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)

Advances in major gastrointestinal surgery and the existence of a significant number of high-risk patients necessitate a detailed knowledge of the metabolic response to surgery and the need for adjunctive nutritional therapy. Such surgery has the potential to cause significant nutritional consequences affecting patient outcome. Often, patients present malnourished preoperatively because of their chronic gastrointestinal disease, advanced age, or comorbidity. Still others are at great risk for developing malnutrition postoperatively secondary to the hypercatabolism of prolonged illness or postoperative complications. In addition, the surgical alterations of the gastrointestinal tract might disrupt normal function sufficiently to result in chronic nutritional deficiencies. Because starvation is no longer an acceptable condition, these concerns need to be recognized prior to surgery, and if indicated, nutritional support must be initiated preoperatively. Placement of feeding jejunostomy catheters for early enteral support should be considered for all high-risk patients. Equally important, surgeons should maintain a watch for future nutritional innovations that will improve their ability to meet patients' nutritional requirements.
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PMID:Nutritional consequences of major gastrointestinal surgery. Patient outcome and starvation. 190 40

1. Indirect calorimetry has been used to measure resting energy expenditure (REE) and the thermogenic response to a test meal (diet-induced thermogenesis) in groups of weight-stable and weight-losing patients with gastrointestinal adenocarcinoma. Average daily intakes of energy and protein were computed from dietary assessment for the week before hospitalization. Results were compared with a control group of patients with benign gastrointestinal disease. 2. Weight-losing cancer patients had a significantly reduced mean total energy and protein intake. 3. There was no significant difference in REE between the groups when results were normalized in terms of metabolic body size (kJ/kg 0.75) and lean body mass (kJ/kg). 4. Diet-induced thermogenesis was reduced in weight-losing cancer patients. 5. It is suggested that the reduction of diet-induced thermogenesis in weight-losing cancer patients is another element of starvation adaptation, subsequent to their weight loss, and that altered thermogenesis does not contribute to the weight loss seen in cancer cachexia.
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PMID:Diet-induced thermogenesis in patients with gastrointestinal cancer cachexia. 276 53

It has been suggested that adaptation to starvation may be impaired in patients with malignant disease and that this may contribute to the development of cancer cachexia. We have investigated this by comparing the body composition, as well as the tissue composition of weight loss, of a group of 49 patients with gastrointestinal carcinomas and 91 patients with benign gastrointestinal disease all of whom had sustained a weight loss greater than 10% of their recalled pre-illness weight. Total body protein was calculated from total body nitrogen measured by in vivo neutron activation analysis which also provided absolute values of sodium, chlorine, phosphorus, and calcium. The masses of muscle and nonmuscle protein were estimated using a validated compartmental analysis. Total body fat was derived using anthropometry. Total body water was estimated from the difference between body weight and the sum of body protein, fat, and minerals. The loss of body weight incurred by patients with both benign and malignant disease was primarily muscle mass and body fat. Both groups of patients retained nonmuscle protein. All patients manifested, with increasing weight loss, a progressive loss of muscle protein, fat, and water, which must represent the tissue composition of weight loss. No significant differences between patients with benign or malignant disease were demonstrated for any of the body composition parameters measured. The results of this study do not support the hypothesis that adaptation to starvation in patients with cancer is in anyway different from that which occurs in patients with benign disease.
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PMID:Body composition in malignant disease. 382 8

A sample of 166 common guillemots (Uria aalge) recovered from Belgian beaches during five wintering seasons, from 1993-1994 to 1997-1998, were examined. At necropsy, postmortem examination including body mass, fat reserves, presence or not of intestinal contents, eventual status of oiling, and pathological changes (cachexia, acute hemorrhagic gastroenteropathy (GEAH)) was attributed to each individual. Mild to severe cachexia, a pathology characterized by moderate to severe atrophy of the pectoral muscle as well as reduced amounts or absence of subcutaneous and/or abdominal fat, was observed for most specimens (85.8%). Heavy metal analyses (Cu, Zn, Fe, Cd, Ni, Cr, and Pb) of the tissues (typically liver, kidney, and pectoral muscle) were performed, and total lipids were determined (liver and pectoral muscle). The guillemots collected at the Belgian coast exhibited higher Cu and Zn concentrations compared to individuals collected in more preserved areas of the North Sea such as the northern colonies. A general decrease of their total body mass as well as liver, kidney, and pectoral muscle mass was associated to increasing cachexia severity. Moreover, significantly increasing heavy metal levels (Cu and Zn) in the tissues as well as depleted muscle lipid contents were observed parallel to increasing cachexia severity. On the contrary the organs' total metal burden barely correlates to this status. These observations tend to indicate a general redistribution of heavy metals within the organs as a result of prolonged starvation and protein catabolism (cachectic status). Such a redistribution could well be an additional stress to birds already experiencing stressfull conditions (starvation, oiling).
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PMID:Heavy metals contamination and body condition of wintering guillemots (Uria aalge) at the Belgian coast from 1993 to 1998. 1109 5

Autophagy is a conserved cellular pathway that maintains intracellular homeostasis by degrading proteins and cytosolic contents of eukaryotic cells. Autophagy clears misfolded and long-lived proteins, damaged organelles and invading microorganisms from cells, and provides nutrients and energy in response to exposure to cell stressors such as starvation. Defective autophagy has recently been linked to a diverse range of disease processes of relevance to gastroenterologists and hepatologists including Crohn's disease, pancreatitis, hepatitis and cancer. The present article provides an overview of the autophagy pathway and discusses gastrointestinal disease processes in which alterations in autophagy have been implicated. The clinical significance of autophagy as a potential therapeutic option is also discussed.
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PMID:Autophagy: a primer for the gastroenterologist/hepatologist. 2217 57

This case highlights the fact that Supratherapeutic INRs direct the attention of the treating physicians' team to the underlying severely debilitating gastrointestinal diseases. Prolonged fasting or starvation reduces vitamin K levels. Such patients are more sensitive to treatment with Vitamin K antagonist-based anticoagulants. Hence, the Supratherapeutic INR can be an objective indicator of chronic loss of appetite with poor nutritional status of the patient and therefore acts as a warning sign for diagnosis of severe debilitating primary gastrointestinal disease.
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PMID:Supratherapeutic international normalized ratio: an indicator of chronic malnutrition due to severely debilitating gastrointestinal disease. 2476 83