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BACKGROUND: Fluoropyrimidines compose the backbone of regimens to treat many common solid tumors, including gastrointestinal (GI), breast and head/neck. As we continue to use these agents routinely, recognition of rare but real toxicities, such as cardiotoxicity, has also improved. The treatment options for patients who have encountered fluoropyrimidine-induced cardiotoxicity are limited as many anti-angiogenic drugs also pose a cardiac risk. PATIENTS AND METHODS: We present a case series of three patients who developed cardiotoxicity in the form of anginal-like symptoms, EKG changes and elevated cardiac enzymes on infusional 5-FU or capecitabine and were subsequently treated with the s-MOX (simplified-mitomycin-oxaliplatin) regimen for their metastatic colorectal cancer (mCRC). All three patients were tested for polymorphic abnormality of DYPD and TYMS. RESULTS: All three patients were treated with s-MOX consisting of mitomycin-C 7 mg/m2 on day 1 and oxaliplatin 85 mg/m2 on days 1 and 15 (1 cycle = 28 days) after they encountered cardiotoxicity to 5-FU and/or capecitabine. None of these patients developed any cardiotoxicity on s-MOX. Overall, the MOX regimen was well tolerated. The most common toxicities included ≤ 2 grade peripheral neuropathy, nausea, vomiting, thrombocytopenia, and anemia. Grade ≥ 3 toxicities included neutropenia (10%), thrombocytopenia (33%), vomiting (8%), and peripheral neuropathy (30%). DYPD gene was normal in all patients and TYMS was abnormal (2R/2R) in one patient. CONCLUSION: This is the first case series that reports the safety and feasibility of s-MOX in patients with mCRC who developed cardiac toxicity to 5-FU or capecitabine. The s-MOX regimen may provide an alternative treatment option for patients who either develop fluoropyrimidine-related cardiotoxicity or who have abnormalities in the DYPD gene.
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INTRODUCTION: To assess tumor control and survival in patients treated with stereotactic radiosurgery (SRS) for 10 or more metastatic brain tumors. METHODS: Patients were retrospectively identified. Clinical records were reviewed for follow-up data, and post-treatment MRI studies were used to assess tumor control. For tumor control studies, patients were separated based on synchronous or metachronous treatment, and control was assessed at 3-month intervals. The Kaplan-Meier method was employed to create survival curves, and regression analyses were employed to study the effects of several variables. RESULTS: Fifty-five patients were treated for an average of 17 total metastases. Forty patients received synchronous treatment, while 15 received metachronous treatment. Univariate analysis revealed an association between larger brain volumes irradiated with 12 Gy and decreased overall survival (p = 0.0406); however, significance was lost on multivariate analysis. Among patients who received synchronous treatment, the median percentage of tumors controlled was 100%, 91%, and 82% at 3, 6, and 9 months, respectively. Among patients who received metachronous treatment, the median percentage of tumors controlled after each SRS encounter was 100% at all three time points. CONCLUSIONS: SRS can be used to treat patients with 10 or more total brain metastases with an expectation of tumor control and overall survival that is equivalent to that reported for patients with four or fewer tumors. Development of new metastases leading to repeat SRS is not associated with worsened tumor control or survival. Survival may be adversely affected in patients having a higher volume of normal brain irradiated.
