To the Editor,
We report a case of severe hypoglycaemia secondary to quinolones in a haemodialysis patient.
Our patient was a 72-year-old man who received haemodialysis three times a week with a tunnelled catheter. He was admitted for severe shivering during a dialysis session. Blood and catheter cultures showed S. maltophilia and E. casseliflavus. The catheter was removed, and antibiotic treatment was initiated with levofloxacin, at 250mg every 48h, and cotrimoxazole once a day.
The patient’s renal failure was then treated medically. The sepsis developed without complication until the second week, when severe hypoglycaemia was detected, with neurological symptoms that persisted for three days. The patient received boluses of glucose at 30% via intravenous administration, and glucose infusion at 10%. Suspecting erroneous intake of oral hypoglycaemic agents, we performed a drug test but found no traces of these drugs. On the other hand, it did reveal the presence of toxic levels of levofloxacin.
The patient’s underlying nephrological disease was a primary membranous glomerulopathy. The patient had been on haemodialysis for more than ten years, and had lost all arteriovenous fistulas. He also had undergone arthrodesis of the right knee, and had multiple infections of this joint. He was hypertensive, and did not suffer diabetes mellitus.
The patient was under normal treatment with water-soluble vitamins, amlodipine, and Venofer.
Physical examination: the patient was in a mild stupor; blood pressure: 120/80; heart rate: 80 beats/min; respiratory rate: 18 breaths/min; jugular: 5cm at 30°. Heart: RR interval 2 times with II/VI grade systolic murmur in the aortic area (no radiation). Lungs: basal crackles. Abdomen was soft, depressible, and painless, with no visceromegaly. Limbs: oedema and arthrodesis of the right knee. Symmetric pulses. No embolic injuries.
Laboratory tests: [Na+]: 136mM; [K+]: 4.5mM; [Cl-]: 100mM; [HCO3-]: 20mM; haemoglobin: 9g/dl; blood urea nitrogen (BUN): 100mg/dl; creatinine: 10mg/dl; thyrotropin (TRH) 1.79mIU/ml; toxicology: 32ug/ml levofloxacin (therapeutic levels: 6ug/dl).
Hypoglycaemia secondary to levofloxacin is a very rare adverse reaction (<0.01%) according to the manufacturer.1 Several authors have described it in elderly patients with advanced chronic renal failure.2-4 The mechanism of this severe complication is caused by an inhibition of the KATP channels in the islets of Langerhans, which enhances calcium influx and the release of insulin filled vesicles. This effect has been demonstrated in a mouse model, and it is similar to that produced by sulfonylureas.5 Our first suspicion was the use of oral hypoglycaemic agents, which is well known to cause severe hypoglycaemia. However, this was ruled out by drug testing, which revealed the presence of high levels of levofloxacin, despite having adjusted the dose for the renal failure in our patient.
We conclude that, in patients with advanced renal failure, quinolones may cause hypoglycaemia as severe as that produced by oral hypoglycaemic agents.
Conflicts of interest
The authors affirm that they have no conflicts of interest related to the content of this article.
