Severe vancomycin-induced thrombocytopenia in a patient with meningitis

2021 ◽  
Vol 14 (8) ◽  
pp. e244209
Author(s):  
Ian Savchenko ◽  
Tatiana Birg ◽  
Oleg Sharipov ◽  
Yulia Davydova
Keyword(s):  
Platelet Count ◽  
Antibiotic Treatment ◽  
Normal Values ◽  
Igg Antibodies ◽  
Vancomycin Therapy ◽  
Drug Induced ◽  
Drug Dependent ◽  
Hospital Acquired ◽  
Platelet Transfusions

Vancomycin is a widely used antibiotic and rarely can cause drug-induced thrombocytopenia. A patient with hospital-acquired meningitis after neurosurgery was treated with systemic and intrathecal vancomycin. On 9th day of antibiotic treatment, the patient’s platelets dropped to 0.68×109/L. Multiple platelet transfusions had minimal influence on platelet count. After cessation of vancomycin therapy, platelets returned to normal values without any additional interventions. Diagnosis of vancomycin-induced thrombocytopenia was confirmed by detection of drug-dependent antiplatelet IgG antibodies.

scholarly journals Characteristics of quinine- and quinidine-induced antibodies specific for platelet glycoproteins IIb and IIIa

Blood ◽  
1991 ◽  
Vol 77 (12) ◽  
pp. 2668-2676 ◽  
Author(s):  
GP Visentin ◽  
PJ Newman ◽  
RH Aster
Keyword(s):  
Immune Response ◽  
Platelet Membrane ◽  
The Other ◽  
Membrane Glycoprotein ◽  
Igg Antibodies ◽  
Drug Induced ◽  
Disulfide Bonding ◽  
Platelet Membrane Glycoprotein ◽  
Drug Dependent

Abstract Recent studies have shown that antibodies characteristic of quinine- and quinidine-induced thrombocytopenia sometimes recognize the platelet membrane glycoprotein (GP) complex IIb/IIIa in addition to their well known target, GPIb/IX. We have investigated the frequency with which drug-induced antibodies bind to GPIIb/IIIa and the nature of their target epitopes. In studies of sera from 13 patients sensitive to quinidine or quinine, we found that 10 contained IgG antibodies specific for both GPIb/IX and GPIIb/IIIa, two reacted with GPIb/IX alone, and one reacted with GPIIb/IIIa alone. In all cases, the presence of drug was required for binding of IgG to target GPs. By immunoabsorption, we found that each of five polyspecific sera contained at least two different antibodies, one reactive with GPb/IX and the other with GPIIb/IIIa. Further studies with eight drug- dependent antibodies (DDAb) specific for GPIIb/IIIa showed that three recognized the GPIIb/IIIa complex only, one recognized GPIIb alone, and three recognized GPIIIa alone. The eighth serum appeared to bind to both GPIIIa alone and to an epitope determined by the GPIIb/IIIa complex. The three antibodies specific for GPIIIa alone also reacted with GPIIIa deglycosylated with endo-H, and with the major (61 Kd) fragment obtained by chymotryptic digestion of GPIIIa but failed to react with reduced GPIIIa. These findings demonstrate that, in drug- induced, immunologic thrombocytopenia, the anti-platelet immune response is typically directed against epitopes on both GPIb/IX and GPIIb/IIIa. The three DDAb we studied that were specific for GPIIIa alone recognize epitopes resistant to chymotrypsin and endo-H treatment that are dependent on intrachain disulfide bonding.

scholarly journals Characteristics of quinine- and quinidine-induced antibodies specific for platelet glycoproteins IIb and IIIa

Blood ◽  
1991 ◽  
Vol 77 (12) ◽  
pp. 2668-2676 ◽  
Author(s):  
GP Visentin ◽  
PJ Newman ◽  
RH Aster
Keyword(s):  
Immune Response ◽  
Platelet Membrane ◽  
The Other ◽  
Membrane Glycoprotein ◽  
Igg Antibodies ◽  
Drug Induced ◽  
Disulfide Bonding ◽  
Platelet Membrane Glycoprotein ◽  
Drug Dependent

