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)

A boy, aged 14 1/2 years, presented with Burkitt leukemia. His renal status was normal before treatment. Chemotherapy (SFOP LMB 86 protocol) was begun Oct. 9, 1986. After the first 2 courses of chemotherapy, the patient had Gram negative sepsis treated with cefotaxime, netilmycine, Vancomycin and ornidazole. During sepsis, nephrotic syndrome developed (albumin 25 g/l, non selective proteinuria 15 g/24 h), with moderately high blood pressure, functional renal failure (creatinine 141 mumols/l, U/P urea = 20), polyuria and tubular damage. Kidney ultrasonography was normal. Needle biopsy showed minimal glomerular lesions, acute tubular lesions, and no deposits in immunofluorescence. The nephrotic syndrome disappeared within 3 weeks, with treatment of leukemia. He is at present in complete remission with a follow-up of 25 months.
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PMID:[Nephrotic syndrome and B leukemia]. 262 44

Induction of intravascular coagulation and inhibition of fibrinolysis by injection of thrombin and tranexamic acid (AMCA) in the rat gives rise to pulmonary and renal insufficiency resembling that occurring after trauma or sepsis in man. Injection of Captopril (1 mg/kg), an inhibitor of angiotensin converting enzyme (ACE), reduced both pulmonary and renal insufficiency in this rat model. The lung weights were lower and PaO2 was improved in rats given this enzyme-blocking agent. The contents of albumin in the lungs were not changed, indicating that Captopril did not influence the extravasation of protein. Renal damage as reflected by an increase in serum urea and in kidney weight was prevented by Captopril. The amount of fibrin in the kidneys was also considerably lower than in animals which received thrombin and AMCA alone. It is suggested that the effects of Captopril on the lungs may be attributable to a vasodilatory effect due to a reduction in the circulating level of Angiotension II and an increase in prostacyclin (secondary to an increase in bradykinin). Captopril may, by the same mechanism, reduce the increase in glomerular filtration that is known to occur after an injection of thrombin, thereby diminishing the aggregation of fibrin monomers in the glomeruli, with the result that less fibrin will be deposited and thus less kidney damage will be produced.
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PMID:Effects of an inhibitor of angiotensin converting enzyme (Captopril) on pulmonary and renal insufficiency due to intravascular coagulation in the rat. 267 Jul 94

We have investigated the responsiveness of protein kinetics to insulin and the role of glucose oxidation rate as a mediator of the protein catabolic response to burn injury and sepsis by assessing the response of leucine and urea kinetics to a 5-h hyperinsulinemic euglycemic clamp with and without the simultaneous administration of dichloroacetate (DCA) (to further increase glucose oxidation via stimulation of pyruvate dehydrogenase activity) in eight severely burned and eight septic patients. Leucine and urea kinetics were measured by the primed-constant infusions of [1(-13)C]leucine and [15N2]urea. Compared with controls, basal leucine kinetics (flux and oxidation) were significantly elevated (P less than 0.01) in both groups of patients. Hyperinsulinemia elicited significant (P less than 0.05) decreases in leucine kinetics in both groups of patients. Consistent with this observation, hyperinsulinemia caused urea production to decrease significantly (P less than 0.05) in both patient groups. The administration of DCA to patients during hyperinsulinemia elicited a significant increase in glucose oxidation rate compared with the clamp rate (P less than 0.05), and the percent of glucose uptake oxidized increased from 45.5 +/- 5.5 to 53.5 +/- 4.8%; yet the response of leucine and urea kinetics to the clamp plus DCA was not different from the response to the clamp alone. These results suggest that the maximal effectiveness of insulin to suppress protein breakdown is not impaired and that a deficit in glucose oxidation or energy supply is probably not playing a major role in mediating the protein catabolic response to severe burn injury and sepsis.
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PMID:Role of insulin and glucose oxidation in mediating the protein catabolism of burns and sepsis. 267 28

Patients who acquire sepsis, ARDS, ARF, or MSOF subsequent to multiple trauma have a high mortality rate. The pathophysiology of these complications is complex and is thought to involve ischemia, the generation of mediators, alterations in regional perfusion, and cellular oxygen use. Because of the critical nature of the patient with these complications, nursing care requires indepth knowledge as well as competent nursing management, necessitating use of both the art and science of nursing.
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PMID:Complications of multiple trauma. 267 90

A 3-year-old girl is reported on who underwent laparotomy for ileocaecal intussusception elsewhere one week following severe gastroenteritis. Immediately after surgery, she developed haemolytic-uraemic syndrome with haemolytic anaemia, thrombocytopenia, increase of urea and creatinine and anuria as well as subsequent peritonitis, enterocolitis and sepsis. Following relaparotomy with establishment of ileostomy, peritoneal dialysis for several days was carried out for treatment of the haemolytic-uraemic syndrome. This case demonstrates that the haemolytic-uraemic syndrome can be treated effectively by peritoneal dialysis despite fresh bowel anastomoses, and that simultaneously occurring peritonitis can be managed by intraperitoneal administration of antibiotics via dialysis fluid.
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PMID:[Peritoneal dialysis in hemolytic-uremic syndrome following ileocecal resection for invagination in postoperative peritonitis]. 275 Mar 44

