Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of urea synthesis as measured by functional hepatic nitrogen clearance (i.e., the relation of urea synthesis rate to blood alpha-amino nitrogen concentration) was studied before and after diet protein supplementation in six healthy subjects and five patients with stable cirrhosis (galactose elimination capacity about 60% of control). Daily protein intake was increased for 14 days by a protein-enriched liquid from (mean +/- S.D.) 1.01 +/- 0.32 g/kg body wt. to 1.62 +/- 0.31 g/kg body wt in the control subjects, and from 0.69 +/- 0.21 g/kg body wt. to 1.50 +/- 0.15 g/kg body wt. in the patients with cirrhosis. This increased the hepatic nitrogen clearance from 27 +/- 10 l/h to 39 +/- 15 l/h in the control subjects (p less than 0.05) and from 15 +/- 6 l/h to 21 +/- 7 l/h in the cirrhosis patients (p less than 0.05). There was no effect on the galactose elimination capacity in any group. Compared to the control subjects, the response in hepatic nitrogen clearance relative to the increase in protein intake was reduced by 60% in the patients. Basal glucagon was 75% higher in the patients and increased by 50% during high protein intake (p less than 0.05), but did not parallel the increase in hepatic nitrogen clearance, and it did not change in the control subjects. The study shows that an increase in protein intake selectively increases liver function with regard to disposal of amino nitrogen; the mechanism is qualitatively intact but quantitatively deficient in patients with cirrhosis of the liver, and does not seem to depend on glucagon.
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PMID:Effects of an increase in protein intake on hepatic efficacy for urea synthesis in healthy subjects and in patients with cirrhosis. 150 Jun 87

Total parenteral nutrition (TPN) has become a mainstay of modern neonatal care for the increasing population of premature infants who survive their initial pulmonary disease. As with other advances in neonatal therapy, hyperalimentation has associated complications and limitations, primary among them its toxicity to the liver. The basic pathologic lesion is bile cholestasis which is probably multifactorial in etiology. Amino acid solutions, excessive calorie-to-nitrogen ratios, and deficient trace elements and antioxidants have all been implicated in this process. Total parenteral nutrition-cholestasis can progress to portal fibrosis and irreversible cirrhosis if long-term hyperalimentation is required. Most at-risk for this iatrogenic condition are those premature infants less than 1500 g birth weight who are exposed to TPN for longer than two weeks. Enteral feedings providing as little as 10 percent of caloric intake are beneficial, and the prognosis for recovery is good once enteral feedings are established.
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PMID:Hyperalimentation associated hepatotoxicity in the newborn. 156 68

Hepatic encephalopathy is a neuropsychiatric syndrome, which can occur in the clinical course of acute (fulminant) or chronic hepatic failure of various aetiology; reversible metabolic abnormalities without neuronal structural changes are frequently found in this condition. High blood ammonia levels, an imbalance between plasma concentrations of branched-chain and aromatic amino acids, false neurotransmitters and neurotransmitters receptor changes in CNS are the commonly recognized pathogenetic mechanism of this syndrome. Protein malnutrition is a frequent occurrence in liver cirrhosis, especially of alcoholic aetiology. High protein diets may precipitate hepatic encephalopathy; protein restriction leads to malnutrition and enhances a negative nitrogen balance. Several clinical studies have shown that vegetable proteins are tolerated better than animal in patients with liver cirrhosis and chronic portal-systemic encephalopathy: encephalopathy index is usually lower after vegetable-protein than animal-protein diet. The favourable therapeutic effect of vegetable diets on nitrogen metabolism can be mainly accounted for by the increased intake of dietary fibers and increased incorporation and elimination of nitrogen in fecal bacteria. Mixture of amino acids enriched with branched-chain amino-acids may contribute to maintain a positive nitrogen balance and minimize muscle wasting in cirrhotics.
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PMID:[The dietary protein contribution and hepatic encephalopathy in cirrhosis]. 162 17

Based on urinary nitrogen excretion, previous studies have indicated increased protein breakdown rates in cirrhosis. However, studies using [1-13C]-leucine infusion methodology have found normal protein breakdown rates. Because abnormal partitioning between extracellular and intracellular leucine exists in cirrhosis, plasma enrichment of leucine's keto acid (KIC), a marker of intracellular leucine, may more accurately reflect protein metabolism than plasma [1-13C]leucine enrichment. Therefore, protein breakdown and oxidation were calculated using both [1-13C]leucine and [1-13C]KIC and compared with urinary nitrogen excretion in seven cirrhotics and seven matched controls after an overnight fast. The ratio of KIC and leucine plasma enrichment was decreased (P less than 0.001) in cirrhosis because of lower KIC enrichment (P less than 0.006). Cirrhotics had increased rates of protein breakdown (P less than 0.006) and protein oxidation (P less than 0.05) based on KIC (P less than 0.006) but not leucine enrichment. In controls, protein oxidation calculated from urinary nitrogen excretion did not differ from KIC results (0.88 +/- 0.08 vs. 0.83 +/- 0.06) but was higher than the leucine method (0.88 +/- 0.08 vs. 0.73 +/- 0.05; P less than 0.01). However, in cirrhotics protein oxidation based on urinary nitrogen was lower than the KIC methodology (P less than 0.01). Therefore, cirrhotics have accelerated rates of protein breakdown and oxidation associated with increased extrarenal nitrogen loss. Furthermore, these results suggest abnormal leucine transport across cell membranes.
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PMID:In vivo differences between the turnover rates of leucine and leucine's ketoacid in stable cirrhosis. 163 76