Recent studies have shown that antibodies characteristic of quinine- and quinidine-induced thrombocytopenia sometimes recognize the platelet membrane glycoprotein (GP) complex IIb/IIIa in addition to their well known target, GPIb/IX. We have investigated the frequency with which drug-induced antibodies bind to GPIIb/IIIa and the nature of their target epitopes. In studies of sera from 13 patients sensitive to quinidine or quinine, we found that 10 contained IgG antibodies specific for both GPIb/IX and GPIIb/IIIa, two reacted with GPIb/IX alone, and one reacted with GPIIb/IIIa alone. In all cases, the presence of drug was required for binding of IgG to target GPs. By immunoabsorption, we found that each of five polyspecific sera contained at least two different antibodies, one reactive with GPb/IX and the other with GPIIb/IIIa. Further studies with eight drug- dependent antibodies (DDAb) specific for GPIIb/IIIa showed that three recognized the GPIIb/IIIa complex only, one recognized GPIIb alone, and three recognized GPIIIa alone. The eighth serum appeared to bind to both GPIIIa alone and to an epitope determined by the GPIIb/IIIa complex. The three antibodies specific for GPIIIa alone also reacted with GPIIIa deglycosylated with endo-H, and with the major (61 Kd) fragment obtained by chymotryptic digestion of GPIIIa but failed to react with reduced GPIIIa. These findings demonstrate that, in drug- induced, immunologic thrombocytopenia, the anti-platelet immune response is typically directed against epitopes on both GPIb/IX and GPIIb/IIIa. The three DDAb we studied that were specific for GPIIIa alone recognize epitopes resistant to chymotrypsin and endo-H treatment that are dependent on intrachain disulfide bonding.

Levofloxacin-Induced Acute Immune-Mediated Thrombocytopenia of Rapid-Onset

2017 ◽  
Vol 31 (2) ◽  
pp. 234-237 ◽  
Author(s):  
Andrew W. Shih ◽  
Andy S. Lam ◽  
Theodore E. Warkentin
Keyword(s):  
Platelet Count ◽  
Drug Exposure ◽  
Rapid Onset ◽  
Chronic Obstructive ◽  
Drug Induced ◽  
Obstructive Pulmonary Disease ◽  
Immune Mediated ◽  
Drug Dependent ◽  
Low Sensitivity ◽  
Count Recovery

Drug-induced immune thrombocytopenia (D-ITP) typically occurs after the patient has been receiving the implicated drug for at least 1 week, due to newly forming drug-dependent antibodies (“typical-onset” D-ITP). A “rapid-onset” form of D-ITP can occur when previous sensitization has occurred, where antibodies have thus already been formed, and a precipitous platelet count fall occurs upon reexposure. Typical-onset D-ITP has been reported after levofloxacin, but the rapid-onset form with a well-documented previous exposure has not been described. We report a 76-year-old male treated with levofloxacin for acute exacerbation of chronic obstructive pulmonary disease. After a single 750 mg oral dose of levofloxacin, his platelet count fell from 187 to 5 × 109/L (nadir) over 4 days. Other causes of thrombocytopenia were ruled out. He had received a previous course of levofloxacin 6 months earlier. Discontinuation of levofloxacin and treatment with intravenous immunoglobulin and dexamethasone resulted in platelet count recovery. Levofloxacin-dependent antibodies were not detectable, consistent with the known low sensitivity of laboratory tests for drug-dependent antibodies, presumably indicating antibodies against levofloxacin metabolites, as is indirectly supported by the abrupt but relatively slow platelet count decline observed. This case illustrates a rapid-onset presentation of levofloxacin-induced D-ITP in the setting of previous drug exposure.

scholarly journals A Case of Hyperacute Severe Thrombocytopenia Occurring Less than 24 Hours after Intravenous Tirofiban Infusion

2018 ◽  
Vol 2018 ◽  
pp. 1-6
Author(s):  
Vineet Meghrajani ◽  
Nitin Sabharwal ◽  
Vinod Namana ◽  
Moustafa Elsheshtawy ◽  
Bernard Topi
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Percutaneous Transluminal Coronary Angioplasty ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Causative Drug ◽  
Drug Eluting ◽  
Drug Dependent ◽  
Transluminal Coronary Angioplasty ◽  
Peripheral Blood Smears

Thrombocytopenia is defined as a condition where the platelet count is below the lower limit of normal (<150 G/L), and it is categorized as mild (100–149 G/L), moderate (50–99 G/L), and severe (<50 G/L). We present here a 79-year-old man who developed severe thrombocytopenia with a platelet count of 6 G/L, less than 24 hours after intravenous tirofiban infusion that was given to the patient during a percutaneous transluminal coronary angioplasty procedure with placement of 3 drug-eluting stents. The patient’s baseline platelet count was 233 G/L before the procedure. Based on the timeline of events during hospitalization and laboratory evidence, it was highly likely that the patient’s thrombocytopenia was the result of tirofiban-induced immune thrombocytopenia, a type of drug-induced immune thrombocytopenia (DITP) which occurs due to drug-dependent antibody-mediated platelet destruction. Anticoagulant-mediated artefactual pseudothrombocytopenia was ruled out as no platelet clumping was seen on the peripheral blood smears. The treatment of DITP includes discontinuation of the causative drug; monitoring of platelet count recovery; or treatment of severe thrombocytopenia with glucocorticoids, IVIG, or platelet transfusions depending on the clinical presentation. The most likely causative agent of this patient’s thrombocytopenia—tirofiban—was discontinued, and the patient did not develop any signs of bleeding during the remainder of his hospital stay. His platelet count gradually improved to 24 G/L, and he was discharged on the sixth hospital day.

