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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension, phosphate retention, hyperfiltration hyalinosis and the natural course of the underlying are well known factors leading to progression of chronic renal failure. Acute bacterial interstitial nephritis occurring in a previously diseased kidney, although well documented in experimental animals, has not been shown to aggravate chronic renal failure in man. We report on 3 cases of acute suppurative interstitial nephritis, due to E. coli urinary infection complicated by septicemia. All had rapid aggravation of previously mild renal failure secondary to chronic interstitial nephritis. Sepsis originated from the urinary tract which in 2 instances had been temporarily obstructed. Renal biopsy disclosed a diffuse interstitial infiltrate containing numerous polymorphonuclear leukocytes. This was superimposed on chronic tubular and interstitial lesions. In 1 case there were glomerular lesions with crescents and mesangial C3 deposits. A 2nd biopsy performed in 2 cases was of prognostic interest. In one case it showed active lesions and the necessity of continuing the treatment and in the other a satisfactory healing allowing cessation of therapy. Treatment was guided by antibiograms, the clinical and urinary signs of activity, renal biopsy findings and antibiotics known to be concentrated in renal tissue. The duration of treatment seemed important for the regression of acute renal lesions. Hematogenous bacterial interstitial nephritis should be considered as a possible cause of aggravation in chronic renal failure.
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PMID:[Acute hematogenic interstitial nephritis of urinary origin: an unrecognized factor in the exacerbation of chronic kidney failure]. 634 71

A number of changes in therapy of uncontrolled diabetes have occurred in recent years. These include low-dose insulin regimens, often routine phosphate repletion, more cautious bicarbonate replacement, infusion of larger fluid volumes, the use of hypotonic solutions in hyperosmolar states, and recently magnesium repletion. These modalities (with the exception of routine magnesium repletion) have been employed at North Central Bronx Hospital since its opening in 1976. Through this retrospective analysis of 275 cases of uncontrolled diabetes we have tried to answer the following questions: What is the outcome of all episodes of uncontrolled diabetes in a municipal hospital population with a uniform treatment protocol? What are the results of treatment with new modalities in various age groups? Are the causes of death different from those tabulated in previous reports? Our results indicate a good outcome in those under the age of 50 yr regardless of the diagnosis of hyperosmolar nonketotic coma (HNC) or diabetic ketoacidosis (DKA). Mortality from DKA was 2% in those under age 50 yr and 26% in the older age group. Surprising was the low mortality in the hyperosmolar group with 0% mortality under age 50 yr and 14% in patients over this age. The major categories of causes of death in the series included sepsis, adult respiratory distress syndrome (ARDS), metabolic, cardiovascular, and shock. With the exception of ARDS, these categories were not different from other reported series. There were few thromboembolic events in this series.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Uncontrolled diabetes mellitus in adults: experience in treating diabetic ketoacidosis and hyperosmolar nonketotic coma with low-dose insulin and a uniform treatment regimen. 641 94

Management of total parenteral nutrition (TPN) in depressed glucose metabolism was investigated clinically and experimentally in view of insulin control and/or new component of carbohydrate solution. Fifty TPN cases out of 837 for 9 years were successfully performed insulin control, while 17 patients were unable to get sufficient calory in spite of insulin administration. Cumulative expired CO2 after injection of radioactive carbohydrate in rats showed that each carbohydrate was utilized in the order of glucose, fructose, maltose, sorbitol and xylitol even in depressed glucose metabolism and that depressed carbohydrate metabolism was improved by adequate insulin injection. Combined use of glucose, fructose and xylitol at 4:2:1 (GFX) was was experimentally revealed to be superior to glucose alone as carbohydrate source of TPN in depressed glucose metabolism. Compared with conventional TPN (C-TPN), GFX-TPN showed lower blood glucose and insulin level in rabbits of sepsis and rats of streptozotocin diabetes. Contents of fructose 2,6 bisphosphate and triglyceride and activities of fructose 6 phosphate 2 kinase, acetyl CoA carboxylase and fatty acid synthetase in liver of these animals supported that GFX had favourable effects on glucose and fat utilization in depressed glucose Blood glucose of early postoperative patients was lower in GFX-TPN than in C-TPN.
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PMID:[Keypoints and compositions of total parenteral nutrition for patients with low glucose tolerance levels]. 643 89