Urinary 15N-ammonia and 15N-urea were measured by gas chromatography-mass spectrometry after the intravenous administration of 15N-ammonia (0.2 mumol/kg/hr) to 6 volunteers and 11 patients with cirrhosis. Urinary 15N-nitrogen excretion as ammonia and urea was measured during the 210-min infusion period, and urea synthesis and ammonia conversion to amino acids were analyzed with a three-compartment model using the nonlinear least-squares method. The rate of urea synthesis in control subjects was 14.1 +/- 1.2 mg/kg/hr (mean +/- S.E.M.), and in cirrhotic patients it was 11.0 +/- 3.2 mg/kg/hr. The cirrhotic group was divided into those with compensated cirrhosis (Child class A patients) and those with decompensated cirrhosis (Child classes B and C patients), and the rates of urea synthesis for these groups were 14.5 +/- 1.5 and 8.9 +/- 1.6 mg/kg/hr, respectively. The difference between decompensated cirrhotic patients and control subjects was statistically significant (p less than 0.001). The percentage of ammonia reutilization of a given dose of 15N-ammonia was 75.9% +/- 2.4% in compensated cirrhotic patients and 82.9% +/- 3.6% in decompensated cirrhotic patients (p less than 0.05). Fasting venous ammonia levels correlated inversely with urea synthesis (p less than 0.001) and correlated positively with ammonia reutilization (p less than 0.05). These results are consistent with a decreased capacity to synthesize urea and an increased capacity to convert ammonia to amino acids in chronic liver failure.
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PMID:Metabolism of 15N-ammonia in patients with cirrhosis: a three-compartmental analysis. 163 43

To delineate the natural clinical course of spontaneous bacterial peritonitis in hepatitis B-related cirrhosis and to determine if it occurs in hepatocellular carcinoma, a prospective survey was conducted in 262 patients over 2 1/2 years. The in-hospital incidence and mortality rates of spontaneous bacterial peritonitis were 21.6% and 36.4%, respectively, in cirrhosis and 7.3% and 50% in hepatocellular carcinoma. In cirrhosis, the cumulative probability of annual recurrence of spontaneous bacterial peritonitis was 47.3%, which was significantly higher than the annual probability of occurrence of 11.3% in those with no previous attack (P less than 0.0001). The cumulative probability of annual survival was 27.6% in the spontaneous bacterial peritonitis patients, significantly lower than the probability of 64.0% in the control group (P = 0.0001). A univariate analysis, with Kaplan-Meier curves compared by the Mantel-Cox test, and subsequent multivariate analysis by stepwise Cox regression procedure were used to evaluate 37 variables recorded immediately after admission. Blood urea nitrogen concentration greater than 10.5 mmol/L urea (greater than 30 mg/dL) and ascitic fluid protein concentration less than 7.35 g/L (less than 735 mg/dL) were found to be the only significant predictors of lower annual survival; ascitic fluid protein concentration less than 7.50 g/L (less than 750 mg/dL) was the only significant predictor of higher annual recurrence. The authors conclude that spontaneous bacterial peritonitis has a high risk of recurrence in hepatitis B-related cirrhosis and that the same disease occurring in patients with hepatocellular carcinoma is related to the underlying cirrhosis rather than the hepatocellular carcinoma.
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PMID:Spontaneous bacterial peritonitis in patients with hepatitis B-related cirrhosis and hepatocellular carcinoma. 165 49

