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Randomized Controlled Trial
. 2009:(2):39-43.

[Effectiveness of nutritional support for the liver-cell deficiency in the liver cirrhosis]

[Article in Russian]
  • PMID: 19552020
Randomized Controlled Trial

[Effectiveness of nutritional support for the liver-cell deficiency in the liver cirrhosis]

[Article in Russian]
I B Khlynov et al. Eksp Klin Gastroenterol. 2009.

Abstract

The aim: To study the efficiency of enteral nutritional support and its impact on clinical-laboratorial markers of hepatocellular failure of the patients with Child-Pue's hepatic cirrhosis type B suffering from trafologic impairment. MATERIAL AND RESEARCH METHODS: 61 patients with Child-Pue's hepatic cirrhosis type B suffering from trafologic impairment took part in the randomized prospective study. The control group (31 patients) got the conventional treatment with lactulose, beta-blocker, spironolactone on the basis of 1.2 g/kg protein weight and 30 kcal/kg body weight per day. There were 30 patients in the second group (the principal one) and in addition to conventional treatment they got the multisubstrate nutritional cocktail of dietary fibers on the basis of 0.3 g/kg protein weight, 7.5 g fibers per day and 10 kcal/kg body weight during 30 days. To evaluate the efficiency of the treatment we analyzed the clinical presentation and the intensity of blood cholinesterase. The stage of hepatic encephalopathy was defined with the affinity numbers test of Retainer. The parameters under study were checked before the treatment, 30 days and 60 days later after the treatment began.

Results: It was found out during the prospective randomized study that the patients under nutritional support showed the positive clinical dynamics (asthenia and hepatic encephalopathy retrogression and the accurate increase of blood cholinesterase from 4365.4 +/- 1028.6 ME up to 5502.7 +/- 1142.6 ME (p < 0.05).

Conclusion: Nutritional support of the patients with Child-Pue's hepatic cirrhosis type B suffering from trafologic impairment is effective and has an accurate impact upon clinical-laboratorial markers of hepatocellular failure.

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