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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose intolerance occurs in patients with sepsis, and resistance to insulin has been thought to be part of this process. To study this phenomenon, peritonitis was produced in rats by cecal ligation and puncture. One group was killed ten hours later (early sepsis). A second group of rats was killed 16 to 24 hours after ligation, just prior to their expected death (late sepsis). Insulin stimulated glucose uptake to the same extent in muscles from rats in early sepsis, late sepsis, and from control rats. Even at an insulin concentration that produced submaximal stimulation of glucose uptake, no difference in glucose uptake between the three groups of muscles was observed. Thus, there was no resistance to the stimulatory action of insulin on glucose uptake by skeletal muscle during early and late sepsis. However, basal glucose uptake by isolated soleus muscle from animals in late sepsis was significantly increased compared with controls when these muscles were incubated in an aerobic environment. Under anaerobic conditions, glucose uptake in these two groups of muscles increased to the same level. This indicates that there is some stimulus that increases glucose uptake in late peritonitis and may explain the hypoglycemia of late experimental or untreated sepsis. This stimulus could be hypoxia or some other factor resulting from decreased blood flow and increased anaerobic metabolism.
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PMID:Studies of peripheral glucose uptake during sepsis. 45 60

Glucose intolerance has been commonly observed in sepsis and has been attributed to a multitude of endocrine and metabolic disorders. From 1977 to 1978, 19 patients were studied using intravenous glucose tolerance tests to evaluate this phenomenon; 15 patients presented with ongoing sepsis and four patients served as stress controls. Glucose intolerance was found to be a significant finding in less than 40% of the septic group. This state of intolerance was noted to be associated with a high mortality rate (60%), whereas glucose tolerance in sepsis was associated with a much improved mortality rate (10%). Hormone levels were correlated with glucose tolerance curves using the parameters of insulin, glucagon, growth hormone, cortisol, and epinephrine levels. Glucose intolerance and a high mortality rate were linked to sustained hyperglucagonemia, which was unresponsive to glucose challenge, and to marked suppression of growth hormone. This apparently represents a decompensated peripheral metabolic energy deficit, which results in the increased mortality rate.
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PMID:The sepsis-glucose intolerance riddle: a hormonal explanation. 47 28

The application of parenteral nutrition in patients in intensive care units can be limited by shock, septicemia and metabolic disorders. Stress- or trauma-induced glucose intolerance sometimes makes it difficult to maintain the caloric requirements with glucose. Sugar substitutes seem to be of advantage in these cases. Meticulous care is essential to avoid severe complications arising from the use of the central venous feeding catheters.
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PMID:[Problems with hyperalimentation in intensive care units (author's transl)]. 82 90

Disturbances in normal glucose metabolism and homeostasis which manifest as hyperglycemia and glucose intolerance are often observed during clinical sepsis. Skeletal and myocardial muscle as well as whole body insulin resistance have been demonstrated in this laboratory and others during experimental and clinical sepsis. The existence of hepatic insulin resistance in sepsis has yet to be fully elucidated. This study was undertaken to assess hepatic insulin resistance during chronic hyperdynamic sepsis. Animals were randomly assigned to a septic (n = 7), sham (n = 7), or control (n = 7) group. Sepsis was induced in anesthetized dogs via a midline laparotomy whereby a fecal-soaked gauze sponge was placed amid the intestines. Sham animals underwent a laparotomy with mechanical manipulation of the intestines but no fecal implant. Control animals had no previous surgery. Sham and control dogs were pair-fed with the septic dogs. On postoperative day 7, after an overnight fast, animals were anesthetized, intubated, and ventilated. Via a left subcostal laparotomy, electromagnetic flow probes were placed to measure hepatic arterial and portal venous blood flows. Cannulae were placed in femoral, portal, and hepatic veins and femoral artery and used to calculate hepatic outputs of glucose, lactate, and oxygen during a basal period and hyperinsulinemic-euglycemic clamps which used intravenous insulin infusions which ranged from 0.4 to 4,000 mU/min. Mean arterial blood pressure decreased with increasing insulin concentrations in septic animals while no change was seen in control or sham animals. In control and sham animals, net hepatic glucose output (NHGO) decreased in response to increasing insulin levels. Septic animals showed no such inverse relationship and, moreover, showed no change in glucose output response to any insulin infusion, i.e., hepatic insulin unresponsiveness during sepsis. Net hepatic lactate output during basal pre-insulin period during sepsis was negative. This was in contrast to the positive outputs in control and sham animals. Glucose infusion rates (GIR) increased during insulin infusion but were not different between groups at any insulin infusion rate. These data demonstrated a hepatic insulin resistance (unresponsiveness) during chronic hyperdynamic, hypermetabolic sepsis.
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PMID:Hepatic insulin resistance during chronic hyperdynamic sepsis. 142 10

