Short-term changes in energy metabolism after 1 month of a regular oral diet in severely malnourished cirrhotic patients.

Malnutrition in patients with liver cirrhosis is currently associated with abnormal fuel metabolism. The aim of this study was to evaluate changes in energy production and substrate oxidation rates in a group of 26 nonanorectic severely malnourished cirrhotic patients in stable clinical condition after 1 month of an oral diet. Child-Pugh score, nutritional status, energy expenditure, rates of nutrient oxidation, and plasma levels of intermediary metabolites in the postabsorptive phase were assessed before and after 1 month of oral nutrition. Upon entry onto the study, caloric and protein intakes were 40.1 +/- 2.0 kcal/kg and 1.44 +/- 0.8 g/kg, respectively. The Child-Pugh score did not change during the study, whereas nutritional status improved as shown by increased muscular midarm circumference, ([MMAC] P < .02), height-creatinine index (P < .05), triceps skinfold thickness ([TST] P < .01), and fat mass (P < .001). Inflammatory state improved during the study, as shown by the decrease of C-reactive protein ([CRP] P < .01) and orosomucoid (P < .001). The ratio of caloric intake to resting energy expenditure (REE) increased (1.53 +/- 0.06 v 1.66 +/- 0.07, P < .05), as well as the rate of glucose oxidation ([Gox] 73.6 +/- 9.9 v 128.1 +/- 10.3 mg/min, P < .001) and urine nitrogen excretion (6.69 +/- 0.47 v 7.96 +/- 0.48 g/d, P < .02). On the other hand, the rate of lipid oxidation (Lox) decreased (67.3 +/- 3.9 v 47.3 +/- 4.9 mg/min, P < .001) and was correlated with the decrease of free fatty acid (FFA) levels (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of liver failure, ascites, and energy expenditure on the response to oral nutrition in alcoholic liver cirrhosis.

The influence of liver failure, ascites, and energy expenditure on the response to oral nutrition was assessed in a group of 55 alcoholic cirrhotic patients. Caloric intake, nutritional status, resting energy expenditure (REE), and Child-Pugh score were evaluated before and after 1 mo of oral nutrition. Patients were severely malnourished, 73% had muscular midarm circumference (MMAC) below the 5th percentile of a reference population, 51% had triceps skinfold thickness below the 25th percentile. Eleven patients were in class A of Child, 19 in class B, and 25 in class C. Twenty-six patients were nonascitic, whereas ascites was resolved in 10 ascitic patients by the end of the study and 19 patients had refractory ascites. Liver damage was more pronounced and did not improve during the study in patients with refractory ascites. Caloric intake was approximately 40 kcal/kg of body weight and was in the same range in the three groups according to Child classification. Fat mass (FM) increased, respectively, from 17.4% +/- 1.7% to 19.5% +/- 1.4%, P < 0.01, in Child A patients; from 17.1% +/- 1.4% to 19.3% +/- 1.4%, P < 0.001, in Child B patients; and from 17.6% +/- 1.5% to 18.8% +/- 1.5%, P < 0.05, in Child C patients. The increase in FM was comparable in the three groups, whereas MMAC and the creatinine/height ratio did not change significantly. FM was lower and did not increase in patients with refractory ascites. Child C patients were characterized by an increase in the rate of glucose oxidation (P < 0.02) and a decrease in the rate of lipid oxidation (P < 0.05). High-density lipoprotein cholesterol and apolipoprotein (Apo) A1 were reliable indices of improvement of liver function in patients with severe liver failure, ApoA1 was also a marker of improvement of metabolic impairment. With respect to the measured REE/predicted REE ratio calculated according to Harris-Benedict equation (r), 19 patients were considered hypermetabolic (r < 1.1), 30 normometabolic (0.9 < r < 1.1), and 6 hypometabolic (r < 0.9). An increase in FM correlated with r (P < 0.01) and was more marked in hypermetabolic patients. In contrast to the other two groups, Child-Pugh score and nutritional status remained unchanged in the hypometabolic patients. These results show that severe liver failure did not preclude improvement of nutritional status provided caloric intake was high. In Child C patients, improvement of nutritional status paralleled improvement of liver function and normalization of oxidative metabolism. Refractory ascites had negative effects on changes in nutritional status and liver function. Despite adequate caloric intake to energy requirements, hypometabolism has a poor prognosis regarding both nutritional status and liver function.

