Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parenteral nutrition associated cholestasis is a condition that challenges even the most astute clinician. The risk:benefit ratio of parenteral nutrition must be individualized for each neonate. The dilemma is based on weighing the risk of progressive cholestasis and its complications against the risk of starvation, malnutrition, and their consequences. Avoiding excessive nutrient infusion and providing even minimal enteral calories may prevent or mitigate cholestasis. Routine monitoring of hepatic function in all neonates receiving parenteral nutrition allows early detection and intervention. Affected infants must be evaluated for treatable causes of neonatal cholestasis. Parenteral nutrition related cholestasis remains a diagnosis of exclusion. Further research is needed to unravel the cause and to define the long-term consequences of parenteral nutrition associated cholestasis.
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PMID:Parenteral nutrition and hepatobiliary dysfunction. 308 61

PCM can be usefully considered in terms of edematous (kwashiorkor-like) and nonedematous (marasmic) forms, as long as the limitations of the traditional terms are kept in mind. The body composition of subjects with undernutrition, or total starvation, both appear to maintain an extracellular fluid volume at a normal level, which increases as a percentage of the shrinking body weight. This is in contrast to patients with hospital malnutrition, in whom there is often an absolute increase in the extracellular volume while the body cell mass is shrinking. Data from the starvation literature suggest that the adult subject must gain approximately 10% of his or her body weight as extracellular expansion before edema is clinically evident. Preliminary evidence indicates that the hospitalized patient with the edematous form of malnutrition is at greater risk for complications and death when undergoing an operation, or requiring intensive care. The depleted patient who shows a rise in a depressed serum albumin after 7 to 10 days of TPN will have an improved prognosis when undergoing the stress of an elective operation. This improvement appears to be more the result of decreasing the expanded extracellular fluid volume than achieving a major increase in protein stores. The severely catabolic patient, particularly during episodes of major infection, can be expected to benefit by a nutritional intake that is carefully designed to provide calorie and nitrogen equilibrium. Nutritional intake high enough to guarantee positive balances of calories and nitrogen should be delayed until the acute catabolic stimulus has subsided, at which time the nutritional objective is to rebuild lost tissue.
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PMID:Forms of malnutrition in stressed and unstressed patients. 308 75

Two patterns of response, that due to starvation or semistarvation and that due the stress, determine whether protein-calorie malnutrition of the adult marasmus variety or hypoalbuminemic malnutrition will occur in any particular nonmalignant disease. The latter condition can have two major components, the neuroendocrine response to injury, which is in large measure mediated by hormones of the hypothalamus and adrenal gland, and the panoply of responses to interleukin-1 production and release by macrophages and monocytes upon activation, usually by phagocytosis. In some cancer patients with weight loss there are many similarities to an interleukin-1 response including increases in resting energy expenditure, whole-body protein flux and synthesis and glucose flux and recycling, hypoalbuminemia and increased albumin catabolic rates, and an adaptive low T3 state that suggest a similar injury/infection response. Separation of cancer patients with malnutrition into those with an injury/infection response and those with simple starvation may explain the heterogeneous response to nutritional support among malnourished cancer patients and suggest new feeding regimens that may uniquely benefit the stress form of cancer malnutrition.
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PMID:Some practical and theoretic concepts in the nutritional assessment of the cancer patient. 309 48