To investigate the effects of bacterial infection on glucose and alanine metabolism, a variety of studies were carried out in rat and monkey models. These included glucose turnover by a pulse-dose technique in infected rats; alanine and glucose production and utilization in control and septic monkeys; in vivo measurement of gluconeogenesis in rats, with and without an alanine load; the in vitro rate of glucose formation from various substrates by isolated liver perfusion and hepatic cells; and in vivo rates of oxidation of glucose labeled with 14C at the 1 or 6 carbon position. In rats, glucose turnover was markedly accelerated 24 hr after inoculation of either 10(4) or 10(7) Streptococcus pneumoniae. Glucose utilization and production were also accelerated during illness and early recovery from a pneumococcal infection in monkeys. The rates of gluconeogenesis as measured by either a pulse technique in rats or continuous infusion of labeled alanine in monkey were significantly elevated during pneumococcal septicemia. During the agonal stages (10(7) of the pneumococcal infection in rat, an alanine load resulted in a decreased rate of labeled glucose production and an increase in plasma glucose when compared to values of fasted control rats. However, early illness caused similar or increased rates of glucose production from alanine in vivo. Similar reduced rates of glucose formation were observed when the isolated livers or hepatocytes from rats during the agonal stages of infection were perfused with excess quantities of gluconeogenic substrates. Thus, in the rat, gluconeogenic capacity (ability to form glucose from excess substrates) appears to decrease only during the agonal stages of pneumococcal infection. During acute pneumococcal sepsis in the rhesus monkey, alanine production and utilization were significantly elevated and it was estimated that over 90% of the newly produced alanine was utilized for glucose synthesis. When arterial--venous differences were measured across the hindquarters, significantly more alanine was released, presumably from skeletal muscle of the septic monkey, compared to the recovery period or in the control groups. Thus, the increase in glucose synthesis in both rat and monkey appears to be correlated with substrate availability and kinetic rate, rather than gluconeogenic capacity of the liver. The major increase in glucose utilization during both S. pneumoniae and Francisella tularensis live vaccine strain (LVS) infections in rat was a progressive elevation in the rate of oxidation via the pentose phosphate shunt in the rat. Further, the rate of oxidation appeared to be correlated with the magnitude of the bacteremia, which is an indication of the severity of the infection...
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PMID:Glucose and alanine metabolism during bacterial infections in rats and rhesus monkeys. 676 54

A patient with acute myelogenous leukemia developed severe hypophosphatemia manifesting by extreme weakness, confusion, loss of sphincter control, nuchal rigidity, hyperesthesia, hemolysis, congestive heart failure and liver dysfunction. The possible causes for this condition were starvation, parenteral glucose and saline administration, sepsis, hypokalemia and treatment with acetazolamide. A dramatic improvement was noted following phosphate administration.
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PMID:Life-threatening hypophosphatemia in a patient with acute myelogenous leukemia. 677 68

A phase I clinical trial was performed to detect adverse reactions in far advanced cancer patients treated with a unique specific cancer immunotherapy. The vaccines consisted of autologous tumor cell membranes and manganese phosphate gel. From 133 patients admitted into the trial, 95 vaccine batches were made. No batch was toxic in animals. One batch was bacteriologically contaminated. Sufficient patients survived or complied to receive 32 complete and 23 partial courses for a total of 707 SC and ID injections. Minor swelling and occasional minimal pain occurred at injection sites. There were two possible vaccine-related systemic reactions but no evidence of tumor transplantation, tumor acceleration, sepsis or autoimmune disease. Subjective and objective improvement occurred in a number of patients. The vaccines are safe. Their efficacy must be determined. The value of ID vaccine skin testing and the unexpectedly little bacteriological contamination require further study.
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PMID:Autologous anticancer antigen preparation for specific immunotherapy in advanced cancer patients. A phase I clinical trial. 715 75

Vitamin B6 deficiency was evaluated in 37 patients with chronic renal failure and in 71 patients undergoing maintenance hemodialysis (HD) or intermittent peritoneal dialysis (PD). Vitamin B6 deficiency was assessed by the in vitro activity of erythrocyte glutamic pyruvic transaminase (EGPT), without (basal) and with (stimulated) the addition of pyridoxal-5-phosphate to the assay, and the EGPT index (stimulated activity ./. basal activity). Basal and stimulated EGPT activities were below normal in the HD patients, and the EGPT index was increased in each group of patients, indicating vitamin B6 deficiency. Supplemental pyridoxine hydrochloride was given to 30 HD patients who received 1.25 to 50 mg/day (37 studies), 6 PD patients who were given 1.25 or 2.5 mg/day (7 studies), and 8 nondialyzed patients with mild to severe renal failure who received 2.5 mg/ day. In all HD patients, 10 or 50 mg/day of pyridoxine hydrochloride rapidly corrected the abnormal EGPT index and maintained normal values; with supplements of 5.0 mg/day or less, the index was often abnormal, particularly in those who were septic or taking pyridoxine antagonists. In PD patients and nondialyzed patients with renal failure, 2.5 mg/day of pyridoxine hydrochloride was inadequate to correct rapidly the abnormal index in all patients. These findings suggest that HD patients should receive 10 mg/day of supplemental pyridoxine hydrochloride (8.2 mg/day pyridoxine). PD patients and patients with chronic renal failure should receive about 5.0 mg/day of supplemental pyridoxine hydrochloride (4.1 mg/day pyridoxine). When sepsis intervenes or vitamin B6 antagonists are taken, 10 mg/day of pyridoxine hydrochloride may be a safer supplement for all patients.
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PMID:Daily requirement for pyridoxine supplements in chronic renal failure. 728 98

