Platelet Consumption and Activation of the Complement System Induced by Infusion of rTNFα and rIFNγ<sup>a</sup>

Nürnberger, W.; Michelmann, I.; Eckhof-Donovan, S.; Böckmann, D.; Petrik, K.; Göbel, Gabriele; Burdach, Stefan; Göbel, U.

doi:10.1111/j.1749-6632.1994.tb12058.x

Cited by 1 publication

(2 citation statements)

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“…In humans, complement activation is responsible for thrombocytopenia associated with infusion of TNF-a and IFN-g for up to 7 days (Nurnberger et al 1994). The thrombocytopenia can be moderate or profound depending on the duration of the infusion.…”

Section: Complement Activationmentioning

confidence: 99%

“…TNF-a inhibitors, either alone or in combination with IFNg, have been linked to mild to severe (approximately CTCAE grades 3-4) thrombocytopenia in up to 6% of patients (Brunasso and Massone 2009;Chen et al 2011;Gerloni et al 2008;Michelmann et al 1997;Nurnberger et al 1994;Pathare, Heycock, and Hamilton 2006;Salar et al 2007). Similar findings were not reported in nonclinical studies.…”

Section: Tumor Necrosis Factor Alpha (Tnf-a) Inhibitorsmentioning

confidence: 99%

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Unexpected Hematologic Effects of Biotherapeutics in Nonclinical Species and in Humans

Everds

Tarrant²

2013

Toxicol Pathol

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Biotherapeutics are expanding the arsenal of therapeutics available for treating and preventing disease. Although initially thought to have limited side effects due to the specificity of their binding, these drugs have now been shown to have potential for adverse drug reactions including effects on peripheral blood cell counts or function. Hematotoxicity caused by a biotherapeutic can be directly related to the activity of the biotherapeutic or can be indirect and due to autoimmunity, biological cascades, antidrug antibodies, or other immune system responses. Biotherapeutics can cause hematotoxicity primarily as a result of cellular activation, cytotoxicity, drug-dependent and independent immune responses, and sequelae from initiating cytokine and complement cascades. The underlying pathogenesis of biotherapeutic-induced hematotoxicity often is poorly understood. Nonclinical studies have generally predicted clinical hematotoxicity for recombinant cytokines and growth factors. However, most hematologic liabilities of biotherapeutics are not based on drug class but are species specific, immune-mediated, and of low incidence. Despite the potential for unexpected hematologic toxicity, the risk-benefit profile of most biotherapeutics is favorable; hematologic effects are readily monitorable and managed by dose modification, drug withdrawal, and/or therapeutic intervention. This article reviews examples of biotherapeutics that have unexpected hematotoxicity in nonclinical or clinical studies.

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Section: Complement Activationmentioning

confidence: 99%

Section: Tumor Necrosis Factor Alpha (Tnf-a) Inhibitorsmentioning

confidence: 99%

Unexpected Hematologic Effects of Biotherapeutics in Nonclinical Species and in Humans

Everds

Tarrant²

2013

Toxicol Pathol

View full text Add to dashboard Cite

show abstract

Platelet Consumption and Activation of the Complement System Induced by Infusion of rTNFα and rIFNγ^a

Cited by 1 publication

References 2 publications

Unexpected Hematologic Effects of Biotherapeutics in Nonclinical Species and in Humans

Unexpected Hematologic Effects of Biotherapeutics in Nonclinical Species and in Humans

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Platelet Consumption and Activation of the Complement System Induced by Infusion of rTNFα and rIFNγa

Cited by 1 publication

References 2 publications

Unexpected Hematologic Effects of Biotherapeutics in Nonclinical Species and in Humans

Unexpected Hematologic Effects of Biotherapeutics in Nonclinical Species and in Humans

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Product

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Platelet Consumption and Activation of the Complement System Induced by Infusion of rTNFα and rIFNγ^a