The relationship between nutritional intervention and circulating thyroid hormones and rapid-turnover proteins was investigated in surgical patients with liver cirrhosis. Fourteen patients with well-compensated liver cirrhosis who were subjected to operations for esophageal varices or hepatoma were divided into two groups. The oral group was offered an oral diet containing 2200 kcal/day before surgery and conventional intravenous infusions of 5% glucose after the operation (500-600 kcal/day). The supplementary parenteral nutrition (SPN) group was offered the same oral diet as the oral group, combined with intravenous 50% glucose, fat emulsion, and branched-chain enriched amino acid solution, 600-1000 kcal and 7.32 g nitrogen/day during the 10 days before surgery and 800-1800 kcal and 7.32-9.76 g nitrogen/day during the first 2 wk postoperative. Plasma triiodothyronine (T3) was higher in the SPN group (1.26 +/- 0.09 ng/ml) than in the oral group (0.91 +/- 0.08 ng/ml) (P less than 0.001), and reverse T3 (rT3) was lower in the SPN group (297 +/- 33 pg/ml) than in the oral group (351 +/- 29 pg/ml (P less than 0.01) on the day of surgery. In addition, SPN significantly attenuated the low T3 and high rT3 levels found in the oral group throughout the 2 postoperative wk. In addition, attenuation of decreases in rapid-turnover proteins was achieved in the SPN group. It is likely that the SPN contributed to the partial correction of liver dysfunction and metabolic imbalance in traumatized cirrhotic patients.
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PMID:Effects of supplementary parenteral nutrition on thyroid hormone patterns in surgical patients with liver cirrhosis. 166 19

The malnourished alcoholic patient requires frequently hospitalization for treatment and an adequate nutritional support is necessary for recovery of their health. The objective of the present study was to evaluate the nutritional value of an enteral diet based on "soya milk", corn sugar, coconut oil and water. Seven alcoholics, males, with 36.4 year mean age, without any clinical evidence of hepatic cirrhosis and/or pancreatitis, were submitted to three periods of metabolic nitrogen balance (NB), with multiple levels of protein intake (0.4, 0.6 and 0.8 grams of proteins/kg of body weight/day). The nitrogen intake (NI), the fecal nitrogen (FN) and the urinary nitrogen (UN) were determined, and the NB and protein digestibility value were calculated. The net protein utilization (NPU) was calculated by correlation studies between the NI and NB, with a value of 101.3%. The mean true digestibility was 100.1% and the mean requirement for that population was 0.5g protein/kg of body weight/day. Using a 97.5% confidence limit, the protein requirement of the enteral diet was calculated to be 0.8g protein/kg of body weight/day. The enteral diet based on "soya milk" can be profitable for this group of patients. It is a good alternative for use in enteral nutrition, easily available, well tolerable, and of high biological value.
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PMID:[Nutritional value of soya milk in the treatment of malnourished alcoholic patients]. 166 22

In the post-absorptive stage L-alanine is the main source of alpha-amino-nitrogen reaching the liver as glucose precursor. This aminoacid has been used as a measure of urea synthesis capacity in several pathologic conditions, but it has not been employed sistematically in patients with liver cirrhosis. We tried to address this issue by evaluating: a) L-alanine plasma levels, b) urea extraformation (UE), and c) ammoniogenesis after oral L-alanine (0.25 and 0.50 g/kg b wt) in healthy control subjects and in patients with nonalcoholic compensated (Child-Pugh's A class) and decompensated (Child-Pugh's B and C) liver cirrhosis. L-alanine plasma levels after oral load were higher and lasted longer in cirrhotics as compared to controls. Furthermore, after L-alanine oral load, significantly higher ammonia plasma levels were observed in cirrhotics than in controls. Changes in the urea extraformation were comparable in cirrhotics and controls. Both delayed L-alanine elimination from plasma and L-alanine-induced hyperammoniemia were more evident in decompensated cirrhotics and related to L-alanine dose.
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PMID:L-alanine plasma levels after oral loads in non-alcoholic liver cirrhosis: relationship with urea extraformation and ammoniogenesis. 174 21

Altered metabolism has been shown to exist in the settings of surgical stress, cancer, cirrhosis, sepsis, and trauma. Each condition is characterized by varying degrees of alteration in metabolic processes, and within a given patient, these metabolic alterations will change as the patient's status changes. Nutrition support is an integral part of the metabolic management of critically ill patients. Metabolic changes impact nutritional substrate requirements and utilization. As the patient's clinical condition deteriorates, clinical signs and symptoms become less reliable in predicting or assessing the existing physiologic state. Objective measurements are needed to define the metabolic status during these physiologic changes. The purpose of this article is to review selected indices that have been used to identify abnormalities in nutritional substrate metabolism. Although some of these tests are readily available and inexpensive, many have not been used outside of the research setting and, therefore, their clinical utility has yet to be determined. However, their use as research tools for defining metabolism warrants their inclusion in order to assist the clinician in interpreting research studies. The biochemical markers discussed include glucose, lactate, pyruvate, triglycerides, beta-hydroxybutyrate, acetoacetate, urinary nitrogen, acute phase proteins, visceral proteins, 3-methylhistidine, plasma amino acids, oxygen consumption, and resting energy expenditure. Each marker is defined in terms of its biochemical significance, and the literature describing changes that occur in various stress states is cited.
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PMID:Overview of biochemical markers used for nutrition support. 190 7


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