Oncovin Disease Interactions

Acute shortness of breath and bronchospasm, some severe and life-threatening, have been reported with the use of vinca alkaloids. These reactions were observed most often during combination therapy with mitomycin C, occurring within minutes to several hours after administration of the vinca alkaloid or up to 2 weeks following the mitomycin dose. Therapy with vinca alkaloids should be administered cautiously in patients with preexisting pulmonary dysfunction. Aggressive treatment may be necessary, including use of supplemental oxygen, bronchodilators, and/or corticosteroids. In patients who develop progressive dyspnea requiring chronic therapy, vinca alkaloid should not be readministered.

The use of vincristine is contraindicated in patients with demyelinating conditions including Charcot-Marie-Tooth syndrome. Neurotoxicity associated with vincristine therapy is dose-related and frequently sequential. Sensorimotor (paresthesia, decreased deep- tendon reflex, ataxia, paralysis), autonomic (constipation and adynamic ileus), and CNS (mental status changes, seizures, coma) neurotoxicity have been reported. Patients with existing neuromuscular or neurologic diseases may be at increased risk for toxicity with vincristine therapy. Therapy with vincristine should be administered cautiously and dosage reduction considered in patients with neurologic dysfunction.

Vincristine can cause constipation. Ileus, bowel obstruction, and colonic pseudo-obstruction have occurred. When using this agent in people at risk of constipation, appropriate measures should be instituted to prevent such complications. A routine prophylactic regimen against constipation is recommended for all patients receiving vincristine.

Vincristine is primarily metabolized by the liver. The influence of severe hepatic impairment on the safety and efficacy of vincristine has not been evaluated. Additionally, fatal liver toxicity and elevated levels of aspartate aminotransferase have occurred in clinical trials. Vincristine should be reduced or interrupted if there is evidence of hepatic toxicity. Therapy with vincristine should be administered cautiously and dosages reduced in patients with compromised hepatic function. Close clinical monitoring of hepatic function is recommended.

Vincristine induces mild, dose-related myelosuppression. The use of vincristine may be contraindicated in patients with known infectious diseases. All patients should be instructed to immediately report any signs or symptoms suggesting infection such as fever, sore throat, or local infection during therapy with vincristine. Clinical monitoring of hematopoetic function is recommended.

Vincristine induces dose-related myelosuppression. Leukopenia, thrombocytopenia, and anemia have been reported, however vincristine does not appear to have a consistent or significant effect on platelets or red blood cells. Patients should be instructed to immediately report any signs or symptoms suggesting bone marrow suppression such as fever, sore throat, local infection, or bleeding. Therapy with vincristine should be administered cautiously in patients with compromised bone marrow reserve. Monitor complete blood counts prior to each dose. If Grade 3 or 4 neutropenia, thrombocytopenia, or anemia develops, consider a dose modification or reduction as well as supportive care measures.

The influence of renal impairment on the safety, efficacy, and pharmacokinetics of vincristine has not been evaluated. Caution and monitoring of renal function is advised in patients with renal impairment.

A syndrome of sudden inappropriate antidiuretic hormone (SIADH) secretion has been reported rarely in association with the use of vincristine. Therapy with vincristine should be administered cautiously in patients with or predisposed to abnormal antidiuretic hormone release and/or suppression.