Platelet Activation Induced by lnterleukin-6: Evidence for a Mechanism Involving Arachidonic Acid Metabolism

Oleksowicz, Leslie; Mrowiec, Zbigniew; Zuckerman, D; Isaacs, Randi; Dutcher, Janice P.; Puszkin, Elena

doi:10.1055/s-0038-1648857

Cited by 83 publications

(57 citation statements)

References 18 publications

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“…In vitro studies confirmed that NEUMEGA' does not increase platelet activity [68]. Ex vivo assay of platelet reactivity in cynomolgus monkeys treated with NEUMEGA@ with elevated platelet counts showed no significant difference in platelet reactivity.…”

Section: Platelet Function and Coagulationmentioning

confidence: 67%

FDA licensure of neumega® to prevent severe chemotherapy&hyphen;induced thrombocytopenia

Kaye

1998

Stem Cells

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This paper discusses background infortransfusions in patients with nonmyeloid mation and the body of clinical data that has malignancies. NEUMEGA@ is recommended been accumulated to demonstrate the efficacy to be used at a dose of SO pgkg S.C. once daily and safety of NEUMEGA@ (recombinant starting the day after chemotherapy ends human interleukin 11) when used to prevent until a platelet count of S0,OOO cells/yl is severe chemotherapy-induced thrombocyachieved after the expected nadir. Stem Cells topenia and reduce the need for platelet 1998;1h(suppl2):207-223

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Section: Platelet Function and Coagulationmentioning

confidence: 67%

FDA licensure of neumega® to prevent severe chemotherapy&hyphen;induced thrombocytopenia

Kaye

1998

Stem Cells

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“…If systemic platelet destruction, eg, caused by endothelial changes, is involved by switching on the bone marrow production of platelets before acute coronary syndromes, then this will probably be mediated by TPO. However, studies that show direct cytokine alteration of platelet function ex vivo 112 raise the possibility that some determinants of platelet function are established after thrombopoiesis.…”

Section: A Proposed Mechanism For the Control Of Platelet Production mentioning

confidence: 99%

A Role for Changes in Platelet Production in the Cause of Acute Coronary Syndromes

Loo

Martin

1999

ATVB

124

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Abstract-Platelets are heterogeneous with respect to their size, density, and reactivity. Large platelets are more active hemostatically, and platelet volume has been found to be increased both in patients with unstable angina and with myocardial infarction. Furthermore, platelet volume is a predictor of a further ischemic event and death when measured after myocardial infarction. Platelets which are anucleate cells with no DNA are derived from their precursor, the megakaryocyte. Therefore, it is suggested that changes in platelet size are determined at thrombopoiesis in the megakaryocyte and that those changes might precede acute cardiac events. Understanding of the signaling system that controls platelet production may also further elucidate the cascade of events leading to acute vascular occlusion in some patients. (Arterioscler Thromb Vasc Biol. 1999;19:672-679.)Key Words: platelets Ⅲ myocardial infarction Ⅲ unstable angina Ⅲ coronary heart disease Ⅲ thrombosis T he biological events that occur in the coronary artery that immediately precede acute coronary syndromes are still not clear. However, platelets are involved, and changes in platelets may be a causal factor in producing a thrombus in the coronary artery.Aspirin is the most widely used antiplatelet drug. As platelets have no nucleus and are therefore unable to synthesize protein de novo, an aspirin-induced functional defect lasts for the whole life span of the platelets (8 to 10 days). 1 The results of large trials 2-4 of the beneficial effect of aspirin treatment in patients with unstable angina are consistent with the hypothesis that platelet activity is causally related to acute coronary syndromes. Both the medium-(12 weeks) 2 and long-term (2 years) 3 risk of cardiac death and myocardial infarction (MI) in patients with unstable angina is reduced. More recently, the significant benefit of antiplatelet therapy with aspirin in protection against acute cardiovascular syndromes and death was further supported in an overview of 145 randomized trials by the Antiplatelet Trialists' Collaboration. 5 Given the known effects of aspirin as an inhibitor of platelet function, these trials are strong evidence that platelets may contribute to the pathophysiology of the acute complications of coronary artery disease. Aspirin is an inhibitor of only one of several specific pathways leading to platelet activation and aggregation. 1 Inhibition of the glycoprotein (GP) IIb/IIIa receptor blocks the binding of fibrinogen, which is the final common pathway of platelet aggregation. 6 Integrelin, which is a GP IIb/IIIa receptor inhibitor, was evaluated in 227 patients with unstable angina and reduced significantly the number and duration of Holter-recorded ischemia compared with aspirin therapy. 7 These recent data are further strong support for the pivotal role of platelets in patients with unstable angina.Circulating platelets are heterogeneous in size, density, and reactivity. 8,9 Changes in these variables may be causal in acute coronary syndromes. 10 Initial plaque ...

