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Rituximab to treat gemcitabine-induced hemolytic–uremic syndrome (HUS) in pancreatic adenocarcinoma: a case series and literature review

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Abstract

Purpose

Hemolytic–uremic syndrome (HUS) is a rare side effect of gemcitabine, which is reported as having a high morbidity and mortality despite interventions with standard HUS therapies including plasmapheresis. The purpose of this report was to describe the successful treatment of gemcitabine-induced HUS (G-HUS) with rituximab. It also aims to summarize the literature regarding the morbidity and mortality of G-HUS in pancreatic adenocarcinoma depending on the treatment given, ultimately providing some guidance for beneficial therapies.

Methods

This is a retrospective report of three patients with pancreatic adenocarcinoma who developed G-HUS and were treated with a combination of therapies including rituximab.

Results

All three patients received a combination of therapies to treat their HUS. One patient appeared to have some benefit with plasmapheresis. Resolution occurred following one course of rituximab for all three patients. This resolution has been long lasting with a minimum of eighteen month's follow-up. Similarly, in our literature review a variety of therapies were utilized, but immune therapies appear to reverse HUS if other therapies are failing.

Conclusion

Rituximab can be an effective therapy for reversal of hemolysis and stabilization of renal function in G-HUS when other therapies fail.

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Acknowledgments

Roche and Prince of Wales Hospital compassionately funded the rituximab doses for these patients.

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Correspondence to Georgia E. Ritchie.

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Conflict of interest

David Goldstein has been an unremunerated advisor to Lilly, Celgene and Roche.

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Ritchie, G.E., Fernando, M. & Goldstein, D. Rituximab to treat gemcitabine-induced hemolytic–uremic syndrome (HUS) in pancreatic adenocarcinoma: a case series and literature review. Cancer Chemother Pharmacol 79, 1–7 (2017). https://doi.org/10.1007/s00280-016-3123-6

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  • DOI: https://doi.org/10.1007/s00280-016-3123-6

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