Benazepril
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Reactions 992 - 13 Mar 2004 ★ S Benazepril First report of metabolic acidosis in a child: case report A 4-year-old boy developed hyperchloraemic metabolic acidosis during treatment with benazepril for nephrotic syndrome. The boy presented with a 10-day history of vomiting and drowsiness 4 months after starting treatment with benazepril 0.3 mg/kg/day; his corticosteroid treatment had been tapered over the last 7 months and discontinued 10 days before presentation. On examination he was tired and asthenic, and laboratory investigations revealed metabolic acidosis with a pH of 7.28, a pCO2 of 20, a base excess of –15, a bicarbonate level of 9.3 and moderate hyperchloraemia. Suppression of hypothalamic-pituitary-adrenal axis function as a side effect of corticosteroid therapy was suspected. A saline and bicarbonate infusion was started and his symptoms improved; metabolic acidosis due to gastroenteritis was diagnosed. He was discharged home, but his anorexia and nausea did not resolve and he was readmitted 2 weeks later. Laboratory investigations again revealed metabolic acidosis. He had mild persistent hyperchloraemia and a urinary pH of 6, and a 24-hour urine collection showed increased excretion of sodium ions and decreased excretion of potassium and chloride ions, with a positive urinary anion gap (149 mEq/L). Proximal renal tubular acidosis was suspected and treatment with oral bicarbonate and saline was started, with a subsequent increase in pH to 7.38. However his vomiting worsened and there was no improvement in his nausea or anorexia. His aldosterone level was found to be < 7.5 pg/mL. The boy’s benazepril dose was decreased to 0.2 mg/kg/day and, within a few days, his blood gases and electrolyte levels had normalised and his clinical condition had improved. One week later benazepril was discontinued, and his aldosterone level increased to 29.4 pg/mL after 10 days; he subsequently made a complete recovery. Author comment: "This is the first description in the literature of a case of hyperchloraemic ACE-inhibitor-induced metabolic acidosis in a child." Bruno I, et al. ACE-inhibitors-induced metabolic acidosis in a child with nephrotic syndrome. Pediatric Nephrology 18: 1293-1294, No. 12, Dec 2003 - Italy 807216115 » Editorial comment: A search of AdisBase and Medline did not reveal any previous case reports of metabolic acidosis associated with benazepril. The WHO Adverse Drug Reactions database contained five reports of acidosis associated with benazepril. 1 Reactions 13 Mar 2004 No. 992 0114-9954/10/0992-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Benazepril
Reactions 992 - 13 Mar 2004
★ SBenazepril
First report of metabolic acidosis in a child: casereport
A 4-year-old boy developed hyperchloraemic metabolicacidosis during treatment with benazepril for nephroticsyndrome.
The boy presented with a 10-day history of vomiting anddrowsiness 4 months after starting treatment with benazepril0.3 mg/kg/day; his corticosteroid treatment had been taperedover the last 7 months and discontinued 10 days beforepresentation. On examination he was tired and asthenic, andlaboratory investigations revealed metabolic acidosis with apH of 7.28, a pCO2 of 20, a base excess of –15, a bicarbonatelevel of 9.3 and moderate hyperchloraemia. Suppression ofhypothalamic-pituitary-adrenal axis function as a side effect ofcorticosteroid therapy was suspected. A saline andbicarbonate infusion was started and his symptoms improved;metabolic acidosis due to gastroenteritis was diagnosed. Hewas discharged home, but his anorexia and nausea did notresolve and he was readmitted 2 weeks later. Laboratoryinvestigations again revealed metabolic acidosis. He had mildpersistent hyperchloraemia and a urinary pH of 6, and a24-hour urine collection showed increased excretion ofsodium ions and decreased excretion of potassium andchloride ions, with a positive urinary anion gap (149 mEq/L).Proximal renal tubular acidosis was suspected and treatmentwith oral bicarbonate and saline was started, with asubsequent increase in pH to 7.38. However his vomitingworsened and there was no improvement in his nausea oranorexia. His aldosterone level was found to be < 7.5 pg/mL.
The boy’s benazepril dose was decreased to 0.2 mg/kg/dayand, within a few days, his blood gases and electrolyte levelshad normalised and his clinical condition had improved. Oneweek later benazepril was discontinued, and his aldosteronelevel increased to 29.4 pg/mL after 10 days; he subsequentlymade a complete recovery.
Author comment: "This is the first description in theliterature of a case of hyperchloraemic ACE-inhibitor-inducedmetabolic acidosis in a child."Bruno I, et al. ACE-inhibitors-induced metabolic acidosis in a child with nephroticsyndrome. Pediatric Nephrology 18: 1293-1294, No. 12, Dec 2003 -Italy 807216115
» Editorial comment: A search of AdisBase and Medline didnot reveal any previous case reports of metabolic acidosisassociated with benazepril. The WHO Adverse Drug Reactionsdatabase contained five reports of acidosis associated withbenazepril.
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Reactions 13 Mar 2004 No. 9920114-9954/10/0992-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
