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Effects and safety of dulaglutide treatment on glucocorticoid-induced hyperglycemia in patients treated with CHOP therapy

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Abstract Purpose: Glucocorticoid-induced hyperglycemia is a serious adverse event of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) therapy and requires chemotherapy dose reduction and drug interruption for remediation. Previous reports have showed that the glucagon-like peptide 1 receptor agonist dulaglutide significantly improves glycemic control in glucocorticoid-induced hyperglycemia. Thus, we aimed to investigate the efficacy and safety of dulaglutide for glucocorticoid-induced hyperglycemia in patients with non-Hodgkin lymphoma treated with CHOP therapy. Methods: Ten newly diagnosed patients with non-Hodgkin lymphoma exhibiting glucocorticoid-induced hyperglycemia during initial cycle CHOP ± rituximab therapy were enrolled. Dulaglutide administration began during the second cycle. Glycemic control parameters (HbA1C, glycoalbumin, and fasting blood glucose) and adverse events were monitored alongside chemotherapy sessions. Results: Of the 10 patients, one patient discontinued CHOP treatment due to progression, one patient due to chemotherapy intolerance, and eight patients were finally evaluated. HbA1c and glycoalbumin reduced significantly post-dulaglutide initiation, thereby suggesting improved glycemic control without adverse events, such as hypoglycemia or pancreatitis. Challenges in glycemic assessment due to simultaneous declines in hemoglobin levels alongside HbA1C were noted. Conclusion: Dulaglutide exhibited promise in effectively managing glucocorticoid-induced hyperglycemia during CHOP therapy without serious adverse events.
Title: Effects and safety of dulaglutide treatment on glucocorticoid-induced hyperglycemia in patients treated with CHOP therapy
Description:
Abstract Purpose: Glucocorticoid-induced hyperglycemia is a serious adverse event of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) therapy and requires chemotherapy dose reduction and drug interruption for remediation.
Previous reports have showed that the glucagon-like peptide 1 receptor agonist dulaglutide significantly improves glycemic control in glucocorticoid-induced hyperglycemia.
Thus, we aimed to investigate the efficacy and safety of dulaglutide for glucocorticoid-induced hyperglycemia in patients with non-Hodgkin lymphoma treated with CHOP therapy.
Methods: Ten newly diagnosed patients with non-Hodgkin lymphoma exhibiting glucocorticoid-induced hyperglycemia during initial cycle CHOP ± rituximab therapy were enrolled.
Dulaglutide administration began during the second cycle.
Glycemic control parameters (HbA1C, glycoalbumin, and fasting blood glucose) and adverse events were monitored alongside chemotherapy sessions.
Results: Of the 10 patients, one patient discontinued CHOP treatment due to progression, one patient due to chemotherapy intolerance, and eight patients were finally evaluated.
HbA1c and glycoalbumin reduced significantly post-dulaglutide initiation, thereby suggesting improved glycemic control without adverse events, such as hypoglycemia or pancreatitis.
Challenges in glycemic assessment due to simultaneous declines in hemoglobin levels alongside HbA1C were noted.
Conclusion: Dulaglutide exhibited promise in effectively managing glucocorticoid-induced hyperglycemia during CHOP therapy without serious adverse events.

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