Rat transforming growth factor alpha (TGF alpha) inhibits glycogen synthesis in rat and guinea pig hepatocyte cultures and counteracts the stimulation of glycogen deposition and activation of glycogen synthase caused by insulin. The EC50 for inhibition of glycogen deposition was 0.2nM. The inhibition of glycogen synthesis was also observed in the absence of extracellular Ca2+ and was not blocked by indomethacin, suggesting that it is not mediated by production of prostaglandins. Since TGF alpha is produced by hepatocytes during liver regeneration and by macrophages during endotoxin stimulation, it may have an autocrine/paracrine effect on hepatic carbohydrate metabolism in these states, and may account for the low hepatic glycogen levels during liver regeneration and the impaired glucose tolerance associated with sepsis.
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PMID:Transforming growth factor alpha inhibits glycogen synthesis and counteracts the stimulation by insulin in hepatocytes. 155 May 64

The complications associated with home parenteral nutrition (HPN) and their relationship to length of therapy were studied. The medical records of 56 patients treated with HPN (age range, 6 months to 82 years) were retrospectively reviewed to study complications associated with HPN. Of the 56 study patients, 30 (53.6%) had complications related to HPN, 18 (32.1%) had complications not related to HPN, and 8 (14.3%) had no complications. Of the 365 total complications noted, 125 (34.2%) were related to HPN. The mean +/- S.D. interval between initiation of HPN and occurrence of a complication was 1.25 +/- 1.73 years (mean +/- S.D.). Patients were more likely to have fluid or electrolyte complications or glucose intolerance in the first year of therapy and catheter-related complications later in the course of treatment. The first episode of septicemia occurred 2.1 +/- 1.8 years (mean +/- S.D.) after the initiation of HPN. The risk of developing catheter-related septicemia was higher for patients on long-term HPN therapy and for young patients. Patients receiving HPN should be carefully monitored for complications such as fluid and electrolyte abnormalities and glucose intolerance, which commonly occur early in the course of therapy; later complications of HPN include catheter-related infection, thrombosis, and breakage or dislodgement.
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PMID:Complications of home parenteral nutrition. 160 Jun 87

The ideal energy substrate for critically ill patients receiving total parenteral nutrition (TPN) remains controversial. While glucose has been proved to have nitrogen sparing properties in postoperative patients, critically ill patients tolerate glucose loads poorly and fat appears to be an obligatory fuel in sepsis. Furthermore, it is not yet certain whether the changes in whole body protein metabolism induced by critical illness are influenced by the nature of the TPN provided. This study was conducted on patients admitted to a surgical intensive care unit (SICU) who fulfilled the criteria of requiring TPN and mechanical ventilation for at least four days. Patients were randomized to receive either glucose (G) or equicaloric proportions of glucose and lipid (GF) as an intravenous energy source. TPN was commenced early, within 24-48 hr of trauma or surgery and admission to the ICU. Nonprotein calorie intake was 125% of calculated basal energy expenditure. Nitrogen balance was calculated from 24-hr urinary urea excretion. Protein synthesis, turnover, and catabolism were measured on Day 4 of the study using an established radiolabeled C14-leucine technique. Degree of sepsis and illness were calculated using published scores. Fifty patients entered the trial but 32 were excluded by Day 4. Of the 18 patients completing an initial four day study, eight went on to complete a second study on the alternative regimen--a total of 26 studies (14 G, 12 GF). Net protein synthesis was achieved in 18 studies (12 G, 6 FG) and positive nitrogen balance by Day 4 in 22 studies. Four patients on the G regimen were withdrawn due to glucose intolerance while none of the patients on GF developed glucose intolerance or hyperlipidaemia. Both whole body protein synthesis and catabolism correlated significantly with degree of sepsis. The type of TPN fuel used, G and GF, did not appear to influence whole body protein dynamics, both regimens achieving greatly improved whole body protein kinetics.
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PMID:The effect of fuel source on amino acid metabolism in critically ill patients. 174 Sep 40

