In the name of God. Vinca alkaloids By: Dr Malek. References. Holland- Frei Cancer Medicine. 6th edition. Kufe DW, Pollock RE, Weichselbaum RR, et al., editors.
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Kufe DW, Pollock RE, Weichselbaum RR, et al., editors.
Sauerland C, Wickham R. Vesicant extravasation Part I: Mechanisms, pathogenesis, and nursing care to reduce risk. Oncology Nursing Forum. -41Hamilton (ON):BC Decker; 2007
Herbal Medicine: Biomolecular and Clinical Aspects. 2nd edition.
Benzie IFF, Wachtel-Galor S, editors.
Boca Raton (FL): CRC Press; 2011
.The Vinca alkaloids are naturally occurring or semisynthetic nitrogenous bases extracted from the pink periwinkle plant Catharanthusroseus
. Many Vinca alkaloids have been extensively evaluated, but only vincristine (VCR), vinblastine (VBL), and vinorelbine (VRL) are approved for use in the United States.
The Vinca alkaloids have dimeric chemical structures composed of two basic multiringed units an indole nucleus (catharanthine), and a dihydroindole nucleus (vindoline), joined together with other complex systems
.the principal mechanisms of cytotoxicity relate to their interactions with tubulin and disruption of microtubule function, particularly of microtubules comprising the mitotic spindle apparatus, leading to metaphase arrest
In cell culture, VCR or VBL enhances methotrexate accumulation in tumor cells, an effect mediated by a Vinca alkaloid-induced blockade of drug efflux
l-Asparaginase may reduce the hepatic clearance of the Vinca alkaloids, particularly VCR, which may result in increased toxicity. To minimize the possibility of this interaction, VCR should be given 12 to 24 h before l-asparaginase
pain and loss of deep tendon reflexes may develop with continued treatment, which may be followed by foot drop, wrist drop, motor dysfunction, ataxia, and paralysis.
Cranial nerves may also be affected rarely, resulting in hoarseness, diplopia, jaw pain
Acute, severe autonomic neurotoxicity is uncommon, but may arise as a consequence of high-dose therapy (greater than 2 mg/m2) or in patients with diminished drug clearance because of altered hepatic function. Toxic manifestations include constipation, abdominal cramps, paralytic ileus, urinary retention, orthostatic hypotension, and hypertension and facial palsies.
VCR treatment in patients with hepatic dysfunction or obstructive liver disease is associated with an increased risk of developing neuropathy because of impaired drug metabolism and delayed biliary excretion
. Although a number of antidotes, including thiamine, vitamin B12, folinic acid, pyridoxine, and neuroactive agents , have been used, these treatments have not been clearly shown to be effective
Neutropenia Charcot-Marie-Tooth disease, hereditary and sensory neuropathy type I, is the principal dose-limiting toxicity of VBL, VDS, and VRL. Thrombocytopenia and anemia are usually less common and less severe.
The onset of neutropenia is usually 7 to 11 days after treatment, and recovery is generally by days 14 to 21.
The Charcot-Marie-Tooth disease, hereditary and sensory neuropathy type I, Vinca alkaloids are potent vesicants and may cause significant tissue damage if extravasation occurs.
If extravasation occurs or is suspected, treatment should be discontinued immediately and aspiration of any residual drug remaining in the tissues should be attempted
The application of local heat and injection of Charcot-Marie-Tooth disease, hereditary and sensory neuropathy type I, hyaluronidase, 150 mg subcutaneously, in a circumferential manner around the needle site are thought to minimize both discomfort and latent cellulitis
Acute cardiac ischemia, chest pains without evidence of ischemia, fever without an obvious source, acute pulmonary effects (alone or in combination with mitomycin C), Raynaud phenomenon, hand-foot syndrome, and pulmonary and hepatic toxicity have also been reported with the Vinca alkaloids.
All of the ischemia, fever without an obvious source, acute pulmonary effects (alone or in combination with Vinca alkaloids have been implicated as a cause of SIADH, and patients who are receiving intensive hydration are particularly prone to severe hyponatremia secondary to SIADH.1
. A 50% dose reduction is often recommended for patients with total bilirubin levels between 1.5 and 3.0 mg/dL (50% dose reduction for bilirubin levels between 2.0 and 3.0 mg/dL is recommended for VRL), and at least a 75% dose reduction for plasma total bilirubin levels above 3.0 mg/dL.