scholarly journals Thrombocytopenia in Young Patient due to Anti Tuberculosis Drugs : A Case Report

2020 ◽  
Vol 6 (1) ◽  
pp. 5
Author(s):  
Aryani Prawita Sari ◽  
Winariani Koesoemaprodjo

Background: Most anti-tuberculosis (ATD) drugs are relatively safe, but unusual serious reactions can occur. Thrombocytopenia is an uncommon but potentially life-threatening complication of certain ATDs and is characterized by rapid destruction of platelets whenever an offending drug is taken by a susceptible person. Rifampicin is the most common cause of thrombocytopenia.Case: A 25 years old woman came with chief complaints, shortness of breath since 1 week before admission and cough with phlegm since 2 months before admission. The patient received antibiotic and ATD. In the course of improving on sepsis and pneumonia, the patient had thrombocytopenia accompanied by melena on day 4 of treatment.Discussion: Thrombocytopenia is defined as a disorder, which showed an abnormality on the low amount of thrombocyte. Thrombocytopenia was commonly cofounded when Complete blood count (CBC) was performed. The majority of the mechanism associated with thrombocytopenia is the immune. Drug-induced Thrombocytopenia (DITP) is an exclusion diagnosis, which is obtained by ruling out other underlying causes that resulted in thrombocytopenia.Conclusion: This case illustrates that the discovery of isolated thrombocytopenia in a patient taking several medications presents a challenging clinical problem. Laboratory confirmation of drug-induced thrombocytopenia at the time of initial presentation is not possible because tests for drug-dependent anti-platelet antibodies are not available in most clinical laboratories. The diagnosis of drug-induced thrombocytopenia can be supported only by resolution of thrombocytopenia after discontinuation of therapy with the suspected drug.

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.


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.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Eric L. Tam ◽  
Padma L. Draksharam ◽  
Jennifer A. Park ◽  
Gurinder S. Sidhu

We describe a case of a 63-year-old woman with advanced colon cancer and liver metastases who was treated with fluorouracil, leucovorin, and oxaliplatin (FOLFOX) and cetuximab chemotherapy. She tolerated 13 cycles of chemotherapy without any significant hematological side effects, but after the 14th cycle, she developed melena and was admitted for severe thrombocytopenia. After supportive care, the platelet counts rapidly improved to 76,000/μL. Upon initiation of FOLFIRI and cetuximab chemotherapy, she again developed rectal bleeding and severe thrombocytopenia with a platelet count of 6000/μL. Lab testing was positive for oxaliplatin and irinotecan drug-dependent platelet antibodies on flow cytometry assay. Drug-induced thrombocytopenia (DITP) is associated with several classes of drugs with several proposed underlying mechanisms. Prospective studies are needed to further address different mechanisms of drug-induced thrombocytopenia.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 731-731
Author(s):  
Daniel W. Bougie ◽  
Jessica Birenbaum ◽  
Scott Ahl ◽  
Richard H. Aster

Abstract Drug-induced immune thrombocytopenia (DITP) is a serious and sometimes life-threatening complication of treatment with many drugs. In most instances (excluding heparin-induced TP), platelet (plt) destruction is caused by antibodies (abs) that recognize distinct epitopes on platelet membrane glycoproteins (GP) only when the sensitizing drug is present in soluble form. How drug at pharmacological levels promotes tight binding of antibody to a specific target is unknown, in part because only polyclonal human abs have been available for study. We sought to produce monoclonal abs (mAbs) that mimic the behavior of human drug-dependent abs to create tools that can be used to study the molecular basis for this interaction. Mice were immunized with GPIIb/IIIa isolated from human platelets together with soluble quinine (Qn), tirofiban (Tf), or eptifibatide (Ef), three drugs that commonly cause DITP. Hybridomas were prepared from splenic B cells using a standard protocol and approximately 550 supernatants from each cultured hybrid line were screened for DDAbs by flow cytometry using normal platelets as targets. To date, 11 Abs that react with GPIIb/IIIa only in the presence of the immunizing drug (2 Qn-, 3 Tf- and 6 Ef-specific) have been identified. Preliminary studies show that the Qn-specific abs bind reversibly to GPIIb/IIIa at 50 nM Qn, a concentration much lower than is achieved pharmacologically, and are not inhibited by Qn at 5 mM, the limit of solubility. Quinidine (Qd) the diastereoisomer of Qn, supports only weak ab binding at a concentration of 50 uM. The tirofiban and eptifibatide-dependent abs recognize GPIIb/IIIa occupied by these RGD ligand-mimetic GPIIb/IIIa inhibitors. In each of these respects, reaction patterns of the three groups of mAbs closely resemble those of abs from patients experiencing TP after treatment with one of these drugs. These findings show that mAbs mimicking the behavior of human drug-dependent abs can be produced by immunizing mice with GP and soluble drug to produce probes suitable for characterizing the molecular basis of ab-drug-target interactions leading to platelet destruction in DITP. It is noteworthy that these mAbs were induced using soluble drug and protein for immunization because this suggests that the immune response leading to DITP does not require the sensitizing drug to be covalently linked to a protein, i.e, does not require the drug to act as a classical hapten.


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.


Blood ◽  
2011 ◽  
Vol 117 (22) ◽  
pp. 5975-5986 ◽  
Author(s):  
José Perdomo ◽  
Feng Yan ◽  
Zohra Ahmadi ◽  
Xing-Mai Jiang ◽  
Roland Stocker ◽  
...  

