scholarly journals Adalimumab‐induced platelet antibodies resulting in severe thrombocytopenia

2021 ◽  
Author(s):  
Henk Jan Boiten ◽  
Sufia Amini ◽  
Frank H.J. Wolfhagen ◽  
Peter E. Westerweel
Keyword(s):  
Severe Thrombocytopenia ◽  
Platelet Antibodies

IgM and IgG Platelet Antibodies in a Case of Infectious Mononucleosis and Severe Thrombocytopenia

2009 ◽  
Vol 32 (2) ◽  
pp. 145-148 ◽  
Author(s):  
M. C. Kappers-Klunne ◽  
H. H. D. M. Vliet
Keyword(s):  
Infectious Mononucleosis ◽  
Severe Thrombocytopenia ◽  
Platelet Antibodies

scholarly journals Acute Immune-Mediated Thrombocytopenia due to Oxaliplatin and Irinotecan Therapy

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Eric L. Tam ◽  
Padma L. Draksharam ◽  
Jennifer A. Park ◽  
Gurinder S. Sidhu
Keyword(s):  
Colon Cancer ◽  
Flow Cytometry ◽  
Severe Thrombocytopenia ◽  
Flow Cytometry Assay ◽  
Drug Induced ◽  
Advanced Colon Cancer ◽  
Platelet Antibodies ◽  
Immune Mediated ◽  
Drug Dependent ◽  
Underlying Mechanisms

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.

scholarly journals Adalimumab-induced platelet antibodies resulting in severe thrombocytopenia

2021 ◽  
Author(s):  
Henk-Jan Boiten ◽  
Sufia Amini ◽  
Frank Wolfhagen ◽  
Peter Westerweel
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Laboratory Tests ◽  
Tumor Necrosis ◽  
Bone Marrow Suppression ◽  
Severe Thrombocytopenia ◽  
Necrosis Factor Alpha ◽  
Platelet Antibodies ◽  
Factor Alpha ◽  
Necrosis Factor

Anti-tumor necrosis factor alpha (TNFα) agents are effective in diseases including Crohn’s disease (CD) but may cause cytopenias. The mechanisms involved in anti-TNFα agents induced thrombocytopenia are scarce. We report a 73-year-old male with Crohn’s disease for which he currently used adalimumab, an anti-TNFα agent. He had received mesalazine and infliximab before the treatment of adalimumab. No comorbidities were present. Routine laboratory tests revealed a deep thrombocytopenia (thrombocytes 24x10*9/L) after which adalimumab was discontinued. Bleeding symptoms included cutaneous hematomas and mild epistaxis. Direct monoclonal antibody-specific immobilization of platelet antigens (MAIPA assay) revealed autoantibodies specific to glycoprotein IIb/IIIa (GPIIb/IIIa) and glycoprotein V (GPV) platelet receptors. There was no bone marrow suppression. Other causes of the thrombocytopenia were ruled out. The platelet count normalized after adalimumab discontinuation. No further interventions were required. Monitoring thrombocyte levels after initiating anti-TNFα agents is recommended, which could lead to prevention of this potential fatal phenomenon.

Megakaryocyte Abnormalities Occur In The Absence Of Cell-Mediated Immunity In a Murine Model Of Passive Immune Thrombocytopenia (ITP)

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3537-3537
Author(s):  
John W. Semple ◽  
Kristin Hunt ◽  
Yu Hou ◽  
Rukhsana Aslam ◽  
Edwin R. Speck ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Immune Thrombocytopenia ◽  
Conflicts Of Interest ◽  
In Vivo Model ◽  
Cell Mediated Immunity ◽  
Severe Thrombocytopenia ◽  
Platelet Destruction ◽  
Platelet Counts ◽  
Antiplatelet Antibodies ◽  
Platelet Antibodies

