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

Despite mounting experimental evidence that cyclosporine inhibits pancreatic islet cell function, clinical data on posttransplant diabetes mellitus (PTDM) in renal allograft recipients in the cyclosporine era are scarce. Between June 1983 and December 1988, 39 of 337 (11.6%) cyclosporine-treated adult renal transplant recipient whose grafts survived longer than 1 year developed PTDM. Of these, 43.6% and 74.4% were diagnosed by 3 and 12 months posttransplant, respectively, and 51.3% were insulin-dependent. Incidence of PTDM was highest in blacks (19.8%) and Hispanics (21.3%) and in those with HLA-A 30 and Bw 42 antigens. Older recipients and those that received cadaveric kidneys were more likely to develop diabetes than those who received living related allografts (14% vs. 5.3%, P less than 0.05). The rate of PTDM appeared to be independent of the type of induction, immunosuppressant therapy, incidence of rejection, total steroid and cyclosporine dose, percentage of body weight gain in the first posttransplant year, and serum creatinine concentration. Actuarial 5-year, decaying from 100% at 1 year, patient and graft survival rates were 87% and 70%, respectively, in the PTDM group compared with 93% and 90%, respectively, in controls. Causes of graft failure among the diabetics included chronic rejection (6), patient death (3), noncompliance with immunosuppressants (2), and sepsis (1). The incidence of infectious complications was significantly higher in the PTDM group compared with the control group (53% vs. 16%, P less than 0.05), with all 5 deaths among the diabetics being sepsis-related.
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PMID:Diabetes mellitus after renal transplantation in the cyclosporine era--an analysis of risk factors. 199 25

Two similar cohorts of low birth weight infants whose size was appropriate for gestational age randomly received either aztreonam-arginine plus ampicillin (n = 15) or gentamicin plus ampicillin (n = 15) for empiric treatment of neonatal sepsis. The regimens were infused together with glucose at greater than 5 mg/kg per minute, and immediate (4 hours) and cumulative (3 days) effects were assessed. Serum arginine and insulin values rose immediately after administration of aztreonam (containing 0.15 mmol of arginine per kilogram), but there were no changes in the gentamicin-treated cohort; no differences occurred in either cohort in serum concentrations of glucose, ammonia, potassium, creatinine, and bilirubin. After 3 days of antibiotic therapy (n = 13), the baseline serum arginine concentration was almost twice as high in the aztreonam group and showed a similar further rise and fall during the 4 hours after infusion; arginine urinary fractional excretion (normalized to creatinine clearance) decreased in the gentamicin group. The indirect bilirubin concentration rose more (p less than 0.001) in the aztreonam-treated infants (5.1 to 11.5 mg/dl (87 to 196 mumol/L] than in the gentamicin-treated infants (5.5 to 8.1 mg/dl (94 to 138 mumol/L)). Thus a modest differential bilirubin response and modestly elevated baseline serum arginine level occurred after the 3-day low-arginine doses of this study; serum ammonia and glucose concentrations were not affected. Aztreonam-arginine in neonates was well tolerated metabolically, and we believe that it can be used safely in conjunction with attention to glucose and bilirubin metabolism.
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PMID:Metabolic tolerance to arginine: implications for the safe use of arginine salt-aztreonam combination in the neonatal period. 204 Sep 35

