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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The energy needs, nutritional status and body composition of 6 undernourished adolescents and young adults with cystic fibrosis (3 male and 3 female) were studied prior to and following a 12 day period of refeeding. Nutritional rehabilitation was attempted with continuous naso-gastric feeding of an elemental diet. The energy needs of the patients were shown to be 25-80% higher than in healthy individuals of the same age, sex and size. Lean body mass as judged by measurement of total body potassium and nitrogen was relatively well preserved, but there was significant wasting of adipose tissue. During the short period of refeeding, body weight, fat and potassium all increased significantly, while fat free body mass and total body nitrogen did not change. A model is proposed for the aetiology of undernutrition in the adolescent and young adult cystic with deteriorating lung function. Based on this model and the finding of the short-term N/G refeeding program described in this paper, we have embarked on a long-term supplementation study in malnourished CF patients who do not respond to dietary counselling and oral supplementation.
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PMID:Energy needs and nutritional rehabilitation in undernourished adolescents and young adult patients with cystic fibrosis. 643 97

Diuretic therapy is the most common cause of potassium deficiency. Although the extent of potassium deficiency usually does not exceed 200 or 300 mEq, under appropriate circumstances such modest deficiency may have important consequences. Factors that tend to increase the incidence or severity of potassium deficiency in patients who take diuretics include high salt diets, large urine volumes, metabolic alkalosis, increased aldosterone production, and the simultaneous use of two diuretics that act on different sites in the renal tubule. There are many serious complications of potassium deficiency, including cardiac arrhythmias, muscle weakness, rhabdomyolysis, glucose intolerance, and several complications that result directly from increased ammonia production, such as protein and nitrogen wasting and hepatic coma. Emphasized herein are those conditions that impose potential danger in patients with mild hypokalemia. Important factors that identify specific causes of potassium deficiency and its treatment are discussed briefly.
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PMID:Diuretic-induced hypokalemia. 649 56

Patients with major injury or illness develop protein wasting, hypermetabolism, and hyperglycemia with increased glucose flux. To assess the role of elevated counterregulatory hormones in this response, we simultaneously infused cortisol (6 mg/m2 per h), glucagon (4 ng/kg per min), epinephrine (0.6 microgram/m2 per min), and norepinephrine (0.8 micrograms/m2 per min) for 72 h into five obese subjects receiving only intravenous glucose (150 g/d). Four obese subjects received cortisol alone under identical conditions. Combined infusion maintained plasma hormone elevations typical of severe stress for 3 d. This caused a sustained increase in plasma glucose (60-80%), glucose production (100%), and total glucose flux (40%), despite persistent hyperinsulinemia. In contrast, resting metabolic rate changed little (9% rise, P = NS). Urinary nitrogen excretion promptly doubled and remained increased by approximately 4 g/d, reflecting increased excretion of urea and ammonia. Virtually all plasma amino acids declined. The increment in nitrogen excretion was similar in three additional combined infusion studies performed in 3-d fasted subjects not receiving glucose. Cortisol alone produced a smaller glycemic response (20-25%), an initially smaller insulin response, and a delayed rise in nitrogen excretion. By day 3, however, daily nitrogen excretion was equal to the combined group as was the elevation in plasma insulin. Most plasma amino acids rose rather than fell. In both infusion protocols nitrogen wasting was accompanied by only modest increments in 3-methylhistidine excretion (approximately 20-30%) and no significant change in leucine flux. We conclude: (a) Prolonged elevations of multiple stress hormones cause persistent hyperglycemia, increased glucose turnover, and increased nitrogen loss; (b) The sustained nitrogen loss is no greater than that produced by cortisol alone; (c) Glucagon, epinephrine, and norepinephrine transiently augment cortisol-induced nitrogen loss and persistently accentuate hyperglycemia; (d) Counterregulatory hormones contribute to, but are probably not the sole mediators of the massive nitrogen loss, muscle proteolysis, and hypermetabolism seen in some clinical settings of severe stress.
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PMID:Role of counterregulatory hormones in the catabolic response to stress. 651 25

