ABSTRACT
The plasma level and pathophysiologic consequences of endothelin-1 [ET1], a potent vasoconstrictor with preferential action on renal vessels, have been investigated in 40 children with chronic liver disease [CLD] [27 males and 13 females; mean age = 8.62 +/- 4.04 years] and 15 sex and age matched clinically healthy children [9 males and 4 females; mean age = 8 +/- 4.17 years]. The children with CLD were divided into 3 subgroups : subgroup I [n = 13] had chronic hepatitis [CH], subgroup II [n = 13] had cirrhosis without ascites and subgroup III [n = 14] had cirrhosis and ascites. The cirrhotic children [n = 27] included 17 children in Child's A class and 10 children in Child's B + C class. Besides routine liver and renal function tests, serum electrolytes as well as a doppler duplex study of the portal vein and the arcuate arteries of both kidneys at the level of the corticomedullary junction, were done to all candidates of the study. The resistive index of renal vessels was calculated. ET-1 level was found to be significantly elevated in all groups of children with CLD. The highest level was in children of subgroup III [x = 4.26 +/- 2.12 ng/ml] followed by those in subgroup II [x = 1.49 +/- 0.61 ng/ml] and lastly came children with CH ie. subgroup I [x = 1.01 +/- 0.46 ng/ml].Children with Child's B+C cirrhosis had a significantly higher level [4.62 +/- 2.4 ng/ml] than those with Child's A cirrhosis [1.93 +/- 1.04 ng/ml]. Serum albumin had a significant negative correlation with ET-1 [r = 0.64] ET-1 level showed a significant negative correlation with serum sodium [r = 0.4]. It correlated positively with portal hypertension as indicated by a positive correlation with portal vein diameter [r = 0.48] and a negative correlation with portal vein flow velocity [r = 0.35]. The resistive index was significantly higher in patients with CLD compared to controls. It showed a significant positive correlation ET-1 [r = 0.49]. Thus, ET-l is elevated in patients with CLD; its elevation being related to the severity of liver disease. It could be involved in the pathophysiology of the hyponatraemia portal hypertension and disturbed renal hemodynamics seen in children with CLD