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

A case of anaerobic sepsis associated with Fusobacterium mortiferum is reported. Blood cultures from a 60-year-old man with type II diabetes mellitus, hypertension, severe atherosclerotic cardiovascular disease, and renal insufficiency revealed on a gramstained smear highly pleomorphic gram-negative bacilli with bizarre forms and round bodies. Growth of the organism on nonselective anaerobic media and analysis of its pattern produced results characteristic of Fusobacterium mortiferum.
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PMID:Anaerobic septicemia secondary to Fusobacterium mortiferum. 371 72

A psoas muscle abscess due to Yersinia enterocolitica developed in a 71-year-old man with mild type II diabetes mellitus. There was no evidence of gastrointestinal infection or septicemia, and treatment with computed tomography-directed percutaneous drainage and cefoxitin resulted in cure. This represents the first known reported case of psoas abscess due to Y. enterocolitica.
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PMID:Psoas muscle abscess due to Yersinia enterocolitica. 672 Jul 35

Among patients hospitalized in 1983-1992 were 416 (239 women) who were immobilized for at least 2 hours due to stroke, orthopedic surgery, or sepsis. 128 (30.8%) had pressure ulcers (PU); 100 (31.2%) had diabetes (DM), including 12 with IDDM and 118 with NIDDM; age (mean +/- SD) was 74.3 +/- 9.5 years. Those with IDDM and NIDDM were younger (70.9 +/- 10.5 and 71.5 +/- 8.4 years, respectively) than the nondiabetic (75.7 +/- 9.6 years; p > 0.05 and < 0.001, respectively). Those with PU were older (76.6 +/- 9.0 vs 73.3 +/- 9.6 years, p < 0.01). Incidence of PU in patients without DM was similar to that in those with NIDDM (30.4 vs 27.1%; no difference even after age-adjustment). However, incidence of PU was significantly higher in those with IDDM than in those without DM (75.0 vs 30.4%, p < 0.01). According to Medline (last 2 years screened), and EBSCO Physician Medline Plus (last 5 years screened), only 5 publications referred to DM as a risk factor for PU. According to our data NIDDM does not appear to be a risk factor for PU, but a causative role for IDDM deserves further study. Increased risk of diabetic foot, infections in ulcers and wounds, and slow healing in DM do not justify considering NIDDM a risk factor for PU.
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PMID:[Is diabetes mellitus a risk factor for pressure ulcers?]. 904 59

Tumor necrosis factor alpha (TNF-alpha) has well-described effects on lipid metabolism in the context of acute inflammation, as in sepsis. Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. Multiple mechanisms have been suggested to account for these metabolic effects of TNF-alpha. These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia.
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PMID:Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. 1087 50

The SOFA score, a new system for patients with sepsis-related diseases, was introduced in 1994 by the "Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine." The purpose of this study was to compare the new SOFA score with the APACHE II and MOD scores. The data on 874 patients from a surgical intensive care unit in an university hospital were analyzed using commercially available software (SPSS for Windows, Version 7.5.2 and MS Excel '97). To compare the different scores, receiver-operating characteristics (ROC)--analyses were applied. The study demonstrated clear correlation between an elevated SOFA score and the mortality of the patients during their ICU stay (score 0-->mortality 0%, 1-->3.6%, 2-->22.5%, 3-->86.7%, respectively r = 0.445; P = 0.01). The ROC analyses of the APACHE II, the MOD and the SOFA scores were comparable (area under the curve: APACHE II 0.73, MOD 0.77, SOFA 0.71). In conclusion, the SOFA score is reliable and might be useful in the daily routine of an intensive care unit.
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PMID:[The SOFA score in evaluating septic illnesses. Correlations with the MOD and APACHE II score]. 1107 90

The vascular actions of insulin may contribute to the increase in glucose uptake by skeletal muscle. We have recently shown that when capillary recruitment by insulin is blocked in vivo, an acute state of insulin resistance is induced. Another agent that may have vascular effects is the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), which has been reported to play an important role in the insulin resistance of obesity, type 2 diabetes, and sepsis in both animals and humans. Thus, in the present study, we have investigated the effect of an intravenous 3-h TNF treatment (0.5 microg x h(1) x kg(-1)) in control and euglycemic-hyperinsulinemic-clamped (10 mU x min(-1) x kg(-1) for 2 h) anesthetized rats. Hind-leg glucose uptake, muscle uptake of 2-deoxyglucose (2-DG), femoral blood flow (FBF), vascular resistance (VR), and capillary recruitment as measured by metabolism of infused 1-methylxanthine (1-MX) were assessed. Insulin alone caused a significant (P < 0.05) increase in FBF (1.7-fold) and capillary recruitment (2.5-fold), with a significant decrease in VR. In addition, hind-leg glucose uptake was increased (fourfold), as was 2-DG uptake in the soleus and plantaris muscles. TNF completely prevented the insulin-mediated changes in FBF, VR, and capillary recruitment and significantly reduced (P < 0.05) the insulin-mediated increase in total hind-leg glucose uptake (by 61%) and muscle 2-DG uptake (by at least 50%). TNF alone had no significant effect on any of these variables. It is concluded that acute administration in vivo of TNF completely blocks the hemodynamic actions of insulin on rat skeletal muscle vasculature and blocks approximately half of the glucose uptake by muscle. It remains to be determined whether these two effects are interdependent.
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PMID:Acute impairment of insulin-mediated capillary recruitment and glucose uptake in rat skeletal muscle in vivo by TNF-alpha. 1107 58

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
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PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

A national survey on permanent hemodialysis catheters was conducted in 99 hemodialysis centers between january 1998 and january 2000. It was a prospective, national and multicentric study. Data were gathered in 1552 patients (mean age 65 +/- 15 years) with chronic end stage renal failure. A questionnaire was filled out each time a permanent hemodialysis catheter was inserted. Two permanent catheters (72%) were inserted under local anesthesia (92%), using the right internal jugular vein (81%) with a percutaneous technique (96%). The two main indications were: end stage chronic renal failure without creation of a vascular access (52%) and dysfunction of a preexisting vascular access (35%). Patients have been followed a mean time period of 58 days and 179 cases of death have been reported. The median duration of catheters was 500 days. The two main causes of catheter removal were creation of a functional A-V fistula (40%) and death of the patient (28%). The incidence of bacteriemia/septicemia was 0.74 episode/patient/1000 days of follow-up while that of any type of infection was 0.85 episode/patient/1000 days. The risk of infection increased with time especially in type 2 diabetes patients.
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PMID:[Permanent catheters for hemodialysis: indications, methods and results. French national survey 1998-2000]. 1181 Sep 93

The present review examines the cytokine response to acute exercise stress, with particular emphasis on the balance between proinflammatory and anti-inflammatory mechanisms, and the release of IL-6. Prolonged endurance exercise induces a sequenced release of pro- and anti-inflammatory cytokines, and IL-6 plays a dominant role. The magnitude of this response bears a general relationship to the intensity of effort, but the duration of activity and many environmental factors also modulate cytokine release. Although many types of cells are capable of producing cytokines, the main source of the exercise-induced IL-6 production appears to be the exercising muscle. The primary function of the additional IL-6 may be to regulate the supply of carbohydrate as muscle reserves of glycogen become depleted. There is also a delayed release of cytokines following eccentric exercise that is related to the repair of muscle injury. Since the production of cytokines is greater with endurance than with resistance exercise, it seems unlikely that they play an important role in the hypertrophy of muscle and bone. More research is needed on a number of important clinical issues where the exercise-induced release of cytokines may have relevance. Exercise-induced cytokine secretion has the potential to provide a simple model of sepsis. Preliminary observations suggest it may also modulate the risk of type 2 diabetes mellitus. Cytokine concentrations are increased in chronic fatigue syndrome, although it is less dear that the cytokine secretion is responsible for fatigue in humans. Exercise-induced modulations in cytokine secretion may contribute to allergies, bronchospasm, and upper respiratory infections in the endurance athlete. Further, the cytokine cascade is involved in the process of atherogenesis, and exercise-induced changes in cytokine production may expose latent HIV to chemotherapeutic agents.
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PMID:Cytokine responses to physical activity, with particular reference to IL-6: sources, actions, and clinical implications. 1249 81

We hypothesized that sepsis during hyperglycemia would activate left ventricular (LV) mitogen activated protein kinase (MAPK) signaling mechanisms and modulate generation of endothelin-1 (ET-1) and nitric oxide (NO) that can contribute to the progression of LV dysfunction. A single injection of streptozotocin (STZ, 60 mg/kg, via tail vein) was used to produce type 2 diabetes in male SD rats. Polymicrobial sepsis and sham-sepsis were induced using single i.p. injection of cecal inoculum and sterile 5% dextrose water, respectively, on the 13th and 27th day following STZ injection. Both 2-week (2-wk) and 4-wk diabetes groups were associated with hyperglycemia and weight loss. LV end diastolic pressure (LVEDP) was significantly increased in 4-wk diabetes but not in 2-wk diabetes group. Plasma concentration of tumor necrosis factor-alpha (TNF-alpha) was significantly increased in 4-wk diabetes+sepsis group as compared to sham, 2-wk diabetes+sepsis and sepsis groups. Elevated plasma and LV ET-1 and NO byproducts (NOx) along with LV preproET-1 and inducible nitric oxide synthase (iNOS) protein expression were observed in 4-wk but not in 2-wk diabetes group. Sepsis further elevated LV iNOS and preproET-1 in 4-wk diabetes group. Up-regulated phosphorylation of LV p38-MAPK, extracellular signal-regulated kinase 1/2 (ERK1/2) and heat shock protein-27 (Hsp27) was observed in 4-wk diabetes group. Sepsis caused a factorial increase in LV p38-MAPK and Hsp27 phosphorylation and iNOS up-regulation but not ERK1/2 following progression from 2-wk to 4-wk diabetes. The study provides evidence that sepsis up-regulated LV iNOS, p38-MAPK phosphorylation and elevated LVEDP during 4-wk diabetes. We concluded that sepsis contributes in the development of LVEDP dysfunction and alteration in signaling mechanisms depending upon the progression from 2-wk to 4-wk diabetes in the rat.
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PMID:Left ventricular mitogen activated protein kinase signaling following polymicrobial sepsis during streptozotocin-induced hyperglycemia. 1533 69


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