How should severe mucositis from capecitabine (Xeloda) be managed? What can be done to prevent this side effect? —Mary Haule, BScN

Mucositis or stomatitis has been reported in up to 22% to 25% of patients receiving capecitabine as a single agent, with 2% to 7% of them experiencing more severe grade 3/4 mucositis.1 Patients beginning therapy with capecitabine or other chemotherapy drugs that may cause mucositis should be counseled regarding oral care, including avoid alcohol-based mouth rinses, use a mild salt and baking soda rinse, brush your teeth with an extra-soft bristled toothbrush after meals and before bed, and ensure dentures fit well and do not rub. Capecitabine’s active metabolites have a long half-life in the body, which makes the use of ice chips to prevent mucositis ineffective in this setting. There has been some study of using pharmacologic agents to prevent mucositis; however, glutamine has not been shown to be effective in this setting and palifermin is not recommended in nontransplant settings.2,3

Patients should be counseled to report symptoms of mucositis, such as oral pain or mouth sores, to their oncology care team. Those who develop mucositis should be managed supportively, with capecitabine or other cancer therapies held as indicated based on the patient’s condition. The goal of supportive therapy is to control pain and maintain hydration while healing occurs. Topical numbing agents, such as “magic mouthwash” may be beneficial. (“Magic mouthwash” ingredients vary based on institutional preferences but frequently include combinations of diphenhydramine, lidocaine, antacids, and other ingredients.) Patients with more severe symptoms may require narcotic pain medications and intravenous hydration, as well as hospital admission to provide supportive care. Patients with heartburn-like symptoms may benefit from the addition of an H2 blocker (eg, famotidine [Pepcid]) or a proton pump inhibitor (eg, omeprazole [Prilosec]). Patients who develop symptoms of an oral infection should receive prompt therapy based on the suspected etiology of the infection (eg, nystatin or another antifungal for thrush).

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Some patients may have dihydropyrimidine dehydrogenase (DPD) deficiency, a condition caused by mutations in the DPD gene resulting in much reduced or total absence of activity of the enzyme responsible for metabolizing the active metabolites of capecitabine and other fluoropyrimidines (eg, fluorouracil [5-FU]). DPD deficiency occurs in approximately 3% to 8% of the population depending on ethnicity.4 Patients with DPD deficiency are at increased risk for adverse effects of capecitabine, including mucositis, and these toxicities may be much more severe than what is typically observed. Patients who develop unusually severe toxicity from capecitabine may be tested for DPD deficiency; treatment with fluoropyrimidines such as capecitabine should be avoided in patients with DPD deficiency in the future.

Lisa Thompson is a clinical pharmacy specialist in oncology at Kaiser Permanente, Colorado.


1. Xeloda [prescribing information]. South San Francisco, CA: Genentech Inc; 2015.

2. Morse MA. Supportive care in the management of colon cancer. Support Cancer Ther. 2006;3(3):158-170.

3. Hensley ML, Hagerty KL, Kewalramani T, et al. American Society of Clinical Oncology 2008 clinical practice guideline update: use of chemotherapy and radiation therapy protectants. J Clin Oncol. 2009;27(1):127-145.

4. Mattison LK, Fourie J, Desmond RA, et al. Increased prevalence of dihydropyrimidine dehydrogenase deficiency in African-Americans compared with Caucasians. Clin Cancer Res. 2006;12(18):5491-5495.