); monoclonal antibodies (eg, abciximab); autoantibody formation (eg, gold); and immune complex formation (eg, heparin). A thorough clinical history is essential in establishing the diagnosis of DITP and should include exposures to prescription medications, herbal preparations and even certain foods and beverages. Clinical and laboratory criteria have been established to determine the likelihood of a drug being the cause of thrombocytopenia, but these criteria can only be applied retrospectively. The most commonly implicated drugs include quinine, quinidine, trimethoprim/sulfamethoxazole and vancomycin. We propose a practical approach to the diagnosis of the patient with suspected DITP. Key features are: the presence of severe thrombocytopenia (platelet nadir <20 × 10 9 /L); bleeding complications; onset 5 to 10 days after first drug exposure, or within hours of subsequent exposures or after first exposure to fibans or abciximab; and exposure to drugs that have been previously implicated in DITP reactions. Treatment involves stopping the drug(s), administering platelet transfusions or other therapies if bleeding is present and counselling on future drug avoidance. The diagnosis can be confirmed by a positive drug re-challenge, which is often impractical, or by demonstrating drug-dependent platelet reactive antibodies in vitro. Current test methods, which are mostly flow cytometry-based, must show drug-dependence, immunoglobulin binding, platelet specificity and *

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Section: Clinical Criteria For Ditpmentioning

confidence: 99%

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Arnold

Nazi

Warkentin

et al. 2013

Transfusion Medicine Reviews

152

144

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“…/3-Lactam anti biotics also suppress colony formation from granulocyte-macrophage progenitors (CFU GM) in semisolid culture (5), indicating that they exert a direct toxic (non-immunogenic) effect on the CFU-GM. Although there are many reports showing the occurrence of thrombocytopenia after prolonged treatment with (3-Iactam antibiotics (6)(7)(8), the effect on megakaryocytes or their progenitors…”

Section: Prolonged Administrationmentioning

confidence: 99%

Suppressive effect of antibiotics on colony formation from human megakaryocyte progenitors (CFU-M) and granulocyte-macrophage progenitors (CFU-GM).

1987

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Abstract-R-Lactamantibiotics, moxalactam (LMOX), cefotaxime (CTX), flomoxef (FMOX), cefamandole (CMD), carbenicillin (CBPC) and sulbenicillin (SBPC), suppressed colony formation from human megakaryocyte progenitors (CFU-M) and granulocyte-macrophage progenitors (CFU-GM) dose-dependently. The suppres sive potencies for both progenitors were weakest for CBPC and SBPC, moderate for LMOX and FMOX, and strongest for CMD and CTX. The stainability of glyco protein Ilb/Illa complex in the megakaryocyte colonies by the monoclonal antibody was decreased by LMOX and CTX. These data suggest that /3-lactam antibiotics directly suppress proliferation of CFU-M and CFU-GM.

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“…[22][23][24][25][26][27][28] No predisposing factors have been identified, and combined with the low incidence of thrombocytopenia with most drugs, has precluded populations at risk for this complication from being prospectively identified with clinical criteria. 22 Thus, standard clinical practice continues to involve measuring the platelet counts of exposed individuals at various intervals and for varying duration.…”

Section: Introductionmentioning

confidence: 99%

Evidence that thrombocytopenia observed in humans treated with orally bioavailable glycoprotein IIb/IIIa antagonists is immune mediated

Billheimer¹,

Dicker²,

Wynn³

et al. 2002

Blood

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Drug-Induced Platelet Destruction

Cited by 100 publications

References 76 publications

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Approach to the Diagnosis and Management of Drug-Induced Immune Thrombocytopenia

Suppressive effect of antibiotics on colony formation from human megakaryocyte progenitors (CFU-M) and granulocyte-macrophage progenitors (CFU-GM).

Evidence that thrombocytopenia observed in humans treated with orally bioavailable glycoprotein IIb/IIIa antagonists is immune mediated

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