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To:
ADC Fetal and Neonatal Edition Letters and ADC Education and Practice Letters
Electronic Letters to:
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Electronic letters published:
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oscar,m jolobe, retired geriatrician manchester medical society, c/o john rylands university library, oxford road, manchester M13 9PP
Send letter to journal:
oscarjolobe{at}yahoo.co.uk oscar,m jolobe
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The use of torasemide in paediatric patients with heart failure(1) is part of an increasing recognition that diuretics which activate the renin- angiotensin-aldosterone system(RAAS)might be detrimental in the long term,given the findings of an observational study using propensity score methods which documented an increased mortality risk(Hazard Ratio 1.31; 95% confidence interval 1.11-1.55; p=0.002)associated with chronic use of non-potassium sparing diuretics vs no diuretic use in the context of chronic heart failure. Of note, this association was noted across a wide spectrum of heart failure patients, including those with Class I and II New York Heart Association symptoms(2). In a subsequent publication, the authors of the study suggested that "clinicians might consider using torasemide instead of furosemide, as the former is less likely to cause neurohormonal activation and may even reverse neurohormone-induced myocardial fibrosis and reduce mortality"(3). These recommendations have relevance also to chronic treatment of patients with hypertension(including those who are minimally symptomatic) when a choice has to be made between competing antihypertensive diuretics, exemplified by torasemide vs thiazides(4). In this context the antialdosterone property of torasemide, to which allusion has already been made(1), compares favourably with the risk of RAAS activation attributable to thiazides such as hydrochlorothiazide(5). The latter has the potential to confer a long-term risk of RAAS-related myocardial fibrosis(3) in addition to imposing a limitation to the antihypertensive potential of this drug class(6). However, given the fact that thiazides already have an established role in childhood hypertension(7), their replacement with torasemide will have to be antedated by studies documenting the degree of RAAS activation attributable to paediatric antihypertensive doses of these agents. References (1) Senzaki H., Kamiyama M., Masutani S et al Efficacy and safety of torasemide in children with heart failure Archives of Disease in Childhood2008:93:768-71 (2) Ahmed A., Husain A., Love TE et al Heart failure, chronic diuretic use, and increase in m ortality and hospitalisation: an observational study using propensity score methods European Heart Journal 2006:27:1431-9 (3) Ahmed A., Young JB., Love TE., Levesque R., Pitt B A propensity-matched study of the effects of chronic diuretic therapy on mortality and hospitalisation in older adults with heart failure International Journal of Cardiology 2008:125:246-253 (4)Baumgart P Torasemide in comparison with thiazides in the treatment of hypertension Cardiovascular Drugs and Therapy 1993:7:63-8 (5)Sassano P., Chatellier G., Billaud E., Corvol P., Menard J Comparison of increase in the enalapril dose and addition of hydrochlorothiazide as second-step treatment of hypertensive patients not controlled by enalapril alone Journal of Cardiovascular Pharmacology 1989:13:314-9 (6)Vaughan ED., Carey RM., Peach MJ., Ackerly JA., Ayers CR The renin response to diuretic therapy A limitation of antihypertensive potential Circulation Research 1978:42:376-81 (7)Lieberman E Approach to treatment of hypertension in childhood and adolescence Journal of Nephrology 1996:9:18-23 |
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