This report describes transient self-limiting hyperglycemia following recreational ingestion of dexamphetamine. Amphetamines are noncatecholamine sympathomimetic amines with central nervous system stimulant activity. Dexamphetamine is used to treat narcolepsy and ADHD (attention deficit/hyperactivity disorder). It may also be abused for recreational purposes. Dexamphetamine, the dextro isomer of d,l-amphetamine sulfate, can induce hyperglycemia in rats (1).

A slender 20-year-old woman presented to her family doctor with a 10-day history of dizziness, nausea, diarrhea, lethargy, and loss of 6 kg in weight over recent months. Her temperature was 37.3°C, blood pressure 120/70 mmHg, and pulse rate 120 bpm. Finger prick blood glucose was 22.9 mmol/l, with 4+ glycosuria and 3+ ketonuria. There was no relevant past medical history. She was taking no prescribed medications. Her great aunt had type 1 diabetes. She was referred to the emergency department with a provisional diagnosis of newly diagnosed type 1 diabetes and ketoacidosis. In the emergency department, there was 2+ glycosuria and trace ketonuria. In venous blood, the pH was 7.45, pCO2 30.3 mmHg, pO2 51.2 mmHg, HCO3− 20.6 mmol/l, and base excess −1.9 mmol/l. Plasma glucose was 19.8 mmol/l. Normal saline was infused intravenously, but initiation of an insulin infusion was delayed inadvertently. Two hours later, the blood glucose had fallen to 13.2 mmol/l and returned to normal over the next 10 h without insulin. A fasting blood glucose the next day was 3.9 mmol/l.

On further inquiry, she admitted to ingesting 30 mg of dexamphetamine tablets 24 h before her presentation. Plasma dexamphetamine level was 4 μg/l at baseline in the emergency department and undetectable 20 h later. Random pre- and postprandial blood glucose recordings over the next 4 days were all <6 mmol/l. The HbA1c was 4.8% (<6%). The emrgency department admission plasma C-peptide was 5.2 nmol/l (0.30–1.20 nmol/l). Later, the fasting C-peptide was 0.57 nmol/l. GAD65 and islet cell auto-antibodies were absent. She declined formal glucose tolerance testing.

Structural analogues of dopamine (DA), including d-amphetamine, induce transient dose-dependent hyperglycemia in rats, possibly as a result of activation of hindbrain DA receptors, inducing epinephrine release from the adrenal medulla and influencing glucoregulation via adrenergic receptors at various sites (1). Other studies (2,3) have found that stimulation of D2 and D3 (but not D1) DA receptors in the brain can elevate blood glucose in rats and support the theory of increased sympathetic adrenal activity as a mechanism. In addition, analogs of DA may directly inhibit insulin release in rat pancreatic islets through α2-adrenergic receptors (4).

During the 1990s, a progressive decline in the perceived risk of recreational drug use was accompanied by increased recreational use of stimulants (5). Prescribed stimulant use in Australia increased fivefold (6). This patient presented with otherwise unexplained hyperglycemia. Resolution of this was associated with clearance of dexamphetamine from the blood. There is a theoretical basis for this in rat studies. Amphetamine use should be considered in the differential diagnosis of atypical hyperglycemic presentations.

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