Abstract The development of immune cytopenias is a well-recognized side effect of many drugs. Quinine- and quinidine-dependent antibodies are classic examples of drug-induced effects that cause severe, life-threatening thrombocytopenia. Whereas the effects of drug-dependent antibodies on platelets have been well documented, their effects on megakaryocyte (Mk) biology are still unclear. We analyzed sera from several quinine-induced thrombocytopenia (QITP) patients on highly pure Mks (98% glycoprotein IIb-positive [GPIIb+]; 92% GPIX+) derived from human CD34+ cells cultured with human thrombopoietin. We demonstrate by flow cytometry and confocal microscopy that QITP IgGs bind Mks efficiently in the presence of quinine. Incubation of day-4 Mks with QITP sera or purified IgG resulted in induction of apoptosis, a significant decrease in cell viability, and an increase in cell death. Furthermore, QITP sera preferentially reduced the number of late GPIX+/GPIbα+ Mks and the number of receptors per cell in the surviving population. Ploidy distribution, lobularity, and average cell size of Mks remained unchanged after treatment. In addition, treated Mks showed a marked decrease in their proplatelet production capacity, suggesting that drug-dependent antibodies hinder platelet production. Therefore, QITP antibodies considerably reduce the proplatelet production capabilities of Mks despite undetectable effects on DNA content, morphology, and cell size.


Blood ◽  
2015 ◽  
Vol 126 (18) ◽  
pp. 2146-2152 ◽  
Author(s):  
Daniel W. Bougie ◽  
Julie Peterson ◽  
Mark Rasmussen ◽  
Richard H. Aster

Key Points Drug-induced modulation of antibody specificity appears to explain the binding of drug-dependent mAbs to αIIb/β3 integrin. Drug-dependent platelet antibodies differ greatly from classic hapten-specific antibodies and may be induced by a quite different mechanism.


2020 ◽  
Vol 9 (7) ◽  
pp. 2212 ◽  
Author(s):  
Caroline Vayne ◽  
Eve-Anne Guéry ◽  
Jérôme Rollin ◽  
Tatiana Baglo ◽  
Rachel Petermann ◽  
...  

Drug-induced immune thrombocytopenia (DITP) is a life-threatening clinical syndrome that is under-recognized and difficult to diagnose. Many drugs can cause immune-mediated thrombocytopenia, but the most commonly implicated are abciximab, carbamazepine, ceftriaxone, eptifibatide, heparin, ibuprofen, mirtazapine, oxaliplatin, penicillin, quinine, quinidine, rifampicin, suramin, tirofiban, trimethoprim-sulfamethoxazole, and vancomycin. Several different mechanisms have been identified in typical DITP, which is most commonly characterized by severe thrombocytopenia due to clearance and/or destruction of platelets sensitized by a drug-dependent antibody. Patients with typical DITP usually bleed when symptomatic, and biological confirmation of the diagnosis is often difficult because detection of drug-dependent antibodies (DDabs) in the patient’s serum or plasma is frequently not possible. This is in contrast to heparin-induced thrombocytopenia (HIT), which is a particular DITP caused in most cases by heparin-dependent antibodies specific for platelet factor 4, which can strongly activate platelets in vitro and in vivo, explaining why affected patients usually have thrombotic complications but do not bleed. In addition, laboratory tests are readily available to diagnose HIT, unlike the methods used to detect DDabs associated with other DITP that are mostly reserved for laboratories specialized in platelet immunology.


Author(s):  
Epameinondas Koumpis ◽  
Konstantina Papathanasiou ◽  
Ioannis Papakonstantinou ◽  
Iliana Tassi ◽  
Anastasia Serpanou ◽  
...  

Thrombocytopenia may be associated with a variety of conditions and risks depending on its severity, ranging from mild epistaxis to life-threating bleeding. Many drugs or herbal remedies can cause thrombocytopenia by either inhibiting platelet production and/or enhancing their destruction from the peripheral blood mediated via an immunological mechanism implicating drug-dependent antibodies. The latter entity is called drug-induced immune thrombocytopenia: a life-threatening, under-recognised condition, which is often a diagnostic challenge. Rifampicin is a widely used, well-tolerated, and effective bactericidal drug. Adverse events, except for gastrointestinal effects, headache, skin rash, and pruritus, are uncommon. The authors herein report on a patient with isolated thrombocytopenia with a recent medical history of brucellosis on rifampicin and doxycycline. Thrombocytopenia was proved to be rifampicin-induced. Also presented is a short review of the literature on this rare subject, which should be of great importance to clinicians.


2021 ◽  
Vol 14 (11) ◽  
pp. e246788
Author(s):  
Vanessa Lopes ◽  
Joana Ramos ◽  
Patrícia Dias ◽  
Arsénio Santos

Idiosyncratic drug-induced agranulocytosis is a rare life-threatening adverse reaction characterised by an absolute neutrophil count <500 cells/μL of blood. Nitrofurantoin has been associated with haematological adverse events, but few agranulocytosis cases worldwide have been reported. We present a case of a 68-year-old woman who presented with fever and agranulocytosis following treatment with nitrofurantoin. Extensive workup for agranulocytosis, including a bone marrow aspirate, was unremarkable. Treatment with nitrofurantoin was discontinued, which led to a complete recovery of the complete blood count. This case stresses the importance of monitoring treatments, given that widely used drugs are not free from severe adverse reactions.


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