Nutritional and metabolic consequences of basal hyperinsulinemia in alcoholic liver cirrhosis: relationship with postprandial changes in erythrocyte insulin-receptor affinity.

The nutritional and metabolic consequences of basal hyperinsulinemia were investigated in a group of 13 alcoholic cirrhotic patients; 7 healthy subjects were studied as a control group. Two groups of patients were defined on the basis of fasting insulin level: group 1 (n = 7) displayed acute hyperinsulinemia (> mean of control group + 2SD), and group 2 (n = 6) had lower insulin levels. Nutrition status was assessed by means of anthropometric parameters; the rates of nutrient oxidation were measured after an overnight fast and 2 h after a standard meal intake. Group 1 had better nutrition status in terms of fat mass than group 2 (p < 0.05). Although the basal rates of nutrient oxidation were in the same range in the three groups, postprandially, the rate of lipid oxidation was significantly different (p < 0.01). Moreover, group 1 showed greater inhibition of postprandial lipid oxidation than the control group (p < 0.05), whereas there was no difference between group 2 and the control group. In the postprandial phase, erythrocyte insulin-receptor binding and affinity increased paradoxically in group 1, whereas they decreased in group 2 and healthy subjects (changes in binding, p < 0.025; changes in affinity, p < 0.01). In conclusion, basal hyperinsulinemia in alcoholic liver cirrhosis is related to more marked inhibition of postprandial lipid oxidation and better-preserved nutrition status and may lead to a paradoxical postprandial increase in insulin-receptor affinity.

Structural changes of glutaraldehyde- treated porcine bioprosthetic valves.

Gross anatomic, histologic, and transmission and scanning electron microscopic observations were made of 29 bioprosthetic valves that had been implanted in patients for up to 115 months. On the basis of these morphologic data, no significant evidence of tissue rejection was seen. However, the durability of these valve bioprostheses is still questionable. Our observation primarily emphasize three factors: (1) disruption of the endothelial cell barrier and the lack of significant host endothelialization even 115 months after transplantation; (2) increased permeability that eased diffusion of circulating host plasma proteins into valve tissue, and increased activity of infiltration processes, eg. calcification and lipid accumulation; and (3) biodegradation of the collagen framework. Each of these factors may contribute further to valve dysfunction. Development of an intimal fibrous sheath seems to occur in porcine bioprostheses that have been implanted for the longest periods of time, but the rate of host tissue ingrowth varies.

[Role of the prevalvular terminal ileum in fecal losses in ileostomized patients]. / Rôle de l'iléon terminal prévalvulaire dans les pertes fécales des iléostomisés.

Fecal losses of water, electrolytes, fat and nitrogen were studied retrospectively in 42 cases (40 patients). To assess the role of the terminal ileum, patients were classified into 2 groups according to the length of resected and/or excluded ileum before the ileocecal junction; group I (n = 17; length less than or equal to 15 cm) and group II (n = 25; length ranging from 15 to 50 cm). In group I, fecal weight and fecal output of sodium, fat and nitrogen were (mean for 24 h) 544 g, 63 mmol, 6.5 g (6.4 p. 100 of ingesta), 2.94 respectively. In group II, fecal outputs were higher; (mean for 24 h) 862 g, 112 mmol, 10.9 g (14.2 p. 100 of ingesta), 4.2 respectively. These differences were statistically significant for fecal weight and fecal output of sodium (p less than 0.001) and for fecal output of fat when expressed as percentage of ingesta (p less than 0.02). These results show that the length of terminal ileum is a major determinant in fecal losses after ileostomy; therefore, it appears to be of major importance to preserve this segment of ileum as much as possible during ileocolic surgery.

[Thermic and metabolic effects of meals in liver cirrhosis assessment of oxidation and storage rates of nutrients]. / Effets thermogénique et métabolique du repas chez le cirrhotique: étude des capacités d'oxydation et de stockage des nutriments.

