Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma proteins, triglyceridemia, body composition and delayed hypersensitivity were determined in 154 critically ill patients after admission. Plasma proteins levels were significantly increased in patients that were subsequently discharged vs. those that died: albumin: 33 +/- 6 g/l vs 28 +/- 6 g/l (p < 10(-6)); transferrin 2,18 +/- 0,65 g/l vs. 1,54 +/0 0,55 g/l (p < 10(-7)); prealbumin: 14,32 +/- 7,79 mg/100 ml vs. 7,28 +/-5,36 mg/100 ml (p < 10(-7)) and triglyceridemia was decreased: 1,07 +/- 0,38 g/l vs. 1,66 +/- 1,12 g/l (p not equal to 10(-3)). Body weight, fat weight and lead body mass were not correlated to subsequent mortality. Muscle cell mass was decreased (-17%, p < 10(-2)) and extracellular water was increased (+14%, p < 10(-4)), in patients who subsequently died. Total body water and visceral cell mass did not change. Initial anergy (tested with 3 antigens: candidin, tuberculin, varidase) did correlate with mortality: 35/62 died when delayed hypersensitivity was negative vs. 13/71 when it was positive (p < 10(-4)). Mortality was associated with decreased total lymphocyte count: 884 +/- 1025 vs. 1270 +/- 870 (p < 0,02) and serum iron: 51 +/- 40 micrograms/100 ml vs. 74 +/- 45 micrograms/100 ml (p < 10(-2)). Sepsis correlated with mortality (p < 10(-3)) and could produce these changes. These results suggest that critically ill paients have a protein-calorie malnutrition syndrom marktly different from that observed in simple starvation. Nutritional therapy must be, in this group of patients, adapted to this concept.
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PMID:[Nutritional status in critically ill patients. Relationship with mortality (author's transl)]. 12 28

Acute and chronic starvation is often associated with childhood cancer. Total parenteral nutrition (TPN) with 20% glucose and 3.0% amino acids, and minerals and vitamins was instituted to treat or prevent malnutrition in 41 children with cancer, ages three months to 18 years. TPN was required for anorexia, vomiting and diarrhea associated with anti-cancer therapy in 33 patients for intestinal complications or surgery in nine, and for preoperative correction of malnutrition in two. During TPN, general nutrition and appearance improved in all patients. Weight gain was noted in most. Despite gastrointestinal complications which usually require the interruption of chemotherapy and irradiation, in 21 children treatment could be continued at full dose with nutritional support by TPN. TPN was discontinued in six patients when blood cultures became positive. Sepsis was treated successfully by removal of the central venous catheter in all six and administration of antibiotics in three. No metabolic complications were noted. TPN appears to be a safe and effective means of combating the malnutrition which may occur with cancer and its therapy.
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PMID:Parenteral nutritional support in children with cancer. 40 34

Four patients from a larger group of 18 patients receiving dextrose-free isotonic (3%) amino acid solution as nutritional support, form the basis of this report. An additional seven patients received intravenous isotonic (5%) dextrose as their sole support in the postoperative period following major elective surgery (average nitrogen balance = -12.3 +/- 2.7 g). All patients were well-nourished as determined by anthropometric measurements. The nonseptic patients receiving infusions of isotonic amino acids demonstrated an improvement in nitrogen balance (= delta 8.5 +2, P less than 0.001) when compared to the postoperative use of 100 to 150 g of glucose. However, sepsis produced a decreased net utilization of the infused crystalline amino acids such that nitrogen balance was similar to the intravenous glucose group (- 10.6 +/- 2.1). This septic response was associated with decreased plasma free fatty acid concentrations and the absence of starvation ketosis and ketonuria. While the nitrogen balance was not different in the septic and the dextrose control groups, deficiencies in plasma amino acid concentrations were observed in the group receiving intravenous infusion of glucose.
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PMID:Effect of deep surgical sepsis on protein-sparing therapies and nitrogen balance. 40 78

During caloric deprivation, the septic host may fail to develop ketonemia as an adaptation to starvation. Because the plasma ketone body concentration is a function of the ratio of hepatic production and peripheral usage, a pneumococcal sepsis model was used in rats to measure the complex metabolic events that could account for this failure, including the effects of infection on lipolysis and esterification in adipose tissue, fatty acid transport in plasma and the rates of hepatic ketogenesis and whole body oxidation of ketones. Some of the studies were repeated with tularemia as the model infection. From these studies, it was concluded that during pneumococcal sepsis, the failure of rats to become ketonemic during caloric deprivation was the result of reduced ketogenic capacity of the liver and a possibly decreased hepatic supply of fatty acids. The latter appeared to be a secondary consequence of a severe reduction in circulating plasma albumin, the major transport protein for fatty acids, with no effect on the degree of saturation of the albumin with free fatty acids. Also, the infection had no significant effect on the rate of lipolysis or release of fatty acids from adipose tissue. Ketone body usage (oxidation) was either unaffected or reduced during pneumococcal sepsis in rats. Thus, a reduced rate of ketone production in the infected host was primarily responsible for the failure to develop starvation ketonemia under these conditions. The liver of the infected rat host appears to shuttle the fatty acids away from beta-oxidation and ketogenesis and toward triglyceride production, with resulting hepatocellular fatty metamorphosis.
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PMID:Role of the liver in regulation of ketone body production during sepsis. 50 Aug 25

