My experience of diuretic-induced hyponatraemia in the elderly is in accordance with the observations made by the authors.1 In my personal series of 61 cases of severe hyponatraemia (plasma sodium <120 mmol/l), compiled over a period of 18 years in patients aged >65, 26 were attributable to thiazide diuretics, culprit drugs in seven other cases being frusemide (three cases), spironolactone on its own (one case), nonsteroidal anti-inflammatory drugs (two cases), carbamazepine, and tricyclic antidepressants (one each). Underlying causes in the other 27 cases included bronchial and other cancers, chest infection, hypoadrenalism, and inappropriate use of hypotonic intravenous fluids. Among the 26 with reversible thiazide-induced hyponatraemia, there were 10 with plasma sodium levels in the range 101–109 mmol/l. Of the 26, 11 had plasma potassium levels less than 3.5 mmol/l. The age range was 74–93 and 22 were women. Hydrochlorothiazide was the offending agent in 12 cases, having been coprescribed with amiloride in 10 instances, and with triamterene in two. Bendrofluazide was the offending agent in nine instances, the dose being 2.5 mg/day in seven instances (coprescribed with amiloride in one instance), and 5.0 mg/day in the other two. Three cases were attributable to cyclopenthiazide, and one each to hydroflumethiazide and to indapamide, respectively. One patient, aged 80, who had become hyponatraemic (plasma sodium 114 mmol/l), while taking bendrofluazide 2.5 mg/day coprescribed with amiloride 5 mg/day, reverted to a plasma sodium of 135 mmol/l after withdrawal of both agents, only to revert to a plasma sodium of 111 mmol/l when inadvertently rechallenged with thiazides, the agent this time being hydrochlorothiazide coprescribed with amiloride. I now utilise torasemide as an adjunctive diuretic in patients with a previous history of thiazide-induced hyponatraemia. The data presented here extend the observations I published previously on this topic.
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