Can Anti-Hypertensives Cause Hypoglycaemia? - A Rare Presentation of Recurrent Hypoglycaemia Secondary to an ACE-Inhibitor

Abstract

Abstract Introduction: Angiotensin-converting enzyme (ACE) inhibitors are commonly prescribed Anti-hypertensives which are first line treatments in patients with Diabetes. We report a rare but significant side-effect of ACE inhibitor treatment, relevant to Diabetic and non-diabetic patients alike. Case Details: We report the case of a 79 year male, with a background of Hypertension (HTN), established on Ramipril and Bendroflumethiazide, who was admitted following an episode of unresponsiveness secondary to Hypoglycaemia, which was initially presumed secondary to Alcohol, the intake of which was minimal. He did not have a history of Diabetes Mellitus. 7 weeks later, he had a similar presentation and as found to be profoundly Hypoglycaemic. On arrival, his observations were unremarkable except for CBG 1.9 and GCS of 14/15, which responded well to IM glucagon, and IV Dextrose. Relevant investigations revealed significantly impaired renal functions and normal CT imaging. There was no history of alcohol intake or intoxication. Management: Following acute management and stabilisation, he was admitted under the Endocrine and Diabetes team, who suspended his regular medications, including his ACE-I. As an inpatient, he underwent extensive biochemical investigations which were unremarkable followed by a prolonged 72 hours fasting test and an Oral Glucose Tolerance Test, wherein no significant drop in Blood Glucose was noted in both. Subsequently, there were no further episodes of hypoglycaemia and he remained asymptomatic whilst off his ACE-I and he was safely discharged. He was followed up in our Endocrine clinic and was found to have no episodes of Hypoglycaemia since discharge and remained asymptomatic. Discussion: We report the rare presentation of recurrent hypoglycaemia in a non- diabetic secondary to ACE-I. Hypoglycaemia may be defined by the Whipple’s triad, a classical triad of hypoglycaemic symptoms, low Blood Glucose levels and relief of symptoms following ingestion of glucose. The mechanism by which ACE-I treatment leads to hypoglycaemia remains unclear. It has been postulated that ACE-I related alterations in the Kininogen-Kinin system, are associated with hypoglycaemia. This mechanism may lead to an increase in Insulin sensitivity, mediated by increased muscle tissue uptake and diminished hepatic glucose production. Another proposed mechanism is the suppressive effect that ACE-inhibitors exhibit on the peripheral sympathomimetic overactivity, thus causing Hypoglycaemia. Exacerbating factors comprise of concurrent renal impairment, as in this case. The first case of ACE-I induced Hypoglycaemia was reported in 1985, with the usage of Captopril. To the best of our knowledge, this is one of the rare peculiar cases wherein an ACE-I has been implicated as the underlying aetiology causing Hypoglycaemia in a Non-Diabetic.