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Cardiac response to exercise in cirrhosis
  1. R H Wachsberg1
  1. 1Professor of Radiology, UMDNJ-University Hospital, 150 Bergen Street, Room C-320, Newark, NJ, USA; wachbrh{at}umdnj.edu
  1. F Wong2,
  2. L Blendis2
  1. 2Department of Gastroenterology and Hepatology, Toronto General Hospital, Toronto, Canada

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Reading the excellent article on the cardiac response to exercise in cirrhosis (Gut 2001;49:268–75), I was surprised that patients without ascites were labelled “preascitic”. The implication is that these are patients have not as yet developed ascites, presumably because their disease is less advanced than in those patients with ascites.

It is well known that many patients with cirrhosis will never develop ascites, regardless of the severity of other sequelae of portal hypertension that have developed or will ultimately develop. This is certainly borne out by my experience at a busy liver transplant centre. I would respectfully suggest that these patients be instead called simply “cirrhotic patients without ascites”.

Authors’ reply

We thank Dr Wachsberg for his comments and apologise for not making ourselves clear. In contrast with cirrhotic patients without ascites, who may well have had ascites and used diuretics sometime in the past, preascites is a well characterised stage in the natural history of cirrhosis. It occurs early in the continuum of cirrhosis. Such patients have never had ascites nor required the use of diuretics, and yet they show evidence of abnormal renal handling of sodium. They maintain sodium balance while on a diet of 100 mmol/day sodium1 but retain sodium when given an acute sodium load such as 200 mmol/day sodium for one week2 or when challenged with an intravenous saline load.3 However, these patients can eventually come to sodium balance, after an intake of 200 mmol/day sodium4 but at the expense of an increase in total and central blood volume,5 together with suppression of renin-angiotensin-aldosterone and sympathetic activities in the supine position.6 The assumption of the erect posture leads to activation of these hormonal systems7 which are responsible for the subtle sodium retention in these patients. Preascites is further characterised by increased dopaminergic activity,8 a possible consequence of the expanded intravascular volume, and elevated plasma nitric oxide levels,9 which partly contributes to the glomerular hyperfiltration observed in these patients.9,10 Finally, preascitic patients also have increased muscle sympathetic nervous activity11 although the significance of this is not clear at present. Thus the preascitic cirrhotic patient is not simply a cirrhotic patient without ascites but rather the syndrome of preascites is a syndrome with well defined characteristics. While many patients in Dr Wachsberg’s busy liver transplant unit may not have ascites, and they may well be receiving their liver transplant for reasons other than ascites, they certainly cannot be confused with preascitic cirrhotic patients.

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