scholarly journals Trombocitopenia Grave Induzida por Fenofibrato

2020 ◽  
Vol 33 (1) ◽  
pp. 58 ◽  
Author(s):  
Ana Clara ◽  
Tiago Martins ◽  
Alexandra Martins ◽  
Ana Baptista ◽  
Mário Lázaro
Keyword(s):  
Immune Thrombocytopenia ◽  
Clinical Case ◽  
Rare Event ◽  
Drug Induced ◽  
Corticosteroid Administration ◽  
Fenofibrate Treatment ◽  
Immune Mediated ◽  
Drug Removal ◽  
Life Threatening ◽  
Purpuric Rash

Drug-induced thrombocytopenia is a common entity in clinical practice. However, having in consideration the severity of the case, it becomes imperative to distinguish non-immune thrombocytopenia from the po-tentially life-threatening immune-mediated forms. The authors report a rare clinical case of a 79-year-old man presenting with purpuric rash and gingival hemorrhage while on fenofibrate treatment (sixth day). The evolu-tion was favorable after drug removal and corticosteroid administration. Drug-associated thrombocytopenia is reported by manufacturers as an extremely rare event. This is the second case report of immune throm-bocytopenia to fenofibrate. The first event was reported for publication in 2015.

scholarly journals Vancomycin-induced Severe asymptomatic Immune Thrombocytopenia; a rare cause

2014 ◽  
Vol 3 (9) ◽  
pp. 42 ◽  
Author(s):  
Yasir Ahmed ◽  
Christopher Sartin ◽  
Imran Umer ◽  
Osama Mukarram ◽  
Renuka Borra
Keyword(s):  
Immune Thrombocytopenia ◽  
Rare Case ◽  
Temporal Relationship ◽  
Clinical Problem ◽  
Drug Induced ◽  
Platelet Antibodies ◽  
Immune Mediated ◽  
Common Causes ◽  
Life Threatening

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.

scholarly journals Case Report: Oxaliplatin-Induced Immune-Mediated Thrombocytopenia

2018 ◽  
Vol 11 (3) ◽  
pp. 880-882 ◽  
Author(s):  
Elizabeth Pan ◽  
Eric Hsieh ◽  
Caroline Piatek
Keyword(s):  
Case Report ◽  
Cancer Therapy ◽  
Cancer Patients ◽  
Immune Thrombocytopenia ◽  
Drug Induced ◽  
Gastrointestinal Malignancies ◽  
Common Cause ◽  
Immune Mediated ◽  
Chemotherapy Agents ◽  
Platinum Derivative

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.

A Comparison of Two Assays for Platelet Antibodies

1979 ◽  
Author(s):  
J.G. Kelton ◽  
A. Giles ◽  
P.B. Neame ◽  
M. Blajchman ◽  
J. Hirah
Keyword(s):  
Multiple Myeloma ◽  
Immune Thrombocytopenia ◽  
Test System ◽  
Healthy Controls ◽  
Fluorescent Assay ◽  
Drug Induced ◽  
Optimal Method ◽  
Platelet Antibodies ◽  
Immune Mediated ◽  
Fluorescence Test

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.

scholarly journals Postanesthetic Severe Oral Angioedema in Patient’s Taking Angiotensin-Converting Enzyme Inhibitor

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Acílio Marques ◽  
Carla Retroz-Marques ◽  
Sara Mota ◽  
Raquel Cabral ◽  
Matos Campos
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Ace Inhibitors ◽  
Clinical Case ◽  
Enzyme Inhibitor ◽  
Converting Enzyme ◽  
Drug Induced ◽  
Life Threatening ◽  
Perioperative Safety ◽  
Improve Patient

Angiotensin-converting enzyme (ACE) inhibitors are the leading cause of a drug-induced angioedema. This occurrence is frequently underdiagnosed, but its relapse can be life-threatening. The authors’ intention in reporting this clinical case is to sound a warning about reviewing attitudes and surveillance to try to improve patient perioperative safety.

Drug-Dependent Murine Monoclonal Antibodies (mAbs) Mimic Antibodies Found in Patients with Drug-Induced Immune Thrombocytopenia (TP).