The efficacy of ceftazidime in the treatment of neonatal sepsis was studied in 42 low birthweight premature babies. Forty-nine courses of ceftazidime (25 mg/kg bd, iv or im were administered. In 19 babies, treatment was stopped after 48 h, the remainder were treated for 5 days or more. Six neonates had bacteriological evidence of infection, one other was pyrexial and 29 had radiological evidence compatible with respiratory tract infection. Eight of the study population died. Only one death was attributed to infection which arose 3 days after completion of a 5-day course of ceftazidime. Two babies developed clinical signs of necrotizing enterocolitis (NEC). Clostridium difficile (7) and Cl. perfringens (2) were isolated from 34 post-treatment faecal samples but not from the two babies with NEC. No faecal sample contained Cl. difficile toxin. Post-treatment cultures from 12 neonates yielded ceftazidime-resistant micro-organisms. Ceftazidime therapy was not associated with significant alteration in serum alanine aminotransferase, urea, creatinine, protein or albumin. Four babies had an eosinophilia, three transient and one following two intrauterine transfusions. Coombs' tests were performed on 17 babies. There were no false positives. The abnormal clotting studies observed in one baby were not due to ceftazidime. In a concurrent pharmacokinetic study, the half-life of ceftazidime was 7.4 (SD +/- 4.1) h following iv administration. Other pharmacokinetic values were C max 74 (SD +/- 20) mg l-1 trough concentration 20 (SD +/- 10) mg l-1. Total body clearance ranged from 0.13 to 2.10 ml min-1 per kg and increased with increasing postnatal age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ceftazidime in the treatment of neonatal infection. 286 90

Cecal ligation and puncture (CLP) has been extensively used as a model of sepsis in adult rats. It is not known if the response to sepsis is similar in young and adult rats. This investigation was done to compare hemodynamic and metabolic alterations in young (four to six weeks of age, 60 to 90 grams) and adult (12 to 14 weeks of age, 270 to 340 grams) rats after CLP. In one series of experiments, survival rate was determined for 96 hours, and in other experiments, mean arterial blood pressure (MAP), heart rate (HR), white blood cell count, hematocrit, platelets, plasma glucose, lactate, amino acids, blood urea nitrogen (BUN), blood and peritoneal cultures and resting energy expenditure (REE) were determined eight and 16 hours after CLP. Levels of glycogen in liver and muscle were determined 16 hours after CLP. Mortality rate was similar in young and adult rats. MAP was stable throughout the course of sepsis, with no significant differences between the two groups of rats. HR was higher in young rats at all times studied. The adult rats became hyperglycemic after CLP while the young were hypoglycemic eight hours after CLP but normalized at 16 hours. Plasma lactate and BUN were similar in the two groups of rats, and no alterations were seen during sepsis. Both young and adult rats became hypoaminoacidemic after CLP. The phenylalanine to tyrosine ratio increased in a similar manner during sepsis in both experimental groups. REE was higher in young than in adult rats, but no significant changes were observed during the course of sepsis in either group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and metabolic alterations during experimental sepsis in young and adult rats. 291 92

In pathological states associated with hypermetabolism, such as acute sepsis, there is marked negative N balance. It has been suggested that the pathway for this response is via leukocyte pyrogen (interleukin I) acting on cyclooxygenase to stimulate prostaglandin release, which then stimulates proteolysis via the lysosomal pathway. In vitro, cyclooxygenase inhibitors decrease proteolysis in muscle tissue from septic rats. We tested this hypothesis in vivo in severely septic patients by using aspirin as the test cyclooxygenase inhibitor. Septic patients (n = 4) were given a primed, constant infusion (183 mg prime, then 37 mg/hr) of 15N-labeled urea for 6 hr to obtain a blood [15N]urea plateau. Blood samples were taken every 30 min. At 180 min 1500 mg of aspirin was given po. If aspirin inhibited protein breakdown, the plateau level should rise, since less cold urea derived from protein breakdown will enter the urea pool. Aspirin did not cause any change in either the BUN concentration, its 15N enrichment, or any of the plasma amino acids. In conclusion, cyclooxygenase inhibition by aspirin in vivo does not decrease protein breakdown in hypercatabolic septic patients.
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PMID:The effect of aspirin on protein breakdown in septic man. 309 51

Subcutaneous infusion ports (SIP) were inserted for chronic venous access during 329 procedures in 300 patients over the past five years at the University of Michigan Medical Center, with a total follow-up experience of 318 patient years. Seventy-four per cent of the SIP were surgically implanted while patients were hospitalized. The SIP were used for chemotherapeutic agents (83.0 per cent), blood products (29.0 per cent) or hyperosmolar total parenteral nutrition (8.5 per cent) and accessed a median of three occasions. Eighty-four per cent were used in an outpatient setting at least part of the time. Thirty-nine per cent of SIP were associated with complications, including local infection or sepsis (16.4 per cent), thrombosis of the catheter or central vein (9.7 per cent) and extravasation from the port secondary to needle dislodgement (6.4 per cent). The risk of complication was slightly higher in those SIP first used ten to 14 days after placement as compared with those used earlier or later (p less than 0.05). In 23 of 32 episodes, clinically diagnosed local infection unassociated with systemic sepsis or skin necrosis was successfully treated without removal of the port using aggressive intravenous and oral antibiotics. Treatment of thrombosis of the catheter with either urokinase or streptokinase infusion was successful in ten of 15 attempts. Seventy-two (22 per cent) of SIP were eventually removed, either after completion of the chemotherapy (20) or because of a complication (52) with 29 SIP being replaced. There was no correlation between the risk of infection or thrombosis and the perioperative use of antibiotics, frequency of SIP use or preoperative white blood cell count, platelet count, coagulation profile, blood urea nitrogen or albumen concentration. SIP provide an excellent method of chronic venous access, having a lower rate of infection and thrombosis in historical comparison with external vascular access devices.
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PMID:Experience with subcutaneous infusion ports in three hundred patients. 312 96

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
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PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24


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