Xeloda Disease Interactions

Because of their cytotoxic effects on rapidly proliferating tissues, antineoplastic agents frequently can, to varying extent, induce myelosuppression. The use of these drugs 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 antineoplastic therapy. Close clinical monitoring of hematopoietic function is recommended.

Capecitabine can cause cardiotoxicity including myocardial infarction, ischemia, angina, dysrhythmias, cardiac failure, sudden death, electrocardiographic changes and cardiomyopathy. These adverse reactions can be more common in patients with a prior history of coronary artery disease.

Capecitabine is metabolized by the liver to fluorouracil (5-FU). Fluorouracil induces bone marrow suppression. Leukopenia, thrombocytopenia, and anemia, some severe, have been reported with capecitabine therapy. Patients should be instructed to immediately report any signs or symptoms suggesting bone marrow suppression such as fever, sore throat, local infection, or bleeding. Close clinical monitoring of hematopoietic function is recommended

Capecitabine is contraindicated in patients with severe renal impairment (creatinine clearance below 30 mL/min). Patients with moderate renal impairment at baseline require a dose reduction. Patients with mild and moderate impairment should be carefully monitored for adverse reactions and prompt interruption of therapy with subsequent dose adjustment might be required depending on the developed adverse events.

Dehydration has been observed in patients receiving capecitabine and it may cause acute renal failure which could be fatal. Patients with asthenia, anorexia, nausea, vomiting or diarrhea may rapidly become dehydrated. Patients should be monitored to prevent and correct dehydration at the onset. If dehydration grade 2 or higher occurs, treatment should be interrupted until dehydration is corrected. Since capecitabine can also induce diarrhea, sometimes severe, patients should be carefully monitored and receive fluid and electrolyte replacement. Standard antidiarrheal treatments are recommended.

Capecitabine is extensively metabolized by the liver. In patients with mild to moderate liver dysfunction due to liver metastases the Cmax and AUC of capecitabine were increased 60%. These patients should be carefully monitored when capecitabine is administered. The effect of severe hepatic dysfunction on capecitabine has not been assessed. Clinical monitoring of hepatic function is recommended for patients with compromised hepatic function.