Glucose dyshomeostasis and insulin resistance are well-documented characteristics of sepsis. The insulin resistance could be manifested in a decreased peripheral glucose uptake and/or an increased hepatic glucose output. To investigate the hepatic and peripheral responses to insulin in a three-day model of sepsis, 14 mongrel dogs were studied. Animals were randomly assigned to a SEPTIC (n = 5), SHAM (n = 4), or CONTROL (n = 5) group. Sepsis was induced in anesthetized dogs via a midline laparotomy with subsequent placement of a fecal-soaked gauze sponge around intestines. SHAM and CONTROL dogs were pair-fed with the SEPTIC dogs. On the third day, animals were anesthetized, intubated, and ventilated. Via a left-side laparotomy, electromagnetic flow probes were placed to measure hepatic arterial and portal venous blood flows. Cannulas were placed in femoral, portal, and hepatic veins and femoral artery to measure hepatic outputs of glucose, lactate, and oxygen during hyperinsulinemic-euglycemic clamps ranging from 0.4 to 4,000 mU insulin/min. Portal venous insulin concentrations in SEPTIC animals were significantly increased compared to CONTROL animals during 0.4 and 4 mU insulin/min infusions. An insulin infusion rate of 40 mU/min significantly decreased net hepatic glucose output (NHGO) in CONTROL animals but did not affect NHGO in SHAM or SEPTIC animals. An insulin infusion rate of 4,000 mU/min significantly decreased NHGO in all groups. An attempt to analyze the ED50 of the three dose-response curves was inconclusive. Glucose infusion rates (GIR) increased during insulin infusion but the GIR were not different between groups at any insulin infusion rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic insulin resistance during canine sepsis. 206 41

The activity of phosphate-dependent glutaminase and glutamine metabolism by tissues known markedly to utilize or synthesize glutamine (or both) were studied in rats made septic by cecal ligation and puncture technique and compared with the same measures in rats that underwent sham operation (laparotomy). Blood glucose level was not markedly different in septic rats, but lactate, pyruvate, alanine, and glutamine levels were markedly increased. Conversely, blood ketone body concentrations were significantly decreased in septic rats. Both plasma insulin and glucagon levels were markedly elevated in response to sepsis. The maximal activity of phosphate-dependent glutaminase was decreased in the small intestine, increased in the kidney and mesenteric lymph nodes, and unchanged in the liver of septic rats. Arteriovenous concentration difference measurements across the gut showed a decrease in the net glutamine removed from the circulation in septic rats. Arteriovenous concentration difference measurements for glutamine showed that both renal uptake and skeletal muscle release of the amino acid were increased in response to sepsis, whereas measurements across the hepatic bed showed a net uptake of glutamine in septic rats. Enterocytes isolated from septic rats exhibited a decreased rate of utilization of glutamine and production of glutamate, alanine, and ammonia, whereas lymphocytes isolated from septic rats showed an enhanced rate of utilization of glutamine and production of glutamate, aspartate, and ammonia. It is concluded that, during sepsis, glutamine uptake and metabolism are enhanced in renal and lymphoid tissue but decreased in that of the small intestine, with increased rates of release by skeletal muscle; however, the liver appears to utilize glutamine in septic rats.
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PMID:Maximal activity of phosphate-dependent glutaminase and glutamine metabolism in septic rats. 206 39

Intermittent hemofiltration (HF) was applied to the treatment of 8 patients (3 men and 5 women) with the grave pattern of acute renal failure (ARF) of prerenal origin. Altogether 23 sessions (from one to six in every patient) were performed with replacement of 44.3 +/- 2.8 1 liquid on the average. Two patients died. Of these, one female patient died from progressive peritonitis and sepsis and the other one from cisplatinum intoxication, bone marrow aplasia and sepsis. The content of blood plasma amino acids (AA), total protein and its fractions was measured before and after HF. Measurements were also made of excretion of those substances with filtrate. Besides, the amount of protein AA catabolized during the procedure was calculated according to the kinetics of urea. The authors hold that ARF-associated changes in the content of AA are primarily determined by adaptive shifts in metabolism. Differences in AA consumption were revealed to depend on the period and quality of adaptation. On the average HF brought about losses of 7.5 g AA and 73.1 g protein with filtrate. At the same time 37.5 g AA underwent oxidation, while urea generation rose 2-fold, amounting to 0.48 mmol/kg bw per hour. It is concluded that in ARF patients undergoing intermittent HF, it is necessary that anabolizing glucose and insulin therapy be applied together with replacement infusion of AA and (or) protein.
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PMID:[Blood plasma amino acids and total protein, their elimination and catabolism during the hemofiltration of patients with acute kidney failure]. 209 95

