Reactions Weekly | 2019
Exenatide/liraglutide/dexamethasone interaction
Abstract
Exacerbation of constipation and false-positive dexamethasone suppression test: 2 case reports In a case series of seven patients, a 75-year-old woman exhibited false positive dexamethasone suppression test following administration of exenatide due to interaction with dexamethasone, and a 49-year-old woman exhibited false positive dexamethasone suppression test following administration of liraglutide due to interaction with dexamethasone. Additionally, the women also developed exacerbation of constipation [routes, time to reactions onsets and outcomes not stated]. Case 1: The woman was hospitalised for diabetes mellitus in April 2016 and received treatment with insulin. She had a history of constipation. During hospitalisation her fasting plasma glucose (FPG) was 118 mg/dL, haemoglobin A1c (HbA1c) was 10.5%, plasma adrenocorticotropic hormone (ACTH) level was 60 pg/mL and serum cortisol level was 12.8 μg/dL. She had been receiving treatment with liraglutide since hospitalisation. Her dose of liraglutide was gradually increased from 0.3 mg/day to 0.9 mg/day. Her chronic constipation was exacerbated by liraglutide therapy. The woman received treatment with sennosides [sennoside] and magnesium oxide for palliation. A low-dose overnight dexamethasone suppression test (DST) was performed during liraglutide therapy to rule out chronic glucocorticoid excessinduced obesity, hypertension and diabetes. However, the the cortisol secretion was not suppressed. A delayed gastric emptying and small bowel transit induced by liraglutide therapy was considered as a cause. Three days after switching from liraglutide to insulin therapy, a low-dose overnight DST was carried out, which revealed the suppression of cortisol secretion. Case 2: The woman was hospitalised for diabetes mellitus in May 2016. Since January 2013, she had been receiving treatment with exenatide 10μg daily and insulin. She had a history of constipation. A physical examination exhibited no Cushing’s symptoms. During hospitalisation her FPG was 89 mg/dL, HbA1c was 8.3%, plasma ACTH was 89 pg/mL and serum cortisol was 10.6 μg/dL. A low-dose overnight dexamethasone suppression test (DST) was performed during exenatide therapy to rule out chronic glucocorticoid excess, but her cortisol secretion was not suppressed. A suspicion of delayed gastric emptying and small bowel transit induced by exenatide was made. A diagnosis of exacerbation of constipation secondary to exenatide was made. Therefore, four days after switching from exenatide to insulin therapy, a low-dose overnight DST was carried out, which revealed the suppression of cortisol secretion. A plasma ACTH and serum cortisol levels for 2 days after the DST to investigate the effect of the absorption delay induced by exenatide on the DST was made. There was no difference between the plasma ACTH and serum cortisol levels in the evening on day 1 exenatide therapy and in the evening on day 8 with insulin treatment. These levels with exenatide treatment in the morning on day 2 were less than with insulin treatment in the morning on day 9. Author comment: We herein report two patients who presented with false-positive results on a dexamethasone suppression test (DST) due to the GLP-1 RAs induced-slow absorption of dexamethasone, a synthetic long-half-life glucocorticoid. We suspected that the delayed gastric emptying and small bowel transit induced by liraglutide might be the cause. We suspected that the delayed gastric emptying and small bowel transit induced by exenatide might be the cause.