Drug-induced immune thrombocytopenia: pathogenesis, diagnosis, and management

被引:226
作者
Aster, R. H. [1 ,2 ]
Curtis, B. R. [1 ]
McFarland, J. G. [1 ]
Bougie, D. W. [1 ]
机构
[1] BloodCtr Wisconsin, Blood Res Inst, Milwaukee, WI 53201 USA
[2] Med Wisconsin, Dept Med, Milwaukee, WI USA
关键词
HEPARIN-INDUCED THROMBOCYTOPENIA; HEMOLYTIC-UREMIC SYNDROME; QUININE-DEPENDENT ANTIBODIES; RED-CELL; QUINIDINE; PURPURA; BINDING; ABCIXIMAB; PLATELETS; SENSITIVITY;
D O I
10.1111/j.1538-7836.2009.03360.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Drug-induced immune thrombocytopenia (DITP) can be triggered by a wide range of medications. Although many cases of DITP are mild, some are characterized by life-threatening bleeding symptoms. The pathogenesis of DITP is complex, in that at least six different mechanisms have been proposed by which drug-induced antibodies can promote platelet destruction. It is possible in many cases to identify antibodies that react with platelets in the presence of the sensitizing drug, but the required testing is technically demanding and not widely available. Therefore, a decision on whether to discontinue an implicated medication in a patient suspected of having DITP must be made on clinical grounds. An algorithm is available that can be helpful in assessing the likelihood that a particular drug caused thrombocytopenia, but the most important aspects of patient management are a high index of suspicion and a careful history of drug exposure in an individual who presents with acute, often severe thrombocytopenia of unknown etiology. How drugs induce platelet-reactive antibodies and how, once formed, the antibodies cause platelet destruction following exposure to the drug is poorly understood. Further studies to address these issues and characterize more completely the range of drugs and drug metabolites that can cause DITP are needed.
引用
收藏
页码:911 / 918
页数:8
相关论文
共 84 条
[41]   Ceftriaxone causes drug-induced immune thrombocytopenia and hemolytic anemia: characterization of targets on platelets and red blood cells [J].
Grossjohann, B ;
Eichler, P ;
Greinacher, A ;
Santoso, S ;
Kroll, H .
TRANSFUSION, 2004, 44 (07) :1033-1040
[42]   TREATMENT OPTIONS IN SULFAMETHOXAZOLE-TRIMETHOPRIM-INDUCED THROMBOCYTOPENIC PURPURA [J].
HERRINGTON, A ;
MAHMOOD, A ;
BERGER, R .
SOUTHERN MEDICAL JOURNAL, 1994, 87 (09) :948-950
[43]   Association between ligand-induced conformational changes of integrin αIIbβ3 and αIIbβ3-mediated intracellular Ca2+ signaling [J].
Honda, S ;
Tomiyama, Y ;
Aoki, T ;
Shiraga, M ;
Kurata, Y ;
Seki, J ;
Matsuzawa, Y .
BLOOD, 1998, 92 (10) :3675-3683
[44]  
Juang Y C, 1992, J Formos Med Assoc, V91, P475
[45]  
Jubelirer SJ, 1999, AM J HEMATOL, V61, P205, DOI 10.1002/(SICI)1096-8652(199907)61:3<205::AID-AJH8>3.0.CO
[46]  
2-9
[47]  
KARPATKIN M, 1977, J LAB CLIN MED, V89, P400
[48]  
KAUFMAN DW, 1993, BLOOD, V82, P2714
[49]   Quinine-associated thrombotic thrombocytopenic purpura-hemolytic uremic syndrome: Frequency, clinical features, and long-term outcomes [J].
Kojouri, K ;
Vesely, SK ;
George, JN .
ANNALS OF INTERNAL MEDICINE, 2001, 135 (12) :1047-1051
[50]  
Kojouri K, 2000, J Okla State Med Assoc, V93, P519