Treatment of Vincristine Extravasation

Bellone, Jack D.

doi:10.1001/jama.1981.03310290019013

Cited by 20 publications

(3 citation statements)

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“…3 Tage lang 4-mal 15-20 min Eisumschläge und Hochlagern der Paravasatstelle (Larson 1982;van Sloten Harwood et al 1984) oder: 25-50 mg Hydrokortison pro geschätztem ml Paravasat subkutan oder intradermal injizieren (Bellone 1981;van Sloten Harwood et al 1984) oder: Paravasatstelle mit 2 Ampullen (à 150 IE) Hyaluronidase (z. B. Kinetin), gelöst in 5 ml 0,9%-iger NaCl-Lösung, infiltrieren, danach Paravasatbereich mit 3 Ampullen Hyaluronidase, gelöst in ca.…”

Section: Doxorubicin Und Epirubicinunclassified

Grundlagen der systemischen Therapie

Schüler¹,

Jäger²,

Krege³

et al. 2009

Uroonkologie

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Section: Doxorubicin Und Epirubicinunclassified

Grundlagen der systemischen Therapie

Schüler¹,

Jäger²,

Krege³

et al. 2009

Uroonkologie

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“…If the agent is injected beneath the skin, immediate attention must be given, and extravasation kits with specific instructions are used. [30][31][32] The major toxicity of vincristine is neurotoxicity and may become dose limiting. 33 Most common is sensory peripheral neuropathy, manifesting as numbness and painful paresthesias, which can progress to muscle weakness and incoordination.…”

Section: Toxicitymentioning

confidence: 99%

20th‐Century Advances in Drug Therapy in Oncology—Part II

Dutcher

Novik

Marcoullis

et al. 2000

The Journal of Clinical Pharma

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Ongoing research in cancer therapy has led to the development of antineoplastic agents which target specific components of the cell cycle. In Part II of this series, we discuss agents which target the mitotic mechanism by inhibiting microtubules. Although many of these agents are being shown to have multiple effects, the Vinca alkaloids and the taxanes are known as antimitotic drugs. They are among the most important anticancer agents currently available, and because of their unique mechanisms, can be combined with a wide variety of other antineoplastic agents in a spectrum of diseases. In addition, in part II, we are discussing agents that target DNA and prevent replication and thus cell growth by inhibiting the enzymes which protect DNA during replication, the topoisomerases. These drugs, too, have unique mechanisms of action and have become major components of combination regimens. The topoisomerase I inhibitors are new drugs derived from an older parent drug, and their full possibilities are still being explored.

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“…Indeed, VCR accumulates at high rates in most organs and tissues with the exception of the brain, eye, and fat (Said & Tsimberidou, 2014;Khalil et al, 2016;Kumar). In this regard, soft-tissue necrosis and ulceration (if accidentally extravagated) (Choy et al, 1979;Bellone et al, 1981), respiratory distress, neurotoxicity and neuropathy (Egbelakin et al, 2011;Muthuraman & Singh, 2011), gastrointestinal toxicities (Cave et al, 2007), hepatotoxicity (Roger 2006;Upmanyu et al, 2011), and infertility (Arnon et al, 2001) have been described in patients who received short-term administration of VCR.…”

Section: Introductionmentioning

confidence: 99%

Sub-Chronic Administration of Vincristine Sulfate Induces Renal Damage and Apoptosis in Rats via Induction of Oxidative Stress and Activation of Raf1-MEK1/2-Erk1/2 Signal Transduction

Shati

2019

Int. J. Morphol.

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SHATI, A. A.Sub-chronic administration of vincristine sulfate induces renal damage and apoptosis in rats via induction of oxidative stress and activation of Raf1-MEK1/2-Erk1/2 signal transduction. Int. J. Morphol., 37(1):273-283, 2019. SUMMARY:In spite of being one of the most powerful anti-cancer drug, the nephrotoxicity of Vincristine (VCR) is not well established in either animals or humans. Hence, this study evaluates the nephrotoxic effect of VCR in rats after sub-chronic long-term administration. Rats were divided into 2 groups (n=10/group) of either control and VCR treated rats (50 mg/kg). Treatments were carried out for 30 consecutive days, after which a series of biochemical and molecular experiments related to kidney function were evaluated. VCR administration significantly decreased the survival rate (69.8 %) and impaired renal function as evidenced by lowered creatinine (Cr) clearance (Ccr), high serum levels of urea and Cr, increased urinary protein levels and resulted in sever cortex pathological alterations, including glomerulus congestion and damage as well as vascular degenerations up to necrosis of both proximal and distal convoluted tubules. Mechanistically, VCR lowered renal antioxidant potential and ATP levels, enhanced lipid peroxidation and induced inflammation. In addition, VCR induced activation of Raf-1-MEK1/2-ERK1/2 signaling pathway leading to downregulation of Bcl-2 and upregulation of P53, Bax, and cleaved caspase-3. In conclusion, these findings show a nephrotoxic effect of VCR sulfate in rats after sub-chronic administration and such effect was mediated by activation of ERK1/2 induced apoptosis.

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Treatment of Vincristine Extravasation

Cited by 20 publications

References 0 publications

Grundlagen der systemischen Therapie

Grundlagen der systemischen Therapie

20th‐Century Advances in Drug Therapy in Oncology—Part II

Sub-Chronic Administration of Vincristine Sulfate Induces Renal Damage and Apoptosis in Rats via Induction of Oxidative Stress and Activation of Raf1-MEK1/2-Erk1/2 Signal Transduction

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