The changes in the regulation of insulin secretion that accompany sepsis are yet to be fully established. We therefore examined insulin secretion both in vivo and in vitro in 2 different models of peritonitis/sepsis in the rat. Sepsis was induced by intraperitoneal injection of Escherichia coli either alone or together with bile. Following sepsis induction, an initial hyperglycemia developed. This hyperglycemia was transient and had vanished after 3 h (coli group) or 9 h (bile group). However, after 24 h, a second phase of hyperglycemia developed in both groups. The glucose elimination rate after intravenous glucose injection (0.5 g/kg) at 4 and 10 h after peritonitis/sepsis induction was retarded and the hyperglycemia that occurred during intravenous glucose infusion (10 mg/min for 30 min) was exaggerated. This is consistent with a reduced glucose uptake. Simultaneously, the plasma insulin responses to glucose were markedly exaggerated. This could be due to a true potentiated insulin secretion or simply to an adaptation to the hyperglycemia. However, also during intravenous arginine infusion (7 mg/min) at 4 h after peritonitis/sepsis induction, the plasma insulin responses were markedly exaggerated. Since only a slight change in plasma glucose occurred during this challenge, the results suggest that sepsis is accompanied by a true hypersecretion of insulin. To verify whether this is directly or indirectly mediated, pancreatic islets were isolated from peritonitis/sepsis animals at 4 h after disease induction and incubated for 45 min in a KRB medium supplemented with different concentrations of glucose. The subsequent insulin secretion was the same in islets from the septic animals as in controls. Hence, our results show that experimental peritonitis/sepsis in the rat is accompanied by (1) glucose intolerance and (2) a true hypersecretion of insulin which is indirectly mediated.
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PMID:Glucose tolerance and insulin secretion in experimental peritonitis in the rat. 220 Jun 90

Seven hundred fifty-eight unselected children entered into the United Kingdom Medical Research Council acute lymphoblastic leukaemia UKALL VIII Study and Trial were studied for differences in early treatment-related toxicity according to the type of intramuscular L-asparaginase received. Two hundred seventy-five received a product obtained from Escherichia coli and 483 the enzyme from Erwinia chrysanthemi. The E. coli patients had a significantly higher incidence of neurotoxicity, pancreatitis, and life-threatening sepsis (4%, 2%, and 20%, respectively) when compared with the Erwinia group (2%, 0%, and 18%). Severe hypersensitivity was seen in one patient from both groups and the incidence of glucose intolerance was not significantly different. These findings indicate that E. coli asparaginase may be more toxic. With a minimum follow up of 4 1/2 years there is no evidence that either product has made a significantly different contribution to disease-free survival.
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PMID:Non-randomised study comparing toxicity of Escherichia coli and Erwinia asparaginase in children with leukaemia. 223 23

Nutrition in acute spinal cord injury is complicated. Not every aspect of nutrition as it relates to the acutely injured spinal cord patient is known. The stress response to injury, fever, infection, sepsis, and surgery alter nutritional needs, as does the spinal cord injury itself. The sequelae of spinal cord injury, including denervation atrophy and paralysis, glucose intolerance, skin and wound breakdown, poikilothermy, anemia, respiratory paralysis, pneumonia, paralytic ileus, gastrointestinal ulcers and hemorrhage, neurogenic bowel and bladder, and depression, all affect the nutritional needs of the patient. Orthopedic appliances, pharmacologic agents, and other injuries can also alter nutritional requirements. Nutritional assessment in acute spinal cord injury is also complex. It should include medical and diet history, physical examination, intake and output measurements, prediction of energy expenditure and protein requirements, or--even better--measurements of energy expenditure with indirect methodology, using the metabolic cart or pulmonary artery catheter. Application of computerized tomography and radioisotope studies may prove valuable in the future. Finally, the direct relationship between nutrition and physiologic alterations of acute spinal cord injury necessitates that the critical care nurse incorporate nutrition-focused thinking into many aspects of the acute spinal cord--injured patient's care.
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PMID:Nutrition in acute spinal cord injury. 226 60


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