P8: CHEMOTHERAPY INDUCED IMMUNE THROMBOCYTOPENIA-AN ENTITY TO KEEP IN MIND!

2016 ◽  
Vol 64 (3) ◽  
pp. 820.2-820
Author(s):  
P Draksharam ◽  
J Park ◽  
G Sidhu
Keyword(s):  
Flow Cytometry ◽  
Platelet Count ◽  
Recovery Time ◽  
Immune Thrombocytopenia ◽  
Chemotherapeutic Agents ◽  
Metastatic Colon Cancer ◽  
Platelet Recovery ◽  
Platelet Antibodies ◽  
Drug Dependent ◽  
Platelet Transfusions

Purpose of StudyThrombocytopenia during chemotherapy is not always due to myelosuppression. We report an unusual case of isolated acute thrombocytopenia after oxaliplatin and irinotecan administration. We reviewed 11 reported cases to better understand the nature of the presentation and variability in response to treatment.Case ReportPatient is a 63 year old female with metastatic colon cancer treated with palliative chemotherapy with FOLFOX. Follwing her 14th cycle she had an episode of acute drop in platelet count to 8,000/microliter. Peripheral smear revealed no evidence of thrombotic microangiopathy. She was managed with supportive platelet transfusions with slow recovery of platelet count. Subsequently she was treated with second line chemotherapy with FOLFIRI. Following the first cycle of Irinotecan, she again had a catastrophic drop in platelets from 136,000/microliter to 6,000/microliter within 10 hours. Due to this recurrent episode, a drug mediated thrombocytopenia was suspected and work up was initiated. She was initially treated with dexamethasone without a significant response. Platelet count normalized after 7 days with supportive platelet transfusions.Methods UsedBlood was tested for drug dependent platelet antibodies by Flow Cytometry at the Platelet and Neutrophil Immunology Laboratory at the Blood Center of Wisconsin.Summary of ResultsThe patient's serum showed evidence of drug dependent platelet antibodies to both oxaliplatin and irinotecan.ConclusionsDrug mediated immune thrombocytopenia is not uncommon. Time to severe acute thrombocytopenia and platelet recovery time varied post exposure of the drug. It is unclear whether steroid or IVIG administration had any effect on the platelet recovery time. Recovery from thrombocytopenia was observed in all 11 cases after the discontinuation of the insulting agent. Confirmation of the presence of drug dependent platelet antibodies against the chemotherapeutic agent by flow cytometry essential for diagnosis. This would be the first reported case of acute thrombocytopenia to two different chemotherapeutic agents in the same patient. Whether the reaction is two different mechanisms or if there is a cross reactivity between Oxaliplatin and Irinotecan has yet to be investigated.

scholarly journals Insertion of central venous catheters in children undergoing bone marrow transplantation: is there a platelet level for a safe procedure?

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Ahmed Elgendy ◽  
Ahmed M. Ismail ◽  
Eslam Elhawary ◽  
Ahmed Badran ◽  
Mohammed Ramadan El-Shanshory
Keyword(s):  
Bone Marrow ◽  
Platelet Count ◽  
Bone Marrow Transplantation ◽  
Postoperative Complications ◽  
Marrow Transplantation ◽  
Central Venous Catheters ◽  
Bleeding Complications ◽  
Safe Procedure ◽  
Central Venous ◽  
Platelet Transfusions