Abstract Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by increased peripheral immune platelet destruction and megakaryocyte defects in the bone marrow. Although ITP was originally thought to be primarily due to humoral mediated autoimmunity it is now evident that T cells can also play a contributing role to the thrombocytopenia. In fact, the exact interplay between platelet destruction, megakaryocyte dysfunction, and the elements of both the humoral and cell mediated immune systems still remain incompletely defined. In murine passive models of ITP, the direct administration of anti-platelet antibodies can result in severe thrombocytopenia which is evident within 24 hours of injection. While most studies have focused on immune platelet destruction in the spleen, an additional possibility is that the anti-platelet antibody also has an effect on megakaryocytes. To unequivocally determine if antiplatelet antibodies have an effect on megakaryocytes in an in vivo model, BALB/c mice were intravenously administered 2 ug of an anti-GPIIbIIIa antibody (MReg30) or 50 uL of a high tittered anti-GPIIIa (anti-β3) serum from BALB/c GPIIIa (CD61) knockout mice immunized with wild type platelets. Platelet counts were assessed over time and the bone marrow and spleens were harvested for histological examination of megakaryocytes. Both preparations of antiplatelet antibodies significantly reduced platelet numbers within 1 day of antibody or serum administration. This thrombocytopenia could be rescued by administration of 2 g/kg of IVIg ip. Compared with naïve control mice, histological (H&E staining) examination of the bone marrow and spleens revealed that megakaryocytes were significantly increased in number and all exhibited abnormalities consistent with apoptosis e.g. pyknotic nuclei. IVIg administration completely prevented these megakaryocyte abnormalities. These results show that passively administered anti-platelet antibodies not only affect platelet counts but also significantly affect megakaryocyte physiology in the absence of cell mediated immunity. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Púrpura trombocitopénica idiopática en el embarazo: a propósito de un caso

2021 ◽  
Vol 81 (04) ◽  
pp. 411-414
Author(s):  
Claudia Milena López-López ◽  
◽  
Luis Carlos Gerena-Pallares
Keyword(s):  
Platelet Count ◽  
First Trimester ◽  
Reticuloendothelial System ◽  
Severe Thrombocytopenia ◽  
Third Trimester ◽  
Platelet Antibodies ◽  
History Of ◽  
First Trimester Of Pregnancy ◽  
Fetal Wellbeing ◽  
Time Of Admission

Idiopathic purple thrombocytopenia is a hemorrhagic pathology, characterized by a decrease in the platelet count during pregnancy, mediated by cells and anti-platelet antibodies, causing the premature destruction of platelets by the reticuloendothelial system, which during pregnancy could lead to a commitment to maternal fetal wellbeing in severe stages. This pathology occurs in 1 out of every 1,000 to 10,000 pregnancies, and corresponds to 3% of thrombocytopenic pregnancies. The goal of management is to maintain platelet counts within safe ranges, recommending starting harmacological management when a platelet count lower than 10,000 / uL is found at any time during pregnancy or 30,000 / uL in the second or third trimester. The case presented corresponds to a 40-yearold woman in the first trimester of pregnancy with a history of chronic idiopathic purple thrombocytopenic, with severe thrombocytopenia at the time of admission to the Hospital. Keywords: Idiopathic thrombocytopenic purpura. Pregnancy. Blood platlets.

scholarly journals Severe Thrombocytopenia Induced by Vancomycin-Dependent Anti-Platelet Antibodies

CHEST Journal ◽  
2017 ◽  
Vol 152 (4) ◽  
pp. A299 ◽  
Author(s):  
Irene Swanenberg ◽  
Samir Bhalla ◽  
Diana Altshuler ◽  
Mark Adelman ◽  
Lilith Colon ◽  
...  
Keyword(s):  
Severe Thrombocytopenia ◽  
Platelet Antibodies

Immune mediated destruction of platelets in dogs with heat stroke: A prospective study

2009 ◽  
Vol 37 (05) ◽  
pp. 314-318 ◽  
Author(s):  
L. Keller ◽  
K. Meichner ◽  
S. Unterer ◽  
K. Hartmann ◽  
I. Zenker
Keyword(s):  
Heat Stroke ◽  
Treatment Protocol ◽  
Severe Thrombocytopenia ◽  
Prospective Evaluation ◽  
Antiplatelet Antibodies ◽  
Time Period ◽  
Immune Mediated ◽  
Standardized Treatment ◽  
A Prospective Study ◽  
Risk For Bleeding

