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.

scholarly journals FP263A COMPARISON BETWEEN BIOIMPEDANCE DATA, LUNG ULTRASONOGRAPHY AND FLUID ACCCUMULATION. THREE CARDS TO DETERMINATE THE STATE OF EUVOLEMIA AND FLUID OVERLOAD IN CRITICAL ILL PATIENTS

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i119-i119
Author(s):  
Francisco Javier Centellas Pérez ◽  
Mercedes Martínez Díaz ◽  
Angela Prado Mira ◽  
Agustín Ortega Cerrato ◽  
Jaime López Tendero ◽  
...  
Keyword(s):  
Fluid Overload ◽  
The State ◽  
Lung Ultrasonography ◽  
Critical Ill Patients ◽  
Critical Ill

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.

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.

scholarly journals Thrombocytopenia in children: a clinico-etiological profile in an urban tertiary care hospital

2018 ◽  
Vol 6 (1) ◽  
pp. 131
Author(s):  
Subramanian V. ◽  
Santosh Kumar K.
Keyword(s):  
Platelet Count ◽  
Viral Infections ◽  
Tertiary Care ◽  
Care Hospital ◽  
Drug Induced ◽  
Medical College ◽  
Clinical Complications ◽  
Paediatric Department ◽  
The Relationship ◽  
Haematological Finding

Background: Thrombocytopenia is a common haematological finding that we come across while managing a sick child. Etiological profile and presentation of thrombocytopenia varies among children. The objective of this study was to study the clinical and laboratory profile of children with thrombocytopenia, associated clinical complications and assess the relationship between platelet levels and severity of disease.Methods: The study was carried out in 644 children between 1 month and 12 years, admitted in Paediatric Department of Raja Rajeshwari medical college and hospital, Bangalore between August 2012 to August 2014.Results: The commonest causes of thrombocytopenia in our study were of infectious aetiology (86.6%). Among Infections Viral infections were the major cause in more than 78% of cases. Other causes included haematological problems, drug induced thrombocytopenia and connective tissue disorders. Bleeding manifestations were present in 33.07% of patients and the commonest bleeds were skin and mucous membranes. Bleeding manifestations were seen most commonly in children with a platelet count less than 50000/µl.Conclusions: Viral Infections were the commonest cause for thrombocytopenia in Children. Platelet count was neither predictive of bleeding manifestations nor predictive of need for platelet transfusion.

scholarly journals Ionized or Total Magnesium levels, what should we measure in critical ill patients?

2021 ◽  
Vol 23 (4) ◽  
Author(s):  
Giuliana Scarpati ◽  
Daniela Baldassarre ◽  
Filomena Oliva ◽  
Gabriele Pascale ◽  
Ornella Piazza
Keyword(s):  
Critical Ill Patients ◽  
Total Magnesium ◽  
Critical Ill

scholarly journals Clinical spectrum and severity of hemolytic anemia in glucose 6-phosphate dehydrogenase–deficient children receiving dapsone

Blood ◽  
2012 ◽  
Vol 120 (20) ◽  
pp. 4123-4133 ◽  
Author(s):  
Allan Pamba ◽  
Naomi D. Richardson ◽  
Nick Carter ◽  
Stephan Duparc ◽  
Zul Premji ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Hemolytic Anemia ◽  
G6pd Deficiency ◽  
Case Reports ◽  
Drug Induced ◽  
Once Daily ◽  
Maximum Decrease ◽  
Life Threatening ◽  
The Mean ◽  
Glucose 6 Phosphate Dehydrogenase

