Safe administration of oral chemotherapy.

High standards of care are desirable for patients in any setting who receive chemotherapy by any route. Patients who self-administer oral chemotherapy are subject to risks of adverse effects similar to those who receive i.v. chemotherapy. Safeguards to prevent medication error in these patients may not be achieved to the same degree as for patients receiving i.v. drugs in an institutional setting. This article describes the differences between typical administration standards for i.v. chemotherapy versus oral chemotherapy. The process of oral chemotherapy provision is examined, with examples of drug characteristics and patient features important in each step. Recommendations are made for improving the care of patients receiving oral chemotherapy medications, particularly in the home setting.

Pharmacology of oral chemotherapy agents.

The abundance of orally formulated chemotherapy agents reflects the expanding role of oral chemotherapy in the care of patients with cancer. Many oral chemotherapy agents have been used for a number of years, and several have been developed recently. Newer agents include the prodrugs capecitabine and temozolomide, the retinoid bexarotene, the immunomodulatory agent thalidomide, the protein kinase inhibitor imatinib, and the epidermal growth factor receptor inhibitors gefitinib and erlotinib. Each agent has unique pharmacologic properties, dosing, and side-effect profiles. This article reviews these agents from a pharmacology perspective.

Primary therapy of Waldenström macroglobulinemia with bortezomib, dexamethasone, and rituximab: WMCTG clinical trial 05-180.

PURPOSE: We examined the activity of bortezomib, dexamethasone, and rituximab (BDR) in patients with symptomatic, untreated Waldenström macroglobulinemia (WM). PATIENTS AND METHODS: A cycle of therapy consisted of bortezomib 1.3 mg/m(2) intravenously; dexamethasone 40 mg on days 1, 4, 8, and 11; and rituximab 375 mg/m(2) on day 11. Patients received four consecutive cycles for induction therapy and then four more cycles, each given 3 months apart, for maintenance therapy. Twenty-three patients received a median of seven cycles of treatment. RESULTS: Median bone marrow disease involvement declined from 55% to 10% (P = .0004), serum immunoglobulin M levels declined from 4,830 to 1,115 mg/dL (P < .0001), and hematocrit increased from 29.8% to 38.2% (P = .0002) at best response. The overall response rates and major response rates were 96% and 83% with three complete responses, two near complete responses, three very good partial responses, 11 partial responses, and three minor responses. Responses occurred at a median of 1.4 months. With a median follow-up of 22.8 months, 18 of 23 patients remained free of disease progression. Peripheral neuropathy was the most common toxicity, and it resolved to grade < or = 1 in 13 of 16 patients at a median of 6.0 months. Four of the first seven treated patients developed herpes zoster, resulting in the institution of prophylactic antiviral therapy. CONCLUSION: The results demonstrate that BDR produces rapid and durable responses, along with high rates of response and complete remissions in WM. Herpes zoster prophylaxis is necessary with BDR, and reversible peripheral neuropathy was the most common toxicity leading to premature discontinuation of bortezomib in 61% of patients. Exploration of alternative schedules for bortezomib administration that includes weekly dosing should be pursued.