Effect of high-dose dexamethasone on patients without diabetes during elective neurosurgery: a prospective study

Abstract

Introduction The peri-operative use of high-dose dexamethasone to reduce cerebral oedema may result in worsening glycaemic control in people with diabetes and glucocorticoid-induced diabetes in susceptible individuals. This study aims to examine the incidence of glucocorticoid-induced diabetes in a cohort of neurosurgical patients receiving high-dose dexamethasone peri-operatively. Materials and methods Adult non-diabetic neurosurgical patients receiving high-dose dexamethasone were prospectively studied. Exclusion criteria included pregnancy, HbA1c > 6.0%, and use of anti-diabetes therapies. The following data were collected: Family history of diabetes, body mass index, fasting glucose, insulin, C-peptide, and HbA1c (prior to surgery and 6 weeks after last dose of dexamethasone). Homeostatic model assessment values were calculated. Peri-operative glucose readings were recorded and 75 g oral glucose tolerance tests performed at the end of 6 weeks. Paired student t tests and multiple linear regressions were used. Results Data from 21 participants (11 women) were available. The mean total dose of dexamethasone was 96 ± 34 mg, and treatment duration was 17 ± 7 days. A total of 105 random blood glucose levels were documented peri-operatively (mean 7.0 ± 1.0 mmol/L). Six weeks following cessation of dexamethasone course, none of the participants developed diabetes, defined either by fasting glucose or by 75 g OGTT. There was a statistically significant increase in the mean HOMA-β from 81.5 to 102.1% (p = 0.01) and a significant decrease in the mean fasting glucose from 5.7 to 4.8 mmol/L (p = 0.001). Conclusions The use of high-dose dexamethasone in this cohort of neurosurgical patients did not result in glucocorticoidinduced diabetes. Hyperglycaemia was transient and had resolved by 6 weeks.

The Magnitude of Dexamethasone-Induced Hyperglycemia in Cataract Surgical Patients with Normal Glucose Metabolism- A Continuous Glucose Monitoring Based Study

“…Because according to the glucose readings delivered from CGM, subjects receiving dexamethasone exhibited the maximum glucose level was less than 11.1 mmo/L, and the SD less than 1.4 mmol/L [17]. Our results in accordance with a previous study reporting that patients receiving high dose of dexamethasone did not resulting in diabetes, and the rise in glucose concentrations were transient and improvement after 6 weeks follow up [4]. In contrast to our study, previously published data showed that about one fth non-diabetic patients receiving dexamethasone therapy were prone to development of diabetes after long-run follow up [5].…”

“…In contrast to our study, previously published data showed that about one fth non-diabetic patients receiving dexamethasone therapy were prone to development of diabetes after long-run follow up [5]. The differences in corticosteroid associated hyperglycemia between the two study may be our study with a relatively short follow up period, because of exposure to a large cumulative dose of dexamethasone may impair glycemic metabolisms [4].…”

“…An impairment of glycemic metabolism or even steroid-induced diabetes may occur in subjects with normal glucose tolerate [3]. Although a pilot study observed that the use of high-dose dexamethasone may not lead to glucocorticoid-induced diabetes [4].…”

The magnitude of dexamethasone-induced hyperglycemia in cataract surgical patients with normal glucose metabolism: a continuous glucose monitoring based study

“…Because according to the glucose readings delivered from CGM, subjects receiving dexamethasone exhibited the maximum glucose level was less than 11.1 mmo/L, and the SD less than 1.4 mmol/L [17]. Our results in accordance with a previous study reporting that patients receiving high dose of dexamethasone did not resulting in diabetes, and the rise in glucose concentrations were transient and improvement after 6 weeks follow up [4]. In contrast to our study, previously published data showed that about one fifth non-diabetic patients receiving dexamethasone therapy were prone to development of diabetes after long-run follow up [5].…”

“…An impairment of glycemic metabolism or even steroid-induced diabetes may occur in subjects with normal glucose tolerate [3]. Although a pilot study observed that the use of high-dose dexamethasone may not lead to glucocorticoid-induced diabetes [4]. Using fasting and 2-hour postprandial glucose levels, and hemoglobin A 1C values, Jeong Y et al observed that non-diabetic patients had a maximum of 20% risk ratio of development of diabetes at 3 or 6 months after dexamethasone therapy [5].…”