scholarly journals Platelet antibodies in immune thrombocytopenia and related conditions

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Volker Kiefel

AbstractPlatelet autoantibodies are a common finding in immune thrombocytopenia (ITP) and in rare cases of antibody-mediated platelet function (“acquired thrombasthenia”). In drug-induced immune thrombocytopenia, antibodies react with platelets only in the presence of the offending drug. Alloantibodies reacting with platelets are induced by transfusion of cellular blood products or during pregnancy. They are responsible for fetal/neonatal alloimmune thrombocytopenia (FNAIT), they are able to cause febrile, nonhemolytic transfusion reactions and they give rise to insufficient platelet increments following platelet transfusions. Two rare transfusion reactions: post-transfusion purpura (PTP) and passive alloimmune thrombocytopenia (PAT) are triggered by platelet alloantibodies. This review discusses the clinical value of tests for platelet antibodies in various clinical situations related to insufficient primary hemostasis.

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Ioanna A. Comstock ◽  
Michelle Longmire ◽  
Richard H. Aster ◽  
Amin A. Milki

Drug-induced immune thrombocytopenia has been associated with hundreds of medications and can lead to devastating consequences for the patient. We present a case of a healthy 33-year-old female undergoing in vitro fertilization who developed a severe drug-induced thrombocytopenia, petechiae, and a large hemoperitoneum after receiving Cefazolin antibiotic prophylaxis for a transvaginal oocyte retrieval. The patient was admitted to the intensive care unit for resuscitation with blood products. The presence of drug-dependent platelet antibodies to Cefazolin was confirmed serologically.


1979 ◽  
Author(s):  
J.G. Kelton ◽  
A. Giles ◽  
P.B. Neame ◽  
M. Blajchman ◽  
J. Hirah

The optimal method for assaying platelet bound antibody is uncertain. We have compared a fluorescent assay (FA) with a (quantitative) antiglobulin consumption assay for platelet associated IgG (PAIgG) in normals and thrombocytopenics with ITP, SLE, non-immune and drug-induced thrombocytopenia. Forty-eight of 49 hospitalized and healthy controls had normal PAIgG levels by the antiglobulin consumption assay (2.6 ± 0.2 fg IgG/platetet, ± SE, normal 0-5 fg) and the FA was negative in 41. The PAIgG level was elevated (20.0 ± 1.9 fq IgG/platdet) in 42 of 45 determinations on ITP patients. The FA was positive in 21. Positivity in the FA test did not relate closely to PAIgG level. The PAlqG was elevated (29.0 - 7.3) in 14 of 15 assays in thrombocytopenic SLE patients. The FA was positive in 3. The PAIgG level was elevated in all 9 patients with drug-induced thrombocytopenia (42.4 ± 23.2) without addition of the drug to the test system. The FA was positive in 5. In 2 of 12 patients with non-immune thrombocytopenia the PAIgG level was slightly elevated (both patients had multiple myeloma) and the FA was positive in 5. The results suggest that the quantitative antiglobulin consumption assay is more sensitive than the fluorescent assay in the diagnosis of immune mediated throinbocytopenia. The significance of the lack of correlation between positivity in the fluorescence test and the PAIgG levels found in patients with ITP is uncertain.


PEDIATRICS ◽  
1975 ◽  
Vol 55 (1) ◽  
pp. 68-74
Author(s):  
P. D. McClure

In children, the term idiopathic thrombocytopenic purpura (ITP) has been loosely applied to at least four conditions; postviral thrombocytopenia, "true" idiopathic thrombocytopenia in which no precipitating factor or associated illness can be found, thrombocytopenia associated with other autoimmune syndromes and drug-induced immune thrombocytopenia. Patients initially thought to have "true" ITP may later develop lupus erythematosus or hemolytic anemia and hence move from one category to another. In 1951 Harrington demonstrated an antiplatelet factor in the serum of patients with ITP. Later this factor was proven to be an antibody of the IgG class and to be present in the blood of all four types of patients. Platelets lightly coated with antibody are sequestered and removed by the reticuloendothelial system in the spleen while more heavily coated platelets may be removed in the liver.2-4 The spleen further contributes to the thrombocytopenia by producing platelet antibodies.5-7 Recently Wybran and others8-10 have shown that cell-mediated immunity to autologous platelets may also be a factor in the pathogenesis of some cases of ITP. In view of the obvious association of ITP and altered immune mechanisms some authors have suggested the term ITP be changed to immunological or immunogenic thrombocytopenic purpura.11, 12 Karpatkin, Garg and Siskind recommend that if a platelet antibody can be demonstrated in the absence of associated disease, the term autoimmune thrombocytopenic purpura (ATP) be applied.13 Since not all patients have demonstrably altered immunity and since the cause of autoantibody production is unclear, we think the term idiopathic thrombocytopenic purpura should be retained at least for those cases in which the precipitating cause (virus or drug) cannot be identified.