Over a 3-year period, 156 of 815 patients admitted to a single institution with acute pancreatitis received total parenteral nutrition (TPN) for 2,572 patient days. Seventy had "simple" acute pancreatitis (group I) and 86 (group II) developed local complex disease (pseudocyst, abscess, or necrotic gland). In groups I and II, respectively, days without oral intake (NPO) were 13.6 +/- 1.5 (SEM) and 24.0 +/- 2.1 (p less than 0.005), hospital days were 19.8 +/- 1.7 and 35.8 +/- 3.2 (p less than 0.005), and duration of TPN was 10.9 +/- 1.0 and 21.0 +/- 2.3 days (p less than 0.005). Thirty-three patients in group I and 53 in group II required exogenous insulin. Alteration of standard formulas was necessary in 87 patients, but cessation of therapy was necessary in only one instance. Twenty catheters were removed for suspected sepsis with only 3 confirmed cases. Fat-based formulas were well tolerated in 15% of patients. During TPN, body weight rose from 95.0 +/- 2.4% to 97.4 +/- 4.3% of ideal in group I and remained at 90.5 +/- 1.8% in group II. Albumin rose from 3.36 +/- 0.10 to 3.50 +/- 0.08 g/dl in group I and from 3.01 +/- 0.07 to 3.35 +/- 0.07 g/dl in group II. The entire cohort differed from 10 randomly chosen patients who did not receive TPN in terms of days NPO (2.8 +/- 0.3) and hospital days (5.5 +/- 0.6). Variables associated with prolongation of hospital stay and time NPO were number of prognostic criteria, local complex disease, and underlying chronic pancreatitis only in select groups. We conclude that during acute pancreatitis, TPN can be administered safely but with careful monitoring and we recommend early aggressive therapy in the subgroups noted above and when underlying malnutrition exists. In the borderline patient, TPN may be administered by peripheral vein until the severity of disease is manifest.
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PMID:Total parenteral nutrition during acute pancreatitis: clinical experience with 156 patients. 212 3

Insulin resistance is a cause for morning hyperglycemia seen in diabetic patients. Other reasons for morning hyperglycemia should be eliminated by performing an insulin response test. Once insulin resistance has been established as the cause of hyperglycemia, a step-by-step process should be used to establish the cause of the insulin resistance. Common causes of insulin resistance include hyperadrenocorticism, acromegaly, hyperthyroidism, and obesity. Hepatic disease, renal insufficiency, and sepsis are other causes of insulin resistance in practice. Less common causes include insulin antibodies, pregnancy, neoplasia, hyperandrogenism, and pheochromocytoma. If the underlying cause cannot be found or resolved, then increased doses of insulin are required to manage the hyperglycemia.
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PMID:Problems in diabetes mellitus management. Insulin resistance. 213 77

1. My aim was to investigate, by mathematical simulation, the errors inherent in the measurement by the primed infusion method of the rate of appearance of glucose in man when turnover was as low or lower than in overnight-fasted normal subjects (control subjects). The simulations were based on published data for means and variances of turnover rates and concentrations in nondiabetic subjects and diabetic patients. 2. Systematic errors (bias) were shown to be considerable whether or not the Steele equation was used, unless run-times were longer than is customary. Errors were greater the lower the turnover rate, and were greatest in patients with diabetes, owing to insulin resistance. Studies of, for example, control subjects, age, obesity, exercise, sepsis and injury, are, however, all likely to be affected. 3. Estimates of variance, within-group means, between-group differences and slopes of rate-concentration relationships were all biased. Entirely spurious results appeared statistically significant. 4. When the Steele equation was not used, run-times had to exceed 3 h in control subjects and 10 h in some diabetic patients to reduce bias to acceptable levels. The nature of the bias depended on how the priming dose/infusion rate ratio was chosen. Each choice implies a particular hypothesis about the values of the rate of appearance of glucose, their variance, and how they are related to concentration. The bias was always such as to favour that hypothesis. 5. When the Steele equation was used, the accessible glucose space (pool fraction x distribution volume) had to be correct to 20-30 ml to avoid unacceptable bias in some patients in runs 4 h long. The space is not known this accurately. Theoretically, in the near-steady metabolic states considered, the pool fraction should be near 1.00, i.e. the accessible space should be near the glucose distribution volume of 200-300 mg/kg. There is some confirmatory experimental evidence. 6. Large random errors from variance of specific (radio)activity measurements when the Steele equation is used can be reduced by a suitable choice of protocols. 7. The propagation of errors is too complex to permit correction of results. It is essential to choose protocols that can be shown to give results that are acceptably bias-free. Ways of doing this are discussed.
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PMID:Errors inherent in the primed infusion method for the measurement of the rate of glucose appearance in man when uptake is not forced by glucose or insulin infusion. 216 67

