Endocrine Abstracts

We would like to present an interesting unusual case of fluoroquinolone induced hypoglycaemia. As per FDA Adverse Event reporting System and medical literature published between 1987–2017, fluoroquinolones are said to have caused about 67 cases of life-threatening hypoglycaemic coma including 13 deaths and 9 permanent disabling injuries, most cases were associated with levofloxacin. Its hypoglycaemic effect is more common in elderly population who are on oral hypoglycaemic agents and insulin but can also happen in non diabetics. Our patient was a sixty seven year old woman who presented with an unwitnessed fall and decreased oral intake. She had a background of learning disability, hypertension, epilepsy, bronchial asthma, chronic iron deficiency anaemia, chronic mild lymphopenia, osteoporosis and previously treated uterine cancer. After clinical review an impression of hospital acquired pneumonia with possible aspiration pneumonia was made along with hyponatraemia secondary to dehydration. She was commenced on intravenous levofloxacin 500 mg twelve hourly and metronidazole 500 mg eight hourly. On first day of admission, venous plasma glucose was noted to be 7.1. She was not known to have diabetes. On third day of admission she was found unresponsive with an early warning score of four, capillary blood glucose was found to be 0.6 mmol/l, this improved with 10% glucose. Blood sugars continued to be low requiring further intravenous glucose. A medication review was undertaken and levofloxacin was discontinued. After 24 hrs of discontinuation of levofloxacin, the hypoglycaemic episodes resolved and her blood glucose later remained > 5 mmol/l throughout the admission.. A short synacthen test showed normal cortisol response (At 0 min – 262 nmol/l, 30 mins- 467 nmol/l). As the patient had no further hypoglycaemic episodes after stopping levofloxacin, a diagnosis of levofloxacin induced hypoglycaemia was made and no further investigation was deemed appropriate at that point. In experimental studies with rat islet cells exposed to quinolones, an increase in insulin secretion via blockade of adenosine triphosphate (ATP)–dependent potassium channels was observed. Thus, the possible mechanism could be increased insulin release via blockade of ATP-sensitive potassium channels in the beta-cells of the pancreas. Health professionals should be aware of the potential risk of severe hypoglycaemia with the use of Fluoroquinolones as it remains antibiotic of choice for many inflammatory conditions and blood glucose monitoring should be recommended if it is prescribed in elderly diabetic patients or in elderly patients who have poor oral intake or in those with other comorbidities to prevent life threatening hypoglycaemia.