Hormonal and substrate profiles and urinary nitrogen and urea excretion were measured in 78 underweight patients admitted for surgical investigation, who were placed into either a normo- or a hyperketonemic group, depending upon their levels of acetoacetate and beta-hydroxybutyrate. The two groups were otherwise similar in terms of weight loss, arm muscle circumference, triceps skinfold thickness, and serum protein levels. Before surgery only one-quarter of them were hyperketonemic displaying mean glucose, insulin, and glucagon levels characteristic of starvation-adaption, and excreted significantly less urinary nitrogen than in normoketonemic group. Those patients who underwent surgery tended to retain their presurgery hormonal and substrate profile. The normoketonemic group excreted significantly greater amounts of urinary nitrogen, depleted body protein to a greater extent as evidenced by larger changes in arm muscle circumference and serum protein levels, and mortality was greater. Interference with insulin-glucagon balance by sepsis and disease is suggested as a possible explanation for the failure of three-quarters of the patients to become starvation-adapted. The implications of this finding on the parenteral feeding of undernourished patients are discussed.
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PMID:Ketosis and nitrogen excretion in undernourished surgical patients. 57 67

Intralipid was used as the main source of calories in the long-term therapy of a patient with severe nutritional failure and cachexia. The treatment was tolerated well for 64 days. The patient died of sepsis after a second therapeutic course which lasted 16 days adn was preceded by an impairment in liver function apparently related to starvation. At autopsy, free fat droplets and extreme foamy swelling of the cytoplasm of the reticuloendothelial cells were found in all examined organs. These findings constitute an unusual example of iatrogenic lipidosis. It is suggested that caution be exerted in the administration of Intralipid to patients with impaired liver function and that serum lipids be maintained regularly during therapy.
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PMID:Latrogenic lipidosis following prolonged intravenous hyperalimentation. 81 19

Host starvation is a common accompaniment to the presence of cancer. Diminished intake is a major contributor to this starvation and does not require that the oropharynx or gastrointestinal tract be the primary site. There is suggestive evidence that the normal adaptive mechanisms of the nontumor-bearing host to starvation that result in body protein conservation are not functioning in the tumor-bearing host. Cancer cachexia has some similarity to the metabolic disturbances of host metabolism that are seen in major injury or sepsis. The growing tumor shows little respect for normal constraints of host tissue growth. With the widespread availability of methods of total parenteral nutrition, the interrelationship of nutrition and host-tumor growth assumes greater importance.
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PMID:Uncomplicated starvation versus cancer cachexia. 86 53

The catabolic effects of starvation alone, or starvation in the presence of pneumococcal sepsis, were compared in rats whose skeletal muscle protein had been tagged 14 days earlier with 14C-phenylalanine. In a fed rat, protein catabolism (as estimated by expired 14CO2) is not constant throughout the day but is highest during the dark hours. Starvation is associated with accelerated protein catabolism and a gradual loss of periodicity. Infection increases the rate of catabolism still further and results in a complete loss of periodicity.
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PMID:Total body protein catabolism in starved and infected rats. 90 62

The restraint model and other models for the production of experimental stress ulcers have been reviewed. The mechanism of experimental stress ulcers appears to depend on an interaction between the presence of acid, changes in mucosal circulation, an increase in the excretion of glycoproteins in the mucus, and a decrease in mitotic activity of the mucosal lining of the stomach. Factors enhancing ulceration are cold, starvation, increased acidity, burns, reflux of bile, endotoxin, adrenalectomy, and hemorrhage. Factors inhibiting ulceration are vagotomy, anticholinergics, elemental diets, vitamin A, antacids, prevention of bile reflux, corticosteroids, epinephrine and norepinephrine, serotonin antagonists, and immediate replacement of blood loss with low molecular weight dextran. The role of sepsis is unclear and more work is needed in this area. Ulcers from intracranial injury are usually associated with the hypersecretion of gastric acid. Stimulation of the hypothalamus, directly or indirectly, with resultant vagal stimulation is thought to be the responsible mechanism for the increase in acid.
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PMID:Experimental stress ulcers: a review. 110 3

Arterial plasma amino acids were measured in 27 patients with serious septic complications after operation, 15 patients following reduction of femoral shaft fractures and nine control patients on the first and third days following uneventful major abdominal surgery. Amino acid concentrations in the controls were similar to those which have been reported during early starvation. The amino acid patterns seen in all groups did not resemble that previously observed following glucocorticoid administration. In the patients with infection, mean phenylalanine concentration (108.0 +/- 46.9 mumoles per liter) was significantly greater than in the controls on the first (p greater than 0.001) or third (p less than 0.001) postoperative days. Four of the septic patients with hyperphenylalaninemia also had elevated arterial methionine concentrations. These observations suggest that many of the patients with sepsis had seriously impaired liver metabolism. In patients with fractures, the concentrations of ornithine (p less than 0.001), taurine (p less than 0.05), and aspartic acid (p less than 0.05) were lower than in controls. No other significant differences of amino acid concentrations were observed. It is difficult to relate these differences to a specific metabolic abnormality.
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PMID:Arterial plasma amino acids in patients with serious postoperative infection and in patients with major fractures. 125 95


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