The thermic effect of food was evaluated in 10 cirrhotic patients and 7 normal controls by indirect calorimetry during 6 hours following intake of a mixed meal supplying 15 kcal/kg of body weight and containing 30, 15 and 55 percent as lipid, protein and carbohydrate calories respectively. The rates of storage and oxidation of nutriments, as well as variations of blood glucose, insulin, plasma lactates, free fatty acids, glycerol, and ketonic corps were also evaluated. The thermogenic response to food was lower (p less than 0.025) and delayed in cirrhotic patients. In cirrhotic patients the rate of glucose oxidation was significantly increased (70.2 +/- 3.9 vs 50.4 +/- 3.9 percent of the glucose load; p less than 0.01) suggesting a defect in glycogen storage. These results can be related to insulin resistance as attested by a larger increase of glucose and insulin levels in cirrhotics than in controls (p less than 0.001 and p less than 0.001, respectively). Compared with controls, lipolysis in cirrhotic patients was more suppressed as shown by a sharper decrease of free fatty acids and glycerol levels (p less than 0.001 and p less than 0.02, respectively). Furthermore, the rate of lipid oxidation decreased more in cirrhotic as compared with controls (p less than 0.001) before becoming completely suppressed. De novo lipogenesis appeared between the 2nd and 4th hours. Consequently, the rate of lipid oxidation was significantly reduced in cirrhotic vs controls (14.3 +/- 5.0 vs 30.5 +/- 3.7 percent of the lipid load; p less than 0.02) showing an increased rate of lipid storage.(ABSTRACT TRUNCATED AT 250 WORDS)

[Energy expenditure and the use of nutriments in cirrhotic patients fasting and at rest. Influence of alcoholic hepatitis and the severity score of the disease]. / Dépenses énergétique et utilisation des nutriments chez le cirrhotique à jeun et au repos. Influence de l'hépatite alcoolique et du score de gravité de la maladie.

Resting energy expenditure and nature of fuels consumed after an overnight fast have been evaluated in 30 cirrhotic patients and 10 normal subjects by indirect calorimetry. Basal metabolic requirements in patients were slightly increased although most of them had as poor nutritional condition assessed by a decreased muscular mass (17.3 +/- 0.8 vs 22.5 +/- 1.2 kg, p less than 0.001). Resting energy expenditure was significantly elevated in 16.7 p. 100 of patients. This hypermetabolic state was related to alcoholic hepatitis. Surface area and the Harris-Benedict equation did not accurately predict the resting energy expenditure. Compared to normal subjects, all patients had higher levels of free fatty acids (0.408 +/- 0.05 vs 0.182 +/- 0.03 mmol/l, p less than 0.001), glycerol (0.109 +/- 0.009 vs 0.035 +/- 0.003 mmol/l, p less than 10(-9)) and ketone bodies (0.137 +/- 0.012 vs 0.099 +/- 0.012 mmol/l, p less than 0.03). The respiratory quotient was lower in cirrhotic patients (0.740 +/- 0.01 vs 0.832 +/- 0.02, p less than 10(-5)). These results show increased lipolysis and a preferential use of fat as fuel substrates in cirrhotic patients: 70 p. 100 of the total calorie expenditure was derived from fat. Fat mobilization was influenced by nutritional status: a positive correlation has been found between fat mass and free fatty acids (p less than 0.02) and between fat mass and glycerol (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging, energy expenditure and nutritional status: evidence for denutrition-related hypermetabolism.

Resting energy expenditure (REE) and nutritional status have been evaluated in 39 elderly inpatients (mean age 84.0 +/- 6.9 years). The nutritional status declined with aging as shown by significant negative correlations between age and, respectively, weight (p < 0.001), fat free mass (FFM) (p < 0.01) and body mass index (BMI) (p < 0.01). The best prediction for REE when considering the whole population was given by FFM (p < 0.001). Increased REE was observed in patients after recent surgery, related to an inflammatory state, as shown by increased plasma levels of C-reactive protein and orosomucoid. Irrespectively of the inflammatory state, REE was also found to be related to the nutritional status: patients who showed a BMI < 20 had higher REE than patients with a BMI > 20 (28.4 +/- 1.3 vs. 22.1 +/- 0.7 kcal/kg of body weight; p < 0.001; 35.7 +/- 1.6 vs. 30.9 +/- 1.0 kcal/kg of FFM; p < 0.02). These results increasingly suggest that elderly patients may suffer from denutrition relevant to hypermetabolism.