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 731-731
Author(s):  
Daniel W. Bougie ◽  
Jessica Birenbaum ◽  
Scott Ahl ◽  
Richard H. Aster
Keyword(s):  
Molecular Basis ◽  
Immune Thrombocytopenia ◽  
Tight Binding ◽  
Human Platelets ◽  
Soluble Form ◽  
Membrane Glycoproteins ◽  
Drug Induced ◽  
Life Threatening ◽  
Drug Dependent ◽  
Covalently Linked

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.

scholarly journals Tuberculosis with Immune Thrombocytopenia an Unusual Association

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 12-12
Author(s):  
Shehab Fareed Mohamed ◽  
Mohammed Alkhatib ◽  
Khaled Elfert ◽  
Ahmed Othman ◽  
Dina Sameh Soliman ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Immune Thrombocytopenia ◽  
English Language ◽  
Conflicts Of Interest ◽  
Bone Marrow Aspiration ◽  
Significant Heterogeneity ◽  
Drug Induced ◽  
Immune Mediated ◽  
Hematological Manifestations ◽  
Idiopathic Thrombocytopenia Purpura

Introduction Tuberculosis (TB) and is the leading infectious cause of death in adult's worldwide.TB can have a wide variety of presentations manifestation. Hematological manifestations of tuberculosis have different forms and one of the rare associated is TB with isolated thrombocytopenia. ITP is relatively common autoimmune bleeding disorder.. However, ITP is very rarely associated with TB with only a few cases reported. Isolated Thrombocytopenia in TB is multifactorial and could be explained by different mechanisms as follows Immune-mediated platelet destruction through antiplatelet antibodies as mycobacterium TB may share antibodies with platelets or platelet-associated immunoglobulin, Tuberculosis-induced hemophagocytosis, Defective platelet production due to bone marrow (BM) infiltration, Hypersplenism, intravascular coagulation, anti-tuberculous treatment (ATT) induced thrombocytopenia. Methodology We reviewed the literature using PubMed, google scholar and English language articles only. We have included all the reported cases of tuberculosis and immune thrombocytopenia if it is associations or initial presentations using the keyword: tuberculosis. Pulmonary tuberculosis, immune thrombocytopenia, Idiopathic thrombocytopenia purpura and we excluded drug induced thrombocytopenia. Our review identified forty-two cases in total, in our review Baseline and clinical characteristics are provided. Results Of the forty-two cases identified, more than one quarter of cases (n=12) were from India; the remainder of the reported cases from thirteen different countries. Gender was nearly equally distributed (males n= 21, females n=20, one case unknown); age ranged from 4 to 74 years. The most reported sites of TB as follows; lung (n=20), disseminated (n=8), lymph nodes (n=6), abdomen (n=4), mediastinum (n=2), spleen (n=1) and knee (n=1). Bone marrow aspiration and biopsy done in 27 cases, three of them (7%) found granuloma and 14 (32%) found to have normal to hyprecellular marrow with increased number of megakaryocytes. Of the forty-two cases, ITP was the first presentation of TB with or without typical TB symptoms and signs in more than three quarters of the cases (n=33), while ITP was discovered in TB patients in routine investigations without obvious bleeding symptoms or signs in only four cases. Hemorrhagic symptoms were reported in most of the cases (n=31), skin manifestations (petechiae/purpura/ecchymosis) being the most common (n=28). The therapeutic approach to TB-associated ITP showed significant heterogeneity with Anti tuberculous treatment and first- and/or second-line treatment for ITP given with or without platelets transfusion. Most of the cases (n=36) achieved full recovery with Anti-tuberculous treatment(ATT) and IVIG ± Steroids. Of the 42 cases, six cases were treated with blood and platelet transfusion for thrombocytopenia which did not normalize the platelet count as thrombocytopenia as expected as this is most likely an immune mediated phenomenon. Conclusion Unfortunately, there are no clear guidelines for management of TB-associated ITP and is anecdotal or observational at best. This highlights the importance of conducting prospective and standardized studies in the future. We found that Anti tuberculous treatment could have play pivotal role in management of ITP in TB Patients. Figure Disclosures No relevant conflicts of interest to declare.

scholarly journals Pathophysiology and Diagnosis of Drug-Induced Immune Thrombocytopenia

2020 ◽  
Vol 9 (7) ◽  
pp. 2212 ◽  
Author(s):  
Caroline Vayne ◽  
Eve-Anne Guéry ◽  
Jérôme Rollin ◽  
Tatiana Baglo ◽  
Rachel Petermann ◽  
...  
Keyword(s):  
Immune Thrombocytopenia ◽  
Clinical Syndrome ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Platelet Factor ◽  
Life Threatening ◽  
Thrombotic Complications ◽  
Drug Dependent

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.

scholarly journals Drug-induced acute pancreatitis: pathogenetic mechanisms

2021 ◽  
pp. 35-43
Author(s):  
O.D. Ostroumova ◽  
◽  
E.S. Akimova ◽  
A.I. Kochetkov ◽  
◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Functional Impairment ◽  
Metabolic Disorders ◽  
Medicinal Products ◽  
Drug Induced ◽  
Cytotoxic Effects ◽  
Medical Practitioners ◽  
Immune Mediated ◽  
Life Threatening ◽  
Hazardous Drugs

Drug-induced (DI) acute pancreatitis (AP) is a difficultly diagnosed disease amounting to 2% among all AP cases that may lead to development of life-threatening complications. This article considers potentially hazardous medicinal products as well as the most significant variants of the pancreas: structural and functional impairment of the pancreatic duct, direct cytotoxic effects, metabolic disorders, vascular disorders, immune-mediated damage to the pancreas and hypersensitivity. The review was performed based on the publications present in the E-library and PubMed databases dated 1965-2020. Due to regular publication of reports on potential associations between specific medicinal products and AP development, medical practitioners must be informed about the potentially hazardous drugs and mechanisms of DI AP development.