Glycolytic intermediates in rat liver show similar changes in both endotoxic and peritonitis shock models suggesting a common etiology. To determine if this parallelism exists for other organs, adult rat hearts were analyzed 5 hours after E. coli endotoxin injection (2 mg/100 gm rat weight) or after sepsis produced by cecal incision. Tissue obtained by freeze-clamp biopsy was deproteinized and the metabolites were enzymatically assayed. Glucocorticoids were injected IV: 1 mg dexamethasone sodium phosphate (DMS) and 3 mg methylprednisolone sodium succinate (MPS) per 100 gm rat weight at time of operation. Glucose-6-phosphate (G6P) and fructose-6-phosphate (F6P) in septic hearts (N = 10) declined 36% and 37% from sham-operated control values (N = 11) of 640 nmole and 136 nmole per gm wet tissue. This finding is consistent with accelerated glycolysis. No changes of other metabolites indicative of severe hypoxic conditions were noted. A 2.5-fold increase in lactate was observed. This may reflect a shift to anaerobiosis in peripheral muscle and greater extraction by heart. Confirming earlier endotoxin rat heart data, glucocorticoids did not prevent decreases in G6P and F6P in septic hearts which declined 37% and 36% below sham controls (N = 10 for pooled glucocorticoid data). Hexose monophosphates in sham animals treated with GC alone were also found to be lowered. Glucocorticoids were synergistic with endotoxin in lowering beta-hydroxybutyrate in heart samples. It is concluded that endotoxin and sepsis produce identical responses on myocardial carbohydrate metabolites and that glucocorticoids do not counter these effects, which reflects the lack of gluconeogenic potential in this organ.
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PMID:Glucocorticoid effect on glycolytic intermediates in septic rat heart. 730 22

Previous work demonstrated that glucose-6-phosphate (G6P) and fructose-6-phosphate (F6P) levels declined early in endotoxemic and septic livers. Since glucocorticoids are known to support hepatic gluconeogenesis in endotoxemia, these agents were tested in a peritonitis model produced by cecal incision in fasted adult male rats. Dexamethasone sodium phosphate (DMS) and methylprednisolone sodium succinate (MPS) were given in doses of 1 mg and 3 mg, respectively, per 100 gm rat weight at time of incision. Freeze-clamp biopsy samples obtained at 5 hr were enzymatically assayed. G6P and F6P in sepsis (N = 12) decreased 50% and 36%, respectively, below sham-operated control values (N = 15) of 236 and 61 nmole/gm wet tissue. The decrease with DMS was 20% and 16% and with MPS was 22% and 23%, showing partial restoration to normal levels. Phosphoenolpyruvate (PEP) did not decline in the moderate, non-terminal stage of peritonitis when compared to the control value (N = 19) of 209 nmole/gm. Treatment with glucocorticoids raised PEP to supernormal levels: DMS (N = 19) a 63% elevation, MPS (N = 12) a 51% elevation above controls in peritonitis rats. The glucocorticoid effect was similar in both rapid endotoxic and the slow peritonitis shock models. It is concluded that hexose monophosphate (HMP) increase is secondary to the support of PEP synthesis with glucocorticoid treatment. Changes in sham-operated control rat livers treated with glucocorticoids did not reach statistical significance.
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PMID:Glucocorticoid action on rat hepatic glycolytic intermediates during experimental peritonitis. 730 24

It has been previously demonstrated that mitochondria isolated from the livers of septic rats display an oxidative phosphorylation capability similar to that of mitochondria from normal hepatocytes. The present study was performed to determine whether this is also true at the level of the whole tissue or was perhaps the result of mitochondrial isolation. To study this, sepsis in rats was produced by cecal ligation and puncture (CLP). 16-19 hr after CLP (late sepsis) rats were sacrificed and the livers removed and placed in ice-cold Krebs Ringer's phosphate buffer. Slices less than 1-mm thick were prepared and placed in the well of a temperature controlled O2 monitor. O2 consumption by liver slices was monitored in buffer equilibrated with 100% O2 (high O2) or room air (low O2). Slices from both septic and sham-operated rats exhibited high initial rates of respiration in high O2 environment (34.3 +/- 3.4 and 31.5 +/- 2.5 microliters/min/gm, respectively). Rates of oxygen consumption were significantly lower after 20 min in high O2 and initially in low O2. Under each environmental condition there was no significant difference in O2 consumption between liver slices from sham-operated and septic rats. The decline in O2 consumption in high O2 was not reversed by resuspending in high O2 buffer but was further inhibited by KCN. These results support the view that depressed O2 consumption in late sepsis is secondary to decreased O2 delivery rather than a primary deficit in oxidative capability of the hepatocytes.
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PMID:Oxidative capability of hepatic tissue in late sepsis. 734 86


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