Endocrine Abstracts

Aim: Check-point inhibitors have revolutionized cancer treatment while introducing a new spectrum of immune-related adverse effects. Hyperglycemia is frequently observed shortly after initiation of immunotherapy. While immune-mediated type 1 diabetes mellitus is currently the only defined condition associated with post-immunotherapy hyperglycemia, it includes only a small fraction of cases (an estimated prevalence of 0.5%). This study was aimed to determine factors associated with glycemic dysregulation following immunotherapy.

Methods: A retrospective study, using the MD-Clone interface, including data from the electronic medical records of all cancer patients treated with checkpoint inhibitors between January 2015 and January 2021.

Results: Among 3384 patients treated with immunotherapy during the study period, a statistically significant increase in glucose levels was observed after the initiation of immunotherapy [mean of maximum glucose levels during the month before immunotherapy 132.3 ± 55.8 mg/dl vs 139.8 ± 64.6 in the month after immunotherapy (P-Value<0.001)]. Glycemic dysregulation was significant among patients treated with glucocorticoids as part of an anti-emetic regimen in protocols combining chemotherapy and immunotherapy or managing immune-related adverse events (n=2168). Mean of maximal glucose level was 136.4 ± 59 mg/dl during the month before immunotherapy and 145.6 ± 68 mg/dl one month after immunotherapy (P< 0.001)]. Among patients who were not treated with glucocorticoids (n=1216), glycemic dysregulation was not found to be significant.

Conclusions: Concomitant glucocorticoid therapy is the primary determinant of post-immunotherapy hyperglycemia. Evaluation of the possibility of a distinct, reversible, autoimmune damage to beta cells would require a prospective study with a dynamic assessment of the beta-cell reserve.