To the Editor: The recent article by Chapman et al1 and a case report published some years previously in the Journal2 indicated that hyponatraemia may occur during indapamide therapy. However, it should be noted that the data came from spontaneous adverse drug reaction reporting, and therefore can give no indication of the incidence or relative risk of hyponatraemia compared with other diuretics. Nor can it give the incidence of hyponatraemia as a proportion of side effects occurring during indapamide therapy.

The presentation of these data appears to cause some confusion, including an interpretation that hyponatraemia was more common with indapamide therapy than other diuretics.3 However, adverse events may be more likely to be reported for drugs which are usually well tolerated. Hyponatraemia led to discontinuation of therapy in only eight out of 3000 patients in the PROGRESS study.3,4 Previous controlled studies of indapamide (2.5 mg or sustained-release 1.5 mg daily) have found no significant overall changes in serum sodium levels.3

Hyponatraemia associated with indapamide therapy may occur with a recommended dose of 2.5 mg, which does not have a significant diuretic effect. Indapamide appears to be useful for treating central diabetes insipidus, raising the possibility that hyponatraemia occurs because of an inappropriate antidiuretic hormone secretion syndrome.6 Indapamide-related hyponatraemia may be more common in elderly women,1 as is the case for hyponatraemia associated with selective serotonin reuptake inhibitors. Hyponatraemia associated with indapamide therapy appears to be sporadic and uncommon and may be avoided by appropriate monitoring of serum electrolyte levels.