Cancer patients have the highest prevalence of malnutrition of any group of hospitalized patients. The potential causes of this malnutrition are numerous, as elements of both starvation and stress are evident in the cancer-bearing host. The presence of the tumor alone may lead to reduced intake of nutrients and treatment modalities of surgery, chemotherapy, and radiation therapy further exacerbate nutritional deficits. It is clear that the tumor requires energy substrates to grow, and that these substrates are exacted from the host. Animal studies identify progressive nutritional depletion concomitant with increasing tumor growth during ingestion of a regular diet. This appears predominantly due to reduced dietary intake in addition to host metabolic alterations. In animal/tumor models deliberate dietary protein depletion results in severe host weight loss, but also causes diminished tumor growth rates. Dietary manipulation in these animal/tumor models have demonstrated methods of improving tumor response to chemotherapy by manipulation of tumor growth rates. In addition, drug-pharmacokinetics have been altered by dietary manipulation. However, data from animal/tumor models are not directly applicable to man since the tumor in animals usually results in the death of the host within six to eight weeks. Nevertheless, controlled laboratory studies in animals provide basic metabolic information which promotes understanding of host/tumor relationships in man. In cancer patients malnutrition has prognostic value, leads to a distortion of body composition with erosion of body protein and fat stores, and compromises the delivery of adequate therapy. There is no direct objective evidence of accelerated tumor growth in humans with cancer who receive nutritional support as part of their treatment regimen. The host benefits to the extent that body composition is at least maintained during the period of nutritional repletion. Thus, nutritional support provides support to the patient during periods of treatment and dietary deprivation. No improvement in the tumor's response to therapy, however, has been demonstrated by this approach.
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PMID:Nutritional support in the cancer-bearing host. Effects on host and tumor. 309 53

In an attempt to elucidate the effect of protein restriction and subsequent refeeding on cardiac muscle function, 133 rat hearts were studied on a Langendorff perfusion apparatus: 19 normal controls, 55 rats during 6 weeks of protein restriction, and 59 rats during 6 weeks of refeeding following starvation. During starvation animals lost 14.3% of body weight and 12.8% in heart weight, both to be gained upon refeeding. Both developed force and force velocity tended to decrease in starving rats compared to control or refeeding rats. This trend was present at time 0, but more so after 60 min of perfusion. Furthermore, these differences became even more obvious and significantly different at the higher heart rates of 300 and 400 beats/min, and less so at 100 or 200 beats/min. These protein malnutrition-associated cardiac function derangements reversed almost completely to normal upon refeeding.
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PMID:Cardiac function during protein malnutrition and refeeding in the isolated rat heart. 309 3

The influence of nutritional status on the resumption of adequate food intake in 101 patients recovering from colorectal cancer operation was examined. Two thirds of these patients were well-nourished; the others were malnourished. Malnutrition criteria were serum albumin of less than 3.5 gm per dl plus any two of the following four factors: recent weight loss greater than 10 per cent or weight for height, mid-arm circumference, and triceps skinfold thickness lower than the tenth percentile. Over half of the well-nourished patients were eating 60 per cent or greater of their caloric requirements by the tenth postoperative day, whereas only one quarter of the malnourished patients had attained this intake. the morbidity and mortality in 33 malnourished patients was 52 and 12 per cent, respectively, compared with 31 and 6 per cent (p less than 0.01) in 68 nourished patients. The duration of postoperative functional starvation in malnourished patients without complications increased to an average of 22 days following a complication and was further prolonged after a complication. Age or operative procedure (curative or palliative) did not influence complication rate. Our data suggest that postoperative nutritional support as either TPN or enteral feeding using an elemental diet is indicated in malnourished patients and in well-nourished patients immediately following a complication requiring therapeutic intervention.
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PMID:Influence of nutritional status on the resumption of adequate food intake in patients recovering from colorectal cancer operations. 309 45

We have previously shown, in an animal model, that viable indigenous bacteria will cross the intact gastrointestinal (GI) mucosa and spread systemically, a process termed bacterial translocation, if the normal bacterial ecology of the gut was sufficiently disrupted to allow bacterial overgrowth or if the animals were severely immunosuppressed. Starvation or protein malnutrition disrupts the normal indigenous GI tract microflora and impairs host antibacterial defenses. Consequently, we tested the effect of the combination of starvation or protein malnutrition plus burn trauma in promoting bacterial translocation from the GI tract. Bacterial translocation was measured by quantitatively culturing the mesenteric lymph nodes, spleens, livers, blood, and peritoneal cavities of normal or burned (30% of total body surface area) CD1 mice deprived of food for three days or fed a low-protein (0.03%) diet. The effect of starvation or protein malnutrition on the gut microflora was determined by quantitatively measuring the levels of bacteria present in the ceca. Both starvation and protein malnutrition increased the cecal levels of gram-negative enteric bacilli and decreased the levels of lactobacilli and strict anaerobes. Surprisingly, neither starvation nor protein malnutrition promoted bacterial translocation, even though these animals lost over 20% of their body weight and the ecology of the gut microflora was disrupted. In fact, the protein-malnourished animals exhibited lower incidences of bacterial translocation than normally nourished animals when both groups were monoassociated with Escherichia coli C-25 or monoassociated and burned. Thus, it appears that protein malnutrition does not promote bacterial translocation, even when combined with burn trauma.
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PMID:Effect of starvation, malnutrition, and trauma on the gastrointestinal tract flora and bacterial translocation. 311 98

