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)

Post-extubation atelectasis (PEA) constitutes the commonest cause of lung collapse in ventilated neonates. The clinical and radiological features of 47 ventilated infants who developed PEA within 24 h of extubation are reported. Three main radiographic patterns of atelectasis were identified: (1) transient unilobar collapse resolving within 12 h of extubation (19 cases), (2) multilobar atelectasis developing over a 48-h period (18 cases), and (3) progressive atelectasis resulting in complete collapse of a whole lung. A similar number of ventilated infants without PEA served as controls. We found a significant association between the incidence of PEA and multiple intubation (P < 0.02), presence of patent ductus arteriosus (P < 0.001) and neonatal sepsis (P < 0.05). Prophylactic physiotherapy is recommended for ventilated infants, particularly those with the above risk factors.
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PMID:Post-extubation atelectasis in ventilated newborn infants. 833 4

Eight cases of ecstasy related acute liver damage referred to a specialised liver unit are described. Two patients presented after collapse within six hours of ecstasy ingestion with hyperthermia, hypotension, fitting, and subsequently disseminated intravascular coagulation with rhabdomyolysis together with biochemical evidence of severe hepatic damage. One patient recovered and the other with evidence of hyperacute liver failure was transplanted but subsequently died, histological examination showing widespread microvesicular fatty change. Four patients presented with acute liver failure without hyperthermia. All four fulfilled criteria for transplantation, one died before a donor organ became available, and two died within one month post-transplantation of overwhelming sepsis. Histological examination showed submassive lobular collapse. Two patients presented with abdominal pain and jaundice and recovered over a period of three weeks; histological examination showed a lobular hepatitis with cholestasis. Patients developing jaundice or with evidence of hepatic failure particularly encephalopathy and prolongation of the international normalised ratio, or both, whether or not preceded by hyperthermia, should be referred to a specialised liver unit as liver transplantation probably provides the only chance of recovery.
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PMID:Acute liver damage and ecstasy ingestion. 867 2

A 42-year-old man with aplastic anemia presented to hospital toxic and septic secondary to central Silastic catheter sepsis. The chronic indwelling catheter fractured during an attempt at removal and the distal remnant embolized to the right ventricular outflow tract and main pulmonary artery precipitating near cardiopulmonary collapse. The thrombosed catheter was successfully retrieved under fluoroscopy by an endovascular snare technique thus avoiding operative intervention in this immunosuppressed, thrombocytopenic and septic individual. The patient had an uneventful recovery.
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PMID:Retrieval of Silastic catheter fragment from heart in septic thromboembolism complicating aplastic anemia. 884 31

Urethan is a commonly used animal anesthetic for nonrecovery laboratory surgery. However, urethan has diverse biological effects that may complicate the interpretation of experimental findings. This study examined the effect of urethan on the response to an intravenous bolus of lipopolysaccharide (LPS; 30 mg/kg) in rats. In instrumented rats, urethan (1.2 gm/kg i.p.) completely prevented the fall in arterial pressure immediately after LPS administration but did not prevent late cardiovascular collapse. In uninstrumented rats, urethan also attenuated indexes of organ injury measured 4 h after LPS administration, including mural bowel hemorrhage, hemoconcentration, hypoglycemia, metabolic acidosis, and lung myeloperoxidase activity, a measure of neutrophil sequestration. The peak increase in tumor necrosis factor-alpha (TNF-alpha) 90 min after LPS administration was reduced 88% by urethan (2,060 +/- 316 vs. 16,934 +/- 847 pg/ml; P < 0.001). In uninstrumented animals, urethan at 1.2 gm/kg reduced the 90% mortality rate of a lethal dose of LPS to 0-10% when given up to 24 h before LPS administration but did not reduce mortality when given 2 h after LPS. Urethan neither directly bound LPS by Limulus assay nor inhibited LPS-stimulated TNF-alpha mRNA expression in cultured mouse peritoneal macrophages, but TNF-alpha mRNA expression was suppressed by serum from a urethan-treated rat. Moreover, rauwolscine, which shares alpha 2-adrenoceptor-blocking activity with urethan, also prevented death from a subsequent 90% lethal dose LPS bolus. We conclude that urethan or its metabolites protect against LPS, in part, by reducing TNF-alpha release and speculate that this may be mediated by alpha 2-adrenoceptors. These actions of urethan make it an undesirable anesthetic agent for in vivo studies of sepsis or LPS.
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PMID:Urethan anesthesia protects rats against lethal endotoxemia and reduces TNF-alpha release. 894 58

