Case Series Open Access
Volume 2 | Issue 1 | DOI: https://doi.org/10.33696/casereports.2.008

Safety and Efficacy of s-MOX Regimen in Patients with Colorectal Cancer Who Developed Cardiotoxicity Following Fluoropyrimidine Administration: A Case Series

  • 1Northwell Health Cancer Institute, Feinstein Institutes of Research and Zucker School of Medicine, Lake Success, New York, USA
  • 2Yale Cancer Center, New Haven, CT, USA
  • 3Tufts Cancer Center, Boston, MA, USA
+ Affiliations - Affiliations

Corresponding Author

Muhammad Wasif Saif, wsaif@northwell.edu

Received Date: June 01, 2020

Accepted Date: July 14, 2020


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.


MOX Regimen, Fluoropyrimidines, Cardiotoxicity, Dihydropyridine Dehydrogenase

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