Plasma and erythrocyte amino acid concentrations in seven female patients in the acute stage of anorexia nervosa were compared with values in the same subjects after refeeding, and with normal controls. We also compared these values with literature values from patients with protein-calorie malnutrition and prolonged starvation in an attempt to identify a biological indicator of severity and prognosis. Our data indicate: (1) Routine laboratory analyses that reflect protein status do not differentiate normal subjects from patients with anorexia nervosa. (2) The plasma aminogram in the acute stage of anorexia nervosa differs from normal, and differs from values reported for both protein malnutrition and prolonged starvation. (3) The Whitehead ratio clearly separates the acutely ill anorectic state from the treated state and from normal controls. (4) Both erythrocyte and plasma amino acid concentrations differ from normal in anorexia nervosa, but changes in erythrocyte concentrations are more obvious. (5) Erythrocyte glycine concentrations are unique, in that values were persistently elevated at all stages of illness in anorexia nervosa. (6) Erythrocyte-to-plasma amino acid ratios do not provide a biological index of severity and prognosis for patients with anorexia nervosa, in contrast to data reported for individuals with protein malnutrition.
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PMID:Plasma and erythrocyte amino acid concentrations in anorexia nervosa. 311 92

The peripheral nitrogen wasting and loss of functional capacity caused by the malnutrition of disease and the immobilization of hospitalization may not be readily reversed by refeeding alone. In order to examine submaximal exercise as an adjunctive anabolic stimulus to intravenous refeeding (IVF) in depleted subjects, 14 volunteers were studied in the postabsorptive (PA) state, after 10 days of total starvation, and again after 10 days of nutritional repletion with I.V. feedings. The subjects were randomized to one group that received IVF alone and one group that performed 1 hour of submaximal (51% of VO2max) stationary bicycle exercise daily during IVF. The exercised group was not significantly different from the nonexercised group in urinary nitrogen balance, resting energy expenditure, extremity amino acid flux, or maximal oxygen consumption. Acute exercise did not induce significant derangements in electrolytes or counter-regulatory hormone concentrations. Ten days of submaximal exercise does not appear to be detrimental in this population recovering from moderate hospitalized malnutrition, but additional anabolic stimulae may be needed for improvements in protein accrual or functional capacity.
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PMID:Submaximal exercise during intravenous hyperalimentation of depleted subjects. 312

Elemental balances, and skeletal muscle membrane potential (Em) and biopsy were utilized to evaluate electrolyte homeostasis and body composition in 11 healthy adult volunteers after 10 days of starvation. This controlled, acute malnutrition was followed by refeeding for 10 days with two different, commonly used, total parenteral nutrition (TPN) solutions. Six subjects were refed with crystalline amino acids and dextrose (dextrose group), while five subjects received amino acids, dextrose, and lipid (lipid group). During starvation, negative balances for potassium, phosphorous, magnesium, and nitrogen were observed in both groups. When compared to starvation, total parenteral nutrition produced statistically significant (p less than 0.05) equilibrium or positive electrolyte and nitrogen balances for both, the dextrose and lipid groups. During TPN, there was a significantly (p less than 0.001) positive chloride balance in the lipid group when compared to the dextrose group. At the conclusion of the 10-day period of TPN, there was a decrease (p less than 0.05) in skeletal muscle Em. This change, in concert with the electrolyte balance data obtained during parenteral repletion, lead us to postulate that restoration of lean tissue protein and cellular function does not occur at a rate which might be inferred from the positive nitrogen balance observed in this model. A persistent defect in cellular function which was evident after starvation, suggests that a brief period of TPN is insufficient to restore skeletal muscle integrity.
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PMID:Effect of starvation and total parenteral nutrition on electrolyte homeostasis in normal man. 312 86


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