Summary Objective: Severe thrombocytopenia is a common sequelae to heat stroke in dogs. So far it has been hypothezised that it is due to disseminated intravascular coagulation. We hypothezised that it is due to immune mediated destruction via antiplatelet antibodies. Material and methods: Prospective evaluation of dogs with heat stroke from May 2005 to August 2008. Dogs that developed severe thrombocytopenia within 5 days of admission were included in the study. All dogs were treated with a standardized treatment protocol. In addition, they received either immunoglobulins or prednisolone. Results: Six dogs were presented with heat stroke during that time period. Four developed a severe thrombocytopenia. All four dogs tested positive for antiplatelet antibodies and did not have elevated D-Dimers at that time. Platelet count in three dogs recovered fully, one dog was euthanized due to liver and renal failure. Conclusion: In those cases thrombocytopenia was due to immune mediated destruction not due to DIC. Clinical rele-vance: Due to the severity of the thrombocytopenia and the high risk for bleeding in those patients, immunosuppressive therapy in addition to DIC prophylaxis should be discussed.

Effect of Congo Red on Blood Platelets and Leucocytes of Rabbits and Cats

1971 ◽  
Vol 26 (03) ◽  
pp. 488-492 ◽  
Author(s):  
Th B. Tschopp ◽  
H.-R Baumgartner ◽  
A Studer
Keyword(s):  
Fatty Acids ◽  
Congo Red ◽  
Platelet Rich Plasma ◽  
Blood Platelets ◽  
Severe Thrombocytopenia ◽  
Ultrastructural Alterations ◽  
Indirect Mechanism

SummaryIn rabbits and cats Congo red administered intravenously causes severe thrombocytopenia and ultrastructural alterations of platelets and leucocytes, similar to those produced by some fatty acids and endotoxin. Transient leucopenia is followed by leucocytosis. In contrast, incubation of Congo red in citrated blood or platelet rich plasma has no effect. Therefore, an indirect mechanism is postulated to explain the in vivo effect of Congo red.

Severe Thrombocytopenia and Platelet Granule Dysfunction Associated with the Combination of Novel Heterozygous Variants in TUBB1 and ITGB3

2019 ◽  
Author(s):  
D. Pillitteri ◽  
S. Sollfrank ◽  
K. Althaus ◽  
S. Heine ◽  
K. Lackner ◽  
...  
Keyword(s):  
Severe Thrombocytopenia

CLINICAL FEATURES AND COAGULATION ABNORMALITIES IN CHILDREN WITH SEPSIS AT DANANG HOSPITAL FOR WOMEN AND CHILDREN

2018 ◽  
pp. 97-103
Author(s):  
Huu Hoi Vo ◽  
Binh Bao Son Bui
Keyword(s):  
Septic Shock ◽  
Clinical Features ◽  
Cross Sectional Study ◽  
Severe Thrombocytopenia ◽  
Cross Sectional ◽  
Hematologic Tests ◽  
Coagulation Abnormalities ◽  
Women And Children ◽  
Key Words Coagulation ◽  
Coagulation Dysfunction

Objective: To determine the relationship between coagulation abnormalities and main clinical features, and hematologic tests. Methods: A descriptive cross-sectional study was conducted in 65 children with sepsis at the PICU, Da Nang Hospital for Women and Children from April 2012 to June 2013. Results: The frequency of internal hemorrhage in septic shock children was significantly higher than in children with sepsis (p < 0.001). The rate of thrombocytopenia was 30.8%, in which 10.8% of the children had severe thrombocytopenia (<50 x 109/l). Hypofibrinogenemia was observed in 30.8% of the patients, in which severe hypofibrinogenemia (≤ 1 g/l) was observed in 16.9% of the children. The frequency of reduced prothrombin ratio was 40%, in which 23.1% of the patients had prothrombin ratio < 50%. 35.4% of the patients had rAPTT > 1.15. Positive D-dimer and DIC were observed in 53.8% and 20% of the patients, respectively. Hemostatic changes showed the significant relationship with hemorrhage and the mortality of sepsis. Conclusion: Children with sepsis, especially septic shock were at high risk of coagulation dysfunction and coagulation abnormalities showed the correlation with hemorrhage and the mortality of sepsis. Key words: coagulation abnormalities, sepsis, children

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