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“…The characteristic feature of RA is the persistence of synovitis, the mechanism of which involves IL-6, which is a cytokine that stimulates the production and activation of platelets [19,20]. Microparticles released from activated platelets in turn prominently induce the release of IL-6 and IL-8 from synovial fibroblasts [21], creating a positive feedback loop of IL-6 production.…”

Section: Discussionmentioning

confidence: 99%

Clinical and structural remission rates increased annually and radiographic progression was continuously inhibited during a 3-year administration of tocilizumab in patients with rheumatoid arthritis: A multi-center, prospective cohort study by the Michinoku Tocilizumab Study Group

Hirabayashi¹,

Munakata²,

Miyata

et al. 2016

Modern Rheumatology

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for the Michinoku Tocilizumab Study Group (2016) Clinical and structural remission rates increased annually and radiographic progression was continuously inhibited during a 3-year administration of tocilizumab in patients with rheumatoid arthritis: A multi-center, prospective cohort study by the Michinoku Tocilizumab Study Group, Modern Rheumatology, 26:6, 828-835, DOI: 10.3109/14397595.2016.1160991 To link to this article: https://doi.org/10. 3109/14397595.2016 Abstract Objective: To evaluate the clinical and structural efficacy of tocilizumab (TCZ) during its longterm administration in patients with rheumatoid arthritis (RA). Methods: In total, 693 patients with RA who started TCZ therapy were followed for 3 years. Clinical efficacy was evaluated by DAS28-ESR and Boolean remission rates in 544 patients. Joint damage was assessed by calculating the modified total Sharp score (mTSS) in 50 patients. Results: When the reason for discontinuation was limited to inadequate response or adverse events, the 1-, 2-, and 3-year continuation rates were 84.0%, 76.8%, and 72.2%, respectively. The mean DAS28-ESR was initially 5.1 and decreased to 2.5 at 6 months and to 2.2 at 36 months. The Boolean remission rate was initially 0.9% and increased to 21.7% at 6 months and to 32.2% at 36 months. The structural remission rates (DmTSS/year 0.5) were 68.8%, 78.6%, and 88.9% within the first, second, and third years, respectively. The structural remission rate at 3 years (DmTSS 1.5) was 66.0%, and earlier achievement of swollen joint count (SJC) of 1 or less resulted in better outcomes. Conclusions: TCZ was highly efficacious, and bone destruction was strongly prevented. SJC was an easy-to-use indicator of joint destruction.

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Platelet Activation Induced by lnterleukin-6: Evidence for a Mechanism Involving Arachidonic Acid Metabolism

Cited by 83 publications

References 18 publications

FDA licensure of neumega® to prevent severe chemotherapy&hyphen;induced thrombocytopenia

FDA licensure of neumega® to prevent severe chemotherapy&hyphen;induced thrombocytopenia

A Role for Changes in Platelet Production in the Cause of Acute Coronary Syndromes

Clinical and structural remission rates increased annually and radiographic progression was continuously inhibited during a 3-year administration of tocilizumab in patients with rheumatoid arthritis: A multi-center, prospective cohort study by the Michinoku Tocilizumab Study Group

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Platelet Activation Induced by lnterleukin-6: Evidence for a Mechanism Involving Arachidonic Acid Metabolism

Cited by 83 publications

References 18 publications

FDA licensure of neumega&reg; to prevent severe chemotherapy&hyphen;induced thrombocytopenia

FDA licensure of neumega&reg; to prevent severe chemotherapy&hyphen;induced thrombocytopenia

A Role for Changes in Platelet Production in the Cause of Acute Coronary Syndromes

Clinical and structural remission rates increased annually and radiographic progression was continuously inhibited during a 3-year administration of tocilizumab in patients with rheumatoid arthritis: A multi-center, prospective cohort study by the Michinoku Tocilizumab Study Group

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FDA licensure of neumega® to prevent severe chemotherapy&hyphen;induced thrombocytopenia

FDA licensure of neumega® to prevent severe chemotherapy&hyphen;induced thrombocytopenia