Protein synthesis and degradation and net uptake and release of amino acids and minerals were investigated in the perfused hemicorpus of acutely uremic and sham-operated control Sprague-Dawley rats. Rats underwent bilateral nephrectomy or sham surgery and were studied 30 hours after surgery. The uremic rats displayed greater urea nitrogen appearance (net urea generation), lower plasma and muscle intracellular concentrations of most amino acids, and increased protein degradation in the hemicorpus as compared with control animals. Muscle protein synthesis was slightly but not significantly decreased in the uremic animals as compared with controls. There was greater net release of phenylalanine, tyrosine, alanine, total nonessential amino acids, total amino acids, potassium, and phosphorus from the perfused hemicorpus of uremic rats and greater release of citrulline from sham rats. Muscle ATP, creatine phosphate, and cyclic AMP, and muscle cathepsin B1, cathepsin D, and alkaline protease activities were not different in the uremic and control rats. These data provide evidence that acutely uremic rats have increased muscle protein wasting which is due to enhanced protein degradation. The cause of the increased muscle protein degradation is unknown.
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PMID:Effect of acute uremia on protein degradation and amino acid release in the rat hemicorpus. 658 68

Head-injury patients studied showed severe wasting immediately after trauma. Nitrogen balance studies were used to determine whether this severe wasting was due to a catabolic state. Patients undergoing elective neurosurgical procedures were used as a control group. The results show that although head-injury patients have a higher protein requirement than the control group, they are not catabolic; their protein requirement is normal.
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PMID:The metabolic response to head injury. 669 58

The classical literature shows that wasting of body protein takes place mainly from the cellular compartment leaving high proportions of extracellular collagen. Whole body nitrogen ( WBN ) is proportional to whole body protein (cellular + extracellular) while whole body potassium ( WBK ) is almost entirely intracellular. WBK might be an adequate index of cellular wasting. WBN was measured by neutron activation and WBK by counting 40K in 29 healthy males and 131 male and female patients with wide ranges of body composition. Our wasted patients with Crohn's disease or ulcerative colitis, had higher WBN / WBK ratios than matched healthy controls and the difference between the two groups was in the cellular ratio (23.6 mol of N/mol of K, 0.33 g of N/mmol of K, 3 mmol of K/g of N). A multiple regression model for all the subjects represented cellular nitrogen by a term in WBK and extracellular nitrogen by simple anthropometric measurements. The partial regression coefficient of WBN on WBK was 22.6 +/- 1.1 (SE) mol of N/mol of K; this was also similar to the cellular ratio. Our results were compatible with extracellular protein (mainly collagen, which is 35% of normal whole body protein) remaining resistant to wasting even when severe loss of cellular protein occurs. The high ratios of WBN / WBK in wasted patients can be explained by this disproportionate wasting of cellular substances and they do not imply alterations in the cellular N/K ratio. We suggested that the stable ratio of WBK to cellular protein makes it an effective index of cellular wasting. The resistance of collagen to wasting and the preponderance of extracellular mass in the fat-free mass of wasted subjects, make WBN and fat-free mass unreliable guides to the extent of wasting.
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PMID:Whole body cellular and collagen nitrogen in healthy and wasted man. 673 80

1. 20 patients before surgery received enteral nutrition for three days (12 g nitrogen, 1800 Kcal). Nitrogen and urea excretions in urine during the second and third day were determined. Eleven patients had a negative nitrogen balance (-2,7 and -2,4 g/day). In these patients urea production rates were 21,1 and 20,1 g/day. An urea production rate exceeding 15 g urea/day is probable an indication for a protein catabolism. The reason for this catabolic state seems to be a decreased protein utilisation (49 and 47 percent) as the result of a metabolic stress situation. This metabolic stress was determined according the stress index (Bistrian). The patients were in a stress situation comparable to postoperative stress (+3,7 and +3,9). The determination of urea production rate and catabolic index seems a suitable tool for defining a catabolic state. 2. 3-met-histidine excretion in urine were measured in seven patients postoperatively. In different periods saline or aminoacids solutions (5% alanine) were infused. During alanine administration protein (+49%)--and 3-met-histidine excretions (+50%) increased. It is not possible to state a catabolic situation out of the 3-met-histidine excretion, because an increased excretion may result from a stimulated protein synthesis in muscle tissue or from an increased muscleprotein wasting. 3. Free amino acid pools in plasma and muscle tissue were analysed in patients with severe illness of liver and pancreas. The free amino acid pattern differed from healthy volunteers. In patients with liver disease significantly increased concentrations of phenylalanine, tyrosine and methionine were found. In patients with acute pancreatitis highly abnormal pattern of intracellular amino acids occurred with decreased concentrations of glutamine, cysteine, histidine, lysine, arginine and ornithine. The highly significant decreased concentrations of glutamine (p less than 0,01) indicate a catabolic situation of these patients. A quantification of the severity of the catabolic state out of amino acid concentrations is not possible.
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PMID:[Biochemical methods for the determination of a clinical protein catabolism]. 679 72