Author(s):  
Kunal Kalra ◽  
Hema Gupta Mittal ◽  
Arti Maria

Abstract Neonatal thrombocytopenia is common and is frequently seen in neonatal sepsis. Drug-induced thrombocytopenia is likely to be missed unless a high index of suspicion is present. Changing of antibiotics for assumed nonresolution of sepsis may lead to persistent thrombocytopenia in a neonate if drug-induced thrombocytopenia is missed. Vancomycin-induced neonatal thrombocytopenia is rarely described in scientific literature. We describe a newborn who was diagnosed with early onset sepsis and vancomycin-induced thrombocytopenia. Other causes of thrombocytopenia such as sepsis, alloimmune thrombocytopenia, thrombosis etc. were excluded. The platelet counts normalized within 72 h of stopping vancomycin. Vancomycin-induced IgM platelet antibodies could not be done in our case (due to financial constraints), but their absence does not exclude the diagnosis of vancomycin-induced thrombocytopenia.


2014 ◽  
Vol 3 (9) ◽  
pp. 42 ◽  
Author(s):  
Yasir Ahmed ◽  
Christopher Sartin ◽  
Imran Umer ◽  
Osama Mukarram ◽  
Renuka Borra

Drug-induced immune thrombocytopenia is a challenging clinical problem that is often overlooked. Vancomycin is a rare cause of immune-mediated thrombocytopenia that can cause severe life-threatening bleeding in an acutely ill patient. The diagnosis requires a temporal relationship with the drug, exclusion of other common causes, and testing for vancomycin-induced platelet antibodies. Here we present a rare case of very severe but asymptomatic vancomycin-induced immune thrombocytopenia that resolved after discontinuation of vancomycin.


2018 ◽  
Vol 11 (3) ◽  
pp. 880-882 ◽  
Author(s):  
Elizabeth Pan ◽  
Eric Hsieh ◽  
Caroline Piatek

Thrombocytopenia is a frequent complication of cancer may be due to a variety of causes including malignancy itself, acute disease processes, or cancer therapy. Systemic cancer therapy is the most common cause of thrombocytopenia in cancer patients observed nearly two-thirds of patients with solid tumors. Thrombocytopenia with traditional chemotherapy agents is most frequently the result of megakaryocyte cytotoxicity. Oxaliplatin is a platinum derivative commonly used in gastrointestinal malignancies and is associated with drug-induced immune thrombocytopenia.


2013 ◽  
Vol 27 (3) ◽  
pp. 137-145 ◽  
Author(s):  
Donald M. Arnold ◽  
Ishac Nazi ◽  
Theodore E. Warkentin ◽  
James W. Smith ◽  
Lisa J. Toltl ◽  
...  

2009 ◽  
Vol 133 (2) ◽  
pp. 309-314
Author(s):  
Barton Kenney ◽  
Gary Stack

Abstract Drug-induced thrombocytopenia was first described in the 19th century, yet our understanding of its pathogenesis continues to evolve. The list of drugs implicated in drug-induced thrombocytopenia is extensive and growing. Many, if not most, of these medications induce thrombocytopenia by immune mechanisms. Because the degree of thrombocytopenia can put patients at risk for serious bleeding, a prompt diagnosis is key to clinical management. The laboratory approach to diagnosing drug-induced thrombocytopenia is 2-pronged. First, nondrug causes of thrombocytopenia must be ruled out. Second, testing for drug-dependent platelet antibodies, available at specialized reference laboratories, often can identify the offending medication, although usually not in time for initial clinical management. Once a medication is suspected of causing thrombocytopenia, it must be discontinued promptly, and the patient should be monitored closely. Thrombocytopenia generally resolves quickly after offending medication withdrawal, and the prognosis of drug-induced thrombocytopenia is then excellent.


Author(s):  
Pradeep Vittal Bhagwat ◽  
R. Rajagopal ◽  
P. S. Murthy ◽  
R. S. V. Kumar

<p class="abstract"><strong>Background:</strong> Chronic renal failure is becoming common entity with increased incidence of diabetes mellitus and resulting diabetic nephropathy. With the availability of renal transplantation services in many centers, increased availability of donors, improved surgical technique and availability of better drugs, the survival of renal transplant recipients has increased. The objective of the study was to study the cutaneous manifestations in renal transplant recipients.</p><p class="abstract"><strong>Methods:</strong> Fifty consenting, consecutive renal transplant recipients attending the OPD and in-patients at Command Hospital Air Force, Bangalore during July 2001 to March 2003 were included in the study. Detailed history was taken and clinical examination was carried out with special emphasis on the Dermatological examination. Relevant investigations were carried out.<strong></strong></p><p class="abstract"><strong>Results:</strong> A total of 50 renal transplant recipients were studied of which 42 (84%) were males and 8 (16%) were females. The age of patients ranged from 16 years to 60 years. Infections were the most common finding, encountered in 38 (76%) patients, followed by drug induced manifestations in 24 (48%) patients. Cellulitis was noted in 1 (2%) patient, viral infections were seen in 18 (36%) patients, fungal infection was the commonest in this study, encountered in 38 (76%) patients. Monomorphic acne was seen in 13 (26%) patients. Hypertrichosis/hirsutism were the commonest drug induced manifestation in this study, seen in 16 (32%) patients.</p><p class="abstract"><strong>Conclusions:</strong> In patients with renal transplantation, superficial fungal infections and viral infections of the skin are seen more commonly. Monomorphic acne and hypertrichosis due to immunosuppressive are also seen frequently. These changes are moderately influenced by the immunosuppressive regimen used.</p>


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