AbstractDrug-induced acute hemolytic anemia led to the discovery of G6PD deficiency. However, most clinical data are from isolated case reports. In 2 clinical trials of antimalarial preparations containing dapsone (4,4′-diaminodiphenylsulfone; 2.5 mg/kg once daily for 3 days), 95 G6PD-deficient hemizygous boys, 24 G6PD-deficient homozygous girls, and 200 girls heterozygous for G6PD deficiency received this agent. In the first 2 groups, there was a maximum decrease in hemoglobin averaging −2.64 g/dL (range −6.70 to +0.30 g/dL), which was significantly greater than for the comparator group receiving artemether-lumefantrine (adjusted difference −1.46 g/dL; 95% confidence interval −1.76, −1.15). Hemoglobin concentrations were decreased by ≥ 40% versus pretreatment in 24/119 (20.2%) of the G6PD-deficient children; 13/119 (10.9%) required blood transfusion. In the heterozygous girls, the mean maximum decrease in hemoglobin was −1.83 g/dL (range +0.90 to −5.20 g/dL); 1 in 200 (0.5%) required blood transfusion. All children eventually recovered. All the G6PD-deficient children had the G6PD A− variant, ie, mutations V68M and N126D. Drug-induced acute hemolytic anemia in G6PD A− subjects can be life-threatening, depending on the nature and dosage of the drug trigger. Therefore, contrary to current perception, in clinical terms the A− type of G6PD deficiency cannot be regarded as mild. This study is registered at http://www.clinicaltrials.gov as NCT00344006 and NCT00371735.

Critical ill patients and flight

2017 ◽  
Vol 10 (4) ◽  
pp. 1079
Author(s):  
Beuy Joob ◽  
Viroj Wiwanitkit
Keyword(s):  
Critical Ill Patients ◽  
Critical Ill

scholarly journals Prophylactic Therapy of Silymarin (Milk Thistle) on Antituberculosis Drug-Induced Liver Injury: A Meta-Analysis of Randomized Controlled Trials

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Lina Tao ◽  
Xiaoyu Qu ◽  
Yue Zhang ◽  
Yanqing Song ◽  
Si-xi Zhang
Keyword(s):  
Liver Injury ◽  
Liver Function ◽  
Randomized Controlled Trials ◽  
Controlled Trials ◽  
Cochrane Central Register ◽  
Prophylactic Therapy ◽  
Antituberculosis Drug ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Randomized Controlled

Background. Prophylactic therapy with silymarin to prevent the development of antituberculosis drug-induced liver injury (anti-TB DILI) has been under debate. We aimed to evaluate the effect of silymarin in the prevention of anti-TB DILI. Methods. We searched MEDLINE, PubMed, Embase, and Cochrane Central Register of Controlled Trials (CENTRAL) up to 30th November 2018. Randomized controlled trials (RCTs) that compared silymarin and placebo to prevent anti-TB DILI were included. All statistical analyses were conducted using STATA 12.0 software. Standardized mean difference (SMD) and risk ratio (RR) with 95% confidence intervals (CIs) were used to evaluate the effect of silymarin. The quality of included studies was assessed according to Cochrane handbook. Funnel plots and Egger’s tests were carried out to evaluate publication bias. Sensitivity analysis was conducted to assess the influence of each study. Results. A total of 1198 patients from five RCTs (585 with silymarin and 613 with placebo groups) were included. Overall, silymarin significantly reduced the occurrence of anti-TB DILI at week 4 [RR: 0.33, 95% CI (0.15, 0.75)]. In addition, silymarin exerted protective effect on liver function in patients undergoing anti-TB drugs [SMD = − 0.15, 95% CI (−0.24, −0.07), P < 0.001 (ALT); SMD =−0.14, 95% CI (−0.23, −0.06), P = 0.001(AST); SMD =−0.12, 95% CI (−0.20, −0.03), P = 0.008 (ALP)]. Silymarin led to similar AEs in placebo groups [OR: 1.09, 95% CI (0.86, 1.39), P = 0.47]. Conclusion. Prophylactic therapy of silymarin is contributed to a noticeably reduced risk of development of anti-TB DILI four weeks after the initiation. In addition, silymarin significantly improved the liver function in patients who are receiving anti-TB drugs.

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