1. The regulation of renal gluconeogenesis was studied in rats made septic by a caecal ligation and puncture technique. 2. Blood glucose concentrations were not markedly different in septic rats, but lactate, pyruvate and alanine concentrations were markedly increased, compared with sham-operated rats. Conversely, blood ketone body concentrations were significantly decreased in septic rats. Both plasma insulin and glucagon concentrations were markedly elevated in response to sepsis. 3. The maximal activities of glucose-6-phosphatase (EC 3.1.3.9), fructose-1,6-bisphosphatase (EC 3.1.3.11), pyruvate carboxylase (EC 6.4.1.1) and phosphoenolpyruvate carboxykinase (EC 4.1.1.49) were markedly decreased in kidneys obtained from septic rats, suggesting diminished renal gluconeogenesis. 4. Renal concentrations of lactate, pyruvate and other gluconeogenetic intermediates were markedly elevated in septic rats, whereas those of acetyl-CoA and fructose 2,6-bisphosphate were decreased and unchanged, respectively. 5. The rate of gluconeogenesis from added lactate, pyruvate and glycerol was decreased in isolated incubated renal tubules from septic rats. 6. Sepsis decreased the arteriovenous concentration difference for glucose, lactate, and alanine. Septic rats showed decreased net rates of glucose production and net rates of removal of lactate and alanine as compared with sham-operated controls. 7. It is concluded that the diminished capacity for renal gluconeogenesis in septic rats could be the result of changes in the maximal activities or regulation of key non-equilibrium gluconeogenic enzymes or both, but the effect of other factors (e.g. toxins) has not been excluded.
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PMID:Metabolic regulation of renal gluconeogenesis in response to sepsis in the rat. 217 16

The effect of sepsis on neutral amino acid transport systems A, ASC, and L, was studied in incubated rat soleus (SOL) muscles. We also examined the effects of plasma from septic rats and of varying concentrations of insulin (10 to 10(5) microU/mL), added in vitro to incubated muscles, on system A amino acid transport. Sepsis was induced by cecal ligation and puncture (CLP) in rats weighing 40 to 60 g. Control rats were sham-operated. System A activity was assessed by determining uptake of 2-(methylamino)isobutyrate (MeAIB) 16 hours after CLP or sham-operation. System ASC was studied by measuring uptake of alpha-aminoisobutyric acid (AIB) in the presence of 25 mmol/L MeAIB and 25 mmol/L 2-amino-2-norbornane carboxylic acid (BCH) to inhibit uptake by systems A and L. System L activity was defined as sodium-independent uptake of cycloleucine. MeAIB uptake was reduced by 28% in muscles of septic rats, while amino acid transport by systems ASC and L was almost identical in muscles from control and septic rats. Addition of plasma from septic rats to incubated normal SOL muscles inhibited MeAIB uptake by 31%. Addition of insulin to the incubation medium resulted in increased uptake of MeAIB, both in nonseptic and septic muscle. The lowest hormone concentration tested that significantly enhanced MeAIB uptake in nonseptic muscle was 10(2) microU/mL and in septic muscle 10 microU/mL. The results suggest that sepsis in rats specifically inhibits amino acid transport system A and that reduced muscle amino acid uptake may be caused by a circulating factor in sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of sepsis on amino acid transport system A and its response to insulin in incubated rat skeletal muscle. 218 70


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