Background: This study aimed to assess whether QT interval prolongation is an independent risk factor for development of hepatorenal syndrome (HRS) in cirrhotic patients with acute
Plasma norepinephrine concentrations are often elevated in patients with hepatic cirrhosis in relation to the stage of disease and possibly in response to a decrease in "effective" arterial blood volume. Since tyrosine, the precursor for catecholamines, is said to influence the rate of catecholamine biosynthesis within the central nervous system and peripheral sympathetic structures, we tested whether basal hypertyrosinemia and increased plasma tyrosine levels after oral loading with l-tyrosine are associated with elevated plasma catecholamine concentrations. Baseline norepinephrine (NE) and epinephrine (E) were significantly higher in 17 patients with decompensated cirrhosis, as compared with 11 healthy controls (NE: 809 +/- 108 pg/ml vs 295 +/- 16 pg/ml; E: 69 +/- 9 pg/ml vs 36 +/- 8 pg/ml). No significant correlation between the basal plasma tyrosine and norepinephrine level could be demonstrated in patients with cirrhosis (r = 0.04). Oral tyrosine loading (100 mg/kg b.w.) administered in six equal doses did not change the level of catecholamines, whereas plasma tyrosine increased two- to three-fold. Even a large single dose (14 g l-tyrosine) failed to alter plasma catecholamines in six cirrhotic patients with marked ascites. We therefore conclude that the enhanced availability of tyrosine in cirrhotics does not influence catecholamine biosynthesis in peripheral sympathetic neurons.
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