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.
By: Dr Malek
.The Vinca alkaloids are naturally occurring or semisynthetic nitrogenous bases extracted from the pink periwinkle plant Catharanthusroseus
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
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.
Patients with antecedent neurologic disorders, such as Charcot-Marie-Tooth disease, hereditary and sensory neuropathy type I, Guillain-Barré syndrome, and childhood poliomyelitis, are highly predisposed to neurotoxicity.
The only known effective intervention for Vinca alkaloid neurotoxicity is discontinuing treatment
Neutropenia is the principal dose-limiting toxicity of VBL, VDS, and VRL. Thrombocytopenia and anemia are usually less common and less severe.
The Vinca alkaloids are potent vesicants and may cause significant tissue damage if extravasation occurs.
The application of local heat and injection of hyaluronidase, 150 mg subcutaneously, in a circumferential manner around the needle site are thought to minimize both discomfort and latent cellulitis
Phlebitis may also occur along the course of an injected vein, with resultant acute inflammation followed by sclerosis.
Mild and reversible alopecia occurs in approximately 10% and 20% of patients treated with VRL and VCR, respectively
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 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
the major role of the liver in the disposition of the Vinca alkaloids implies that dose modifications should be considered for patients with hepatic dysfunction