We present a 56-year-old man referred to Endocrinology for assessment of hypokalaemia whilst admitted with facial swelling and dental pain. Relevant history included hypertension previously managed with lercanidipine, hydrochlorothiazide and telmisartan; type 2 diabetes on metformin; and erectile dysfunction. Blood tests revealed severe hypokalaemia (2.4mmol/L), with a metabolic alkalosis (VBG pH 7.50, bicarbonate 36mmol/L, CO2 47mmHg, chloride 93mmol/L) and ECG changes. He required up to 90mmol of intravenous potassium replacement per day. Systolic blood pressure during the admission peaked at 180 mmHg. Urine sodium excretion was elevated at 324 mmol/day (reference: 40 - 220 mmol/day). Urine potassium excretion was 93.0 mmol/day (reference: 40 – 100 mmol/day).
Hypertension workup revealed renin-aldosterone ratio of 20 (renin 31.7mIU/L, aldosterone 637pmol/L) and mild elevation of serum normetanephrines of 1407pmol/L (reference < 900pmol/L). CT imaging demonstrated normal adrenal glands.
The patient eventually disclosed use of alprostadil 10mcg intracavernous injection for erectile dysfunction at least three times per week. He was reported excess caffeine intake - 1.5L of Coca Cola and multiple cups of coffee most days. Given the metabolic alkalosis, a diagnosis of pseudo-aldosteronism due to alprostadil was made. Withholding alprostadil in hospital led to normalisation of potassium and he was discharged on oral replacement. The patient was recommended to stop alprostadil and decrease caffeine intake. He has declined outpatient follow-up.
Alprostadil is a prostaglandin E1 analogue used to treat erectile dysfunction via intracavernosal injection, dilating the cavernosal arteries and relaxing smooth muscle of the corpus cavernosum and spongiosum. Hypokalaemia has been reported in neonates receiving prostaglandin E1 infusions for management of congenital heart disease, termed “Pseudo-Bartter syndrome”. Electrollyte and water imbalances induced by exogenous prostaglandin administration has also been documented in animal models. Proposed mechanisms include activation of the renin-angiotensin-aldosterone system and enhanced glomerular filtration leading to increased urinary sodium and potassium excretion.