Observations on the Nitrogen Metabolism of Patients with Portal Cirrhosis

Rudman, Daniel; Akgün, Suat; Galambos, John T.; McKinney, Alexander S.; Cullen, Annette B.; Gerron, Glynda G.; Howard, Carolyn H.

doi:10.1093/ajcn/23.9.1203

Cited by 28 publications

(6 citation statements)

References 15 publications

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“…Previously, protein loads were thought to be a common precipitating factor for HE[23,27]. However, protein restriction worsens the nutritional status of cirrhotic patients[10,50] and a report by Córdoba et al[49] showed that diets with a normal-high protein content (1.2 g/kg per day) are metabolically more adequate than low-protein diets and can be administered safely to cirrhotic patients with episodic HE.…”

Section: Discussionmentioning

confidence: 99%

“…Exclusion criteria in this group were present or former HE and variceal bleeding within one week before the study. The high protein meal was used to predict the likelihood of HE developing following a shunt procedure[23]. To test for covert HE, the “number connection test” (NCT)[24] was performed in all patients and an electroencephalogram[25] was recorded in Child-Pugh stage C patients.…”

Section: Methodsmentioning

confidence: 99%

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Protein tolerance to standard and high protein meals in patients with liver cirrhosis

Campollo

Sprengers

Dam

et al. 2017

WJH

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AIMTo investigate the plasma amino acid response and tolerance to normal or high protein meals in patients with cirrhosis.METHODSThe plasma amino acid response to a 20 g mixed protein meal was compared in 8 biopsy-proven compensated cirrhotic patients and 6 healthy subjects. In addition the response to a high protein meal (1 g/kg body weight) was studied in 6 decompensated biopsy-proven cirrhotics in order to evaluate their protein tolerance and the likelihood of developing hepatic encephalopathy (HE) following a porto-caval shunt procedure. To test for covert HE, the “number connection test” (NCT) was done on all patients, and an electroencephalogram was recorded in patients considered to be at Child-Pugh C stage.RESULTSThe changes in plasma amino acids after a 20 g protein meal were similar in healthy subjects and in cirrhotics except for a significantly greater increase (P < 0.05) in isoleucine, leucine and tyrosine concentrations in the cirrhotics. The baseline branched chain amino acids/aromatic amino acids (BCAA/AAA) ratio was higher in the healthy persons and remained stable-but it decreased significantly after the meal in the cirrhotic group. After the high protein meal there was a marked increase in the levels of most amino acids, but only small changes occurred in the levels of taurine, citrulline, cysteine and histidine.The BCAA/AAA ratio was significantly higher 180 and 240 min after the meal. Slightly elevated basal plasma ammonia levels showed no particular pattern. Overt HE was not observed in any patients.CONCLUSIONPatients with stable liver disease tolerate natural mixed meals with a standard protein content. The response to a high protein meal in decompensated cirrhotics suggests accumulation of some amino acids but it did not precipitate HE. These results support current nutritional guidelines that recommend a protein intake of 1.2-1.5 g/kg body weight/day for patients with cirrhosis.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Protein tolerance to standard and high protein meals in patients with liver cirrhosis

Campollo

Sprengers

Dam

et al. 2017

WJH

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“…In comparison with quantitative measurement of global liver function using foreign substances such as galactose elimination rate a n d antipyrine clearance, the daily urea-nitrogen synthesis rate assesses the production of endogenous urea. This method was originally proposed by Rudman et al in 1970 andthen by Galambos in 1978' ',". Hansen a n d Poulsen16 demonstrated that, before and after resection of 70 per cent liver tissue in rats, determination of urea-nitrogen synthesis rate was a more useful assessment than the galactose elimination rate a n d antipyrine clearance.…”

Section: Discussionmentioning

confidence: 99%

Limited hepatic resection for selected cirrhotic patients with hepatocellular or cholangiocellular carcinoma: A prospective study

Paquet¹,

Koussouris²,

Mercado³

et al. 1991

British Journal of Surgery

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From 1 January 1983 to 1 January 1989 123 cirrhotic patients with hepatocellular cancer (n = 122) or cholangiocarcinoma (n = 1) were screened using liver function tests, alpha-fetoprotein determination, ultrasonography with biopsy (and in selected cases computed tomography or nuclear magnetic resonance), laparoscopy and angiography, Child-Pugh classification and urea-nitrogen synthesis rate. Twenty-three patients were selected for surgical resection because the tumour was smaller than 5 cm, not centrally located and at least 1 cm away from main structures; there was no evidence of multicentricity or metastatic disease; and the Child-Pugh classification was A or B and the urea-nitrogen synthesis rate at least 6 g/day. Upper gastrointestinal endoscopy was used routinely to identify oesophageal varices which were present in 17 cases; ten patients with a history of variceal haemorrhage (43 per cent) had preoperative endoscopic sclerotherapy. In cases with recurrent haemorrhage, surgery was used to prevent intraoperative and postoperative bleeding. Tumour resection was carried out using controlled hypotension and hepatoduodenal ligament clamping. Twelve bisegmentectomies, ten segmentectomies and one atypical resection were performed. The operative mortality rate was 13 per cent with liver failure and sepsis as the causes of death. The 'recurrence rate' was 26 per cent and the late mortality rate for the whole group up to 1 January 1990 was 30 per cent; 13 patients were still alive. The 12-month survival rate was 77 per cent and after 5 years it was 49 per cent. Thus, surgical resection of small liver tumours is the treatment of choice in this selected group of patients.

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“…On the other hand, an excessive degree of positive nitrogen balance was observed in these patients upon institution of a high protein diet (120 g/day) after a period of 8-10 days on the low protein diet. This excessive degree of nitrogen balance was associated with a subnormal uri nary excretion of urea and no gain in body weight, suggesting that it was caused by a decrease in the synthesis of urea (151). Although estimates of total body nitrogen balance do not seem to be altered signifi cantly in cirrho sis, there are profound alterations in the distribution of nitrogen between the liver and other organs, and in intermediary nitrogen metabolism.…”

Section: Nitrogen Balancementioning

confidence: 99%

Liver Disease and Protein Needs

Mezey

1982

Annu. Rev. Nutr.

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Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

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Observations on the Nitrogen Metabolism of Patients with Portal Cirrhosis

Cited by 28 publications

References 15 publications

Protein tolerance to standard and high protein meals in patients with liver cirrhosis

Protein tolerance to standard and high protein meals in patients with liver cirrhosis

Limited hepatic resection for selected cirrhotic patients with hepatocellular or cholangiocellular carcinoma: A prospective study

Liver Disease and Protein Needs

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