Abstract Background Bone marrow transplantation (BMT) is a therapeutic procedure for the management of several hematological diseases and malignancies in pediatric population. Central venous catheters (CVCs) play a pivotal role during the process of BMT. The aim of this study was to compare the complications of CVCs placements in children undergoing BMT with platelet levels above and below 50,000/μL and also to detect if there is a platelet count for a safe insertion. This prospective study included all children who had placements of tunneled CVCs during BMT at our hospital between March 2017 and March 2020. Procedures were divided into two groups accordingly to preoperative platelet counts (above and below 50,000/μL). Data were compared between both groups regarding postoperative complications including bleeding or catheter-related blood stream infections (CRBSIs). Results Forty-six CVC insertions were performed in 40 patients. There were 20 procedures below 50,000/μL (median 27,500; range 5000–42,000) inserted with perioperative platelet transfusions, and their postoperative levels were median 59,500/μL, range 18,000–88,000. Allogeneic BMT was adopted in 39 patients (97.5%). Beta thalassemia major was the commonest indication (21/40, 52.5%), followed by acute lymphocytic leukemia in six patients (15%). There were nine postoperative complications (bleeding n = 2 and CRBSIs n = 7) encountered in all placements. Four of them occurred in insertions below 50,000/μL (two bleeding complications that managed conservatively, and two CRBSIs). Post-procedural morbidities regarding bleeding or CRBSIs did not differ significantly between both groups (p value = 0.099 and 0.695, respectively). Conclusions Postponement of CVC insertions in thrombocytopenic children due to the fear of potential complications seems unwarranted, as it has no significant impact on the morbidity. Placements of such catheters can be safe under cover of perioperative platelet transfusions irrespective of the preoperative platelet count.

Postendarterectomy heparin-induced thrombocytopenia

1988 ◽  
Vol 69 (4) ◽  
pp. 632-634 ◽  
Author(s):  
Larry A. Rogers
Keyword(s):  
Platelet Count ◽  
Vascular Surgery ◽  
Carotid Endarterectomy ◽  
Potential Problem ◽  
Anticoagulation Therapy ◽  
Massive Bleeding ◽  
Drug Induced ◽  
Heparin Induced Thrombocytopenia ◽  
Content Type ◽  
Fine Print

✓ Two episodes of massive bleeding from a sutured arteriotomy were observed within 30 hours after carotid endarterectomy. The patient had received anticoagulation therapy with heparin for 72 hours prior to surgery. A platelet count of 93,000/cu mm was demonstrated following the second hemorrhage. The potential problem of drug-induced thrombocytopenia following vascular surgery is discussed.

Pantoprazole-induced Thrombocytopenia: Unresponsive to Corticosteroid and Thrombocyte Concentrate Transfusion

2021 ◽  
pp. 089719002110647
Author(s):  
Widyati ◽  
Nurul Latifah ◽  
Maya Ramadhani
Keyword(s):  
Platelet Count ◽  
Prophylactic Therapy ◽  
Immune Mechanism ◽  
Drug Induced ◽  
Stress Ulcers ◽  
Present Case Report ◽  
Once Daily ◽  
Mucosal Disease ◽  
Critical Ill Patients ◽  
Critical Ill

Introduction Pantoprazole is a proton pump inhibitor (PPI) class drug that is widely used in the treatment of SRMD (stress-related mucosal disease in critical ill patients. PPI are one class of drugs used commonly both for treatment and prophylactic therapy for stress ulcers in intensive care unit (ICU). Case We report a case of a 51-year old male who was referred to PKU Hospital. He was admitted to ICU with diagnosis of Hyperosmolar Hyperglymic State and bronchopneumonia. Thrombocytopenia was noted in admission. There was more than 70% decrease in platelet count after initiation of pantoprazole. Patient received Thrombocyte Concentrate (TC) transfusion and corticosteroid iv for several days, but only had minor increase in platelet count. The platelets recovered after stopping pantoprazole. Discussion In the present case report, another exposures to parenteral pantoprazole in a dose of 40 mg once daily reproduced the same adverse drug reaction. In comparison to lansoprazole, thrombocytopenia from pantoprazole is more severe that necessitate TC transfusion and corticosteroid trial. However, in the present case, TC transfusion and corticosteroid fail to escalate platelet count. This finding suggests probability of non-immune mechanism of pantoprazole-induced thrombocytopenia. Conclusion Pantoprazole may induce thrombocytopenia with new features that were immediately developed, resulting a decrease in platelet count >70%. The mechanism found in this case may be non-immune. Drug-induced thrombocytopenia is one of the rare complications that has to be kept in mind with the use of pantoprazole.

Drug-Induced Thrombocytopenia

2009 ◽  
Vol 133 (2) ◽  
pp. 309-314
Author(s):  
Barton Kenney ◽  
Gary Stack
Keyword(s):  
At Risk ◽  
19Th Century ◽  
Clinical Management ◽  
Drug Induced ◽  
Medication Withdrawal ◽  
Platelet Antibodies ◽  
Patients At Risk ◽  
Drug Dependent ◽  
The 19Th Century ◽  
Prompt Diagnosis

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.

Heparin-induced thrombocytopenia: when a low platelet count is a mandate for anticoagulation

Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel
Keyword(s):  
Platelet Count ◽  
Heparin Therapy ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated ◽  
Number Of Patients ◽  
Increased Risk ◽  
Antibody Levels

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.

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