Hepato-gastroenterology · 2003
Serum concentrations of insulin-like growth factor-I (IGF-I) in patients with liver cirrhosis.
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Vyzantiadis T, Theodoridou S, Giouleme O, Harsoulis P, Evgenidis N, Vyzantiadis A
Аннотация
BACKGROUND/AIMS: Insulin-like growth factor-I is an important anabolic polypeptide with various effects. The circulating insulin-like growth factor-I is mainly liver derived. The aim of this study was to determine insulin-like growth factor-I serum levels in patients with cirrhosis and to clarify their association with patients' clinical condition and the etiology of cirrhosis.
METHODOLOGY: Forty patients with liver cirrhosis were enrolled. Cirrhosis was in 22 cases induced by virus, in 10 due to primary biliary cause and in the rest 8 of alcoholic origin. The Child score index was found as A (n = 26), B (n = 9), C (n = 5). Twenty, age-matched healthy subjects, were used as a control group. Serum insulin-like growth factor-I was measured by an immunoradiometric assay in all subjects.
RESULTS: Serum insulin-like growth factor-I levels in liver cirrhosis were found very significantly lower than in healthy individuals (57.4 +/- 7.0 ng/mL vs. 198.8 +/- 16.3 ng/mL, p = 0.0000001). In liver cirrhosis insulin-like growth factor-I was negatively correlated with spleen enlargement (r = -0.46, p = 0.0031). Child B and C patients showed significantly reduced insulin-like growth factor-I levels in comparison to patients staged as Child A (28.9 +/- 3.0 ng/mL vs. 72.8 +/- 9.3 ng/mL, p = 0.0016). The comparison of 12 patients with viral induced cirrhosis (Child A) to 14 patients with non-viral cirrhosis, of the same clinical stage, showed non-significant difference (84.2 +/- 16 ng/mL vs. 63.1 +/- 10.3 ng/mL, p = 0.27).
CONCLUSIONS: Insulin-like growth factor-I synthesis is disturbed in liver cirrhosis and reflects the severity of the clinical stage. It represents a good marker of hepatic function. The etiology of cirrhosis does not seem to influence its levels.
METHODOLOGY: Forty patients with liver cirrhosis were enrolled. Cirrhosis was in 22 cases induced by virus, in 10 due to primary biliary cause and in the rest 8 of alcoholic origin. The Child score index was found as A (n = 26), B (n = 9), C (n = 5). Twenty, age-matched healthy subjects, were used as a control group. Serum insulin-like growth factor-I was measured by an immunoradiometric assay in all subjects.
RESULTS: Serum insulin-like growth factor-I levels in liver cirrhosis were found very significantly lower than in healthy individuals (57.4 +/- 7.0 ng/mL vs. 198.8 +/- 16.3 ng/mL, p = 0.0000001). In liver cirrhosis insulin-like growth factor-I was negatively correlated with spleen enlargement (r = -0.46, p = 0.0031). Child B and C patients showed significantly reduced insulin-like growth factor-I levels in comparison to patients staged as Child A (28.9 +/- 3.0 ng/mL vs. 72.8 +/- 9.3 ng/mL, p = 0.0016). The comparison of 12 patients with viral induced cirrhosis (Child A) to 14 patients with non-viral cirrhosis, of the same clinical stage, showed non-significant difference (84.2 +/- 16 ng/mL vs. 63.1 +/- 10.3 ng/mL, p = 0.27).
CONCLUSIONS: Insulin-like growth factor-I synthesis is disturbed in liver cirrhosis and reflects the severity of the clinical stage. It represents a good marker of hepatic function. The etiology of cirrhosis does not seem to influence its levels.