To evaluate the effect ketone bodies on protein metabolism beta-hydroxybutyrate was infused into healthy nonobese and obese subjects and insulin dependent diabetics in the postabsorptive state and into obese subjects after 3 days and 3-10 wks of starvation. In association with blood ketone increments of 1-2 mM, plasma alanine fell by 25-35% in all treatment groups. Furthermore, the hypoalaninemic effect of beta-hydroxybutyrate was equally demonstrable in fasted subjects, in whom alanine was already reduced. In association with repeated 12 hr infusions of beta-hydroxybutyrate in subjects fasted 5-10 wks, urinary nitrogen fell by 30%, returning to baseline after cessation of the infusions and paralleling the changes in plasma alanine. When endogenous ketonemia was produced by isocaloric carbohydrate restriction (less than 25 gm/day), protein ingestion was associated with a 40-50% greater increase in plasma branched chain amino acids as well as a reduced rise in plasma insulin. The enhanced rise in branched chain amino acids was attributable to decreased net utilization since intravenous leucine also produced a 40% greater elevation in plasma leucine after carbohydrate restriction. When nitrogen balance was compared during hypocaloric (400 Kcal) feeding of a pure protein diet and a mixed diet containing 50% protein and 50% carbohydrate, no significant differences were observed. Isocaloric replacement with carbohydrate failed to accentuate nitrogen wasting, despite a marked lowering of blood and urinary ketones. Our findings support the possibility that ketone bodies contribute to the reduction in proteolysis and decrease in muscle alanine release which characterizes prolonged starvation. However, when endogenous hyperketonemia is induced by carbohydrate restriction, plasma insulin declines and the disposal of ingested protein is impaired. Furthermore, the addition of carbohydrate during hypocaloric feeding reduces hyperketonemia, but does not enhance negative nitrogen balance. These observations suggest that dietary carbohydrate and insulin also promote nitrogen retention and that ketogenic, high protein diets do not confer a unique protein sparing advantage.
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PMID:The effect of ketone bodies and dietary carbohydrate intake on protein metabolism. 694 62

Quantitative measurement was made of body composition in patients with several forms of neoplastic disease. Total body nitrogen was determined by means of the prompt gamma neutron activation technique; total body potassium was measured with the use of a whole body counter. The mass and protein content of the muscle compartment and nonmuscle lean tissue were estimated by application of the technique of compartmental analysis. Total body water, determined simultaneously with the use of tritium label, provided a measure of lean body mass. From these data, the body fat can be inferred. The prompt gamma neutron activation and whole body counting techniques represent a considerable advance over the balance and radioisotope techniques used in earlier studies. The new techniques make possible sequential studies over prolonged periods of time with a considerable degree of accuracy. The loss of body weight by patients with solid tumors consisted primarily of the loss of muscle mass and body fat. Even in severe wasting, the patients appear to retain significant amounts of body fat. It is the skeletal muscle which is predominantly lost; the visceral life-supporting system is, to a considerable extent, spared. The nonmuscle tissue including the visceral fraction did not change in this study, and actually appeared to increase in size when comparison was made with the normal contrast population. The loss of total body water was slight in the cancer patients studied.
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PMID:Compartmental body composition of cancer patients by measurement of total body nitrogen, potassium, and water. 720 97

To assess whether increasing dietary protein and calorie intake can ameliorate the negative nitrogen balance induced by 70 to 120 mg/d prednisone, we studied nitrogen intake and net urea generation rate in patients undergoing hemodialysis for 10 to 14 days after renal transplantation. Seven patients receiving prednisone with moderately restricted protein (0.73 +/- 0.03 g/kg of body weight per day) and calorie (20 +/- 4 kcal/kg of body weight per day) intake had high urea nitrogen generation rates (199 +/- 18 mg/kg.d) and protein catabolic rates (1.45 +/- 0.12 g/kg.d) and were in marked negative protein balance (-0.72 +/- 0.12 g/kg.d). An increase in protein (1.30 +/- 0.06 g/kg.d) and calorie (33 +/- 3 kcal/kg.d) consumption in another eight prednisone-treated patients resulted in protein balance (-0.02 +/- 0.12 g/kg.d) without further increasing urea generation (174 +/- 9 mg/kg.d). Six control patients undergoing hemodialysis after surgery who were not receiving prednisone had lower urea generation rates (109 +/- 15 mg/kg.d) and were in nitrogen balance. Nitrogen wasting is therefore not an inevitable consequence of high-dose glucocorticoid therapy and can be effectively prevented by simple nutritional modification without increasing hemodialytic requirements.
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PMID:Prevention of prednisone-induced negative nitrogen balance. Effect of dietary modification on urea generation rate in patients on hemodialysis receiving high-dose glucocorticoids. 725 63


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