HbA1c is Associated with Hyperglycemia After Local Dexamethasone Injection in Diabetes Mellitus Patients: A Cohort...

Glucocorticoids (GCs) are often administered locally to inhibit the synthesis and release of pro-inflammatory cytokines, thereby alleviating local pain. While GCs are known to exacerbate hyperglycemia, we previously reported changes in glucose levels following a single-dose dexamethasone injection in patients who did not have diabetes mellitus (DM). In patients without DM, blood glucose levels increased on the first day but were generally not critical. However, the exact changes in blood glucose levels due to GCs and the risk factors for blood glucose elevation in DM patients remain unclear.

To measure changes in glucose levels following a single-dose dexamethasone injection in patients with DM and identify the risk factors for hyperglycemia.

Cohort study.

Gifu University Hospital, Japan.

Fifty DM patients undergoing elective pulsed radiofrequency of the lumbar or sacral nerve root or radiofrequency of the lumbar medial branch of the posterior primary ramus were analyzed. Each patient received 0.1 mg/kg of dexamethasone and was subjected to interstitial glucose monitoring using a continuous glucose monitoring system. Hyperglycemia was defined as a blood glucose level >= 200 mg/dL. The area under the curve (AUC) for glucose levels >= 200 mg/dL was calculated. Risk factors for hyperglycemia were analyzed using an ordinal regression model, with AUC as the objective variable and 4 factors (glycosylated hemoglobin [HbA1c], age, body mass index, and pre-procedure glucose levels) as explanatory variables. Nonlinear regression models were used to predict the blood glucose trends.

Blood glucose levels increased immediately after the dexamethasone injections. The median (interquartile range) maximum glucose level was 328 (250-386) mg/dL, with a median time to peak of 592 (400-700) min. Among the 4 factors, age and HbA1c level were significant predictors of hyperglycemia (P = 0.035 and 0.023, respectively). Patients treated with insulin were predicted to have significantly higher blood glucose levels than those treated for DM with non-insulin medications or no pharmacological medications (P < 0.001).

Firstly, GCs are metabolized by cytochrome p450 3A4, and medications that affect this pathway may alter the clearance of GCs. Some of our patients were taking medications that influenced the cytochrome pathway. Secondly, preoperative insulin management details (dosing, timing, and types) were not fully documented. Thirdly, stress-induced hyperglycemia could not be ruled out. Finally, patients' meal timing and caloric intake were not recorded.

Patients with DM experienced significant hyperglycemia even after a single dose of dexamethasone. Age and HbA1c levels were risk factors for hyperglycemia. Higher preprocedural HbA1c levels, reflecting poorer daily glucose control, were associated with increased blood glucose levels.