Drug-Induced Immune Thrombocytopenia

2014 ◽  
Vol 27 (5) ◽  
pp. 430-439 ◽  
Author(s):  
Teresa Kam ◽  
Maurice Alexander
Keyword(s):  
Data Collection ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Immune Thrombocytopenia ◽  
Treatment Options ◽  
Diagnosis And Treatment ◽  
Drug Induced ◽  
Laboratory Findings ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated

Thrombocytopenia is commonly seen in laboratory findings, especially in critically ill patients. Although the incidence is rare, drug-induced immune thrombocytopenia (DITP) is a serious complication that is often overlooked as a cause of thrombocytopenia. Over the last century, extensive research and data collection have been done in an attempt to better characterize DITP. Heparin-induced thrombocytopenia is the most common DITP and has distinct pathogenesis, diagnosis, and treatment options. However, other offending medications are less well known and have triggered many questions and constant search for answers. This review will discuss both drug-induced immune-mediated and nonimmune-mediated thrombocytopenias, with a focus on immune-mediated processes. Thrombocytopenia caused by chemotherapy will not be discussed in this article.

Platelets: An Update on Diagnosis and Management of Thrombocytopenic Disorders

Hematology ◽  
2001 ◽  
Vol 2001 (1) ◽  
pp. 282-305 ◽  
Author(s):  
Keith R. McCrae ◽  
James B. Bussel ◽  
Pier M. Mannucci ◽  
G. Remuzzi ◽  
Douglas B. Cines
Keyword(s):  
Single Agent ◽  
Pregnant Patient ◽  
Drug Induced ◽  
Platelet Factor ◽  
Alternative Interventions ◽  
Diagnosis And Management ◽  
Asymptomatic Patients ◽  
Immune Mediated ◽  
Life Threatening ◽  
Refractory Itp

Abstract Thrombocytopenia in the pregnant patient may result from a number of causes, most of which involve either immune-mediated platelet destruction or platelet consumption. Many of these disorders share clinical and laboratory features, making accurate diagnosis difficult. Moreover, uterine evacuation is indicated in the therapy of some disorders, while in others alternative interventions may allow the pregnancy to be carried to term. These and other issues are discussed as part of a comprehensive review of the differential diagnosis and management of thrombocytopenia in pregnancy. The term “refractory ITP” is used with reference to two distinct groups of patients: 1) patients in whom the platelet count cannot be easily increased, including those who are poorly responsive to initial single agent treatment, and 2) those with persistent thrombocytopenia despite the use of conventional therapies. An approach to management of the former group will be presented, followed by a discussion of patients with chronic refractory ITP. The latter will include presentation of new data on the role of Helicobacter pylori in ITP and whether its treatment ameliorates thrombocytopenia, as well as the use of rituximab and other modalities. Thrombotic microangiopathies such as thrombotic thrombocytopenic purpura (TTP) are rare, but life threatening causes of thrombocytopenia. Ultra-large multimers of von Willebrand factor (vWF) aggregate platelets intravascularly, and congenital or immune-mediated deficiencies of a metalloprotease that cleaves these ultra-large multimers may cause TTP. However, little information exists concerning the behavior of this protease in other physiological and pathological conditions. Levels of this protease have now been measured in healthy individuals of different ages, full-term newborns, pregnant women and a patients with variety of pathologic conditions, and these data will be reviewed herein. Heparin-induced thrombocytopenia/thrombosis (HIT/T) remains the most common antibody-mediated, drug-induced thrombocytopenic disorder, and a leading cause of morbidity and mortality. Based on clinical correlations and murine models, there is increasing evidence that antibodies to complexes between platelet factor 4 (PF4) and heparin cause HIT/T, and the molecular composition of the relevant antigen has also become better defined. However, the introduction of sensitive ELISAs to measure anti-PF4/heparin antibodies has complicated diagnosis in some settings in which the incidence of such antibodies in unaffected patients exceeds the incidence of the disease. In addition, the FDA approval of Lepirudin and Argatroban has expanded the repertoire of agents available for therapy of HIT/T and may change the approach to management of asymptomatic patients with thrombocytopenia. However, the optimal use of these drugs in commonly encountered settings remains in evolution, and a need for alternative approaches to prevention and treatment is evident.

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