In order to evaluate the role of underlying disease in the high mortality observed in acute renal failure (ARF) and risk factors related to the development of oliguric ARF in renal allograft recipients, two groups were selected: 34 patients with native kidneys, aged 16 and 57 years, and presenting ischemic ARF caused by cardiovascular collapse, with no signs of infection at the time of diagnosis; and 34 renal allograft recipients who developed ARF immediately after transplantation, without rejection. ARF was defined either as 30% increase of basal plasmatic creatinine in patients with native kidneys or nonnormalization of plasmatic creatinine at day 5 after transplantation in renal allograft recipients; oliguria as diuresis < or = 400 mL/24 h. There were no differences in age, male frequency, oliguria presence and duration, need for dialysis, and infection episodes for renal allograft recipients and patients with native kidneys. The development of sepsis (3% and 41%) and death rate (3% and 44%) were higher in patients with native kidneys (p < 0.01). The renal allograft recipients with both oliguric (n = 18) and nonoliguric (n = 16) ARF were evaluated and no difference was observed in the recipient's age, donor's age, cold ischemia time, time elapsed until plasmatic creatinine normalization, donor's plasmatic creatinine or urea, and mean arterial pressure. No differences were observed between the groups regarding frequency of infection episodes during ARF and frequency of death. In conclusion, renal allograft recipients presented a lower death rate and were less susceptible to sepsis. Cold ischemia time, age, and hemodynamic characteristics of the donor did not affect the development of oliguria.
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PMID:Acute renal failure in renal allograft recipients and patients with native kidneys. 910 1

1. Colchicine is a highly active alkaloid used in the treatment of gouty arthritis and pseudogout. In overdose colchicine inhibits cell division effecting organs with a high rate of cell turn-over, such as the gastrointestinal tract and bone marrow. Early fatality results from cardiovascular collapse and respiratory failure, however pancytopenia and overwhelming septicaemia can occur later. 2. We describe a case of suicidal ingestion of 25-30 mg of colchicine in a previously healthy 43-year-old woman. Initial symptoms were mainly gastrointestinal. By day 5 she had developed severe pancytopenia and early sepsis, which were successfully treated using granulocyte colony stimulating factor (G-CSF) 600 micrograms s.c. 3. In vitro G-CSF is produced by the haematopoietic system. However, G-CSF can now be produced by recombinant DNA cloning technology and thus is available clinically. 4. There is no recognised antidote for colchicine poisoning and treatment is symptomatic. Fab fragments may have a promising future in eliminating colchicine from the body, but are currently not clinically available. In those patients that survive the initial phase of poisoning, G-CSF offers an effective method of treating the pancytopenia and preventing overwhelming septicaemia. Daily monitoring of the patient's haematological status is strongly recommended.
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PMID:Granulocyte-colony stimulating factor in the treatment of colchicine poisoning. 915 49

Despite their age, patients younger than 50 years who have collapse of their femoral condyles caused by steroid associated avascular necrosis have few options except total knee arthroplasty. There have been no specific reports of the results of total knee replacements for this disease. Between 1980 and 1993, 31 porous coated anatomic total knee replacements were performed in 21 patients younger than 50 years of age with avascular necrosis of the femoral condyles and tibial plateaus. There were 17 women and 4 men, with an average age of 36 years (range, 22-48 years). Seventeen of 21 patients had systemic lupus erythematosus, and all patients had a history of corticosteroid use. Patients underwent a complete clinical and radiographic evaluation at final followup that averaged 8.2 years (range, 2-16 years). Overall, there were 17 good and excellent results (55%). Eleven knees were revised for aseptic loosening (37%), and 3 additional knees (10%) ultimately were revised for deep sepsis. All 6 knees in patients with no diagnosis of systemic lupus erythematosus had excellent clinical results. There were only 11 of 25 successful outcomes (44%) in the patients with systemic lupus erythematosus. There were no differences in results when patients were stratified by degree of steroid use, cemented versus cementless fixation, or activity level.
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PMID:Total knee arthroplasty for corticosteroid associated avascular necrosis of the knee. 917 Mar 73

Diminished availability of oxygen at the cellular level might account for organ dysfunction in sepsis. Although the classical forms of tissue hypoxia due to hypoxemia, anemia, or inadequate perfusion all might be important under some conditions, it seems increasingly likely that a fourth mechanism, namely cytopathic hypoxia, might play a role as well. The term cytopathic hypoxia is used to denote diminished production of adenosine triphosphate (ATP) despite normal (or even supranormal) PO2 values in the vicinity of mitochondria within cells. At least in theory, cytopathic hypoxia could be a consequence of several different (but mutually compatible) pathogenic mechanisms, including diminished delivery of a key substrate (e.g., pyruvate) into the mitochondrial tricarboxylic acid (TCA) cycle, inhibition of key mitochondrial enzymes involved in either the TCA cycle or the electron transport chain, activation of the enzyme, poly-(ADP)-ribosylpolymerase (PARP), or collapse of the protonic gradient across the inner mitochondrial membrane leading to uncoupling of oxidation (of NADH and FADH) from phosphorylation of ADP to form ATP. Tantalizing, but limited, data support the view that cytopathic hypoxia occurs in both animals and patients with sepsis or endotoxemia.
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PMID:Cytopathic hypoxia in sepsis. 924 46

Sepsis is a major clinical problem in intensive care. The mortality in septic shock is high, and predominantly due to cardiovascular collapse and multiple organ dysfunction. In sepsis high levels of circulating hyaluronan have been found, correlating to disease severity and prognosis. The reason behind the increased levels could be both decreased hepatic uptake and increased peripheral synthesis. Thus, plasma hyaluronan may be a clinically useful marker of hepatic dysfunction and possibly also an indicator of the increased inflammatory and reparative activity in different organs in septic conditions.
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PMID:Hyaluronan turnover in relation to infection and sepsis. 926 May 70

The As4.1 cell line was established from a mouse kidney tumor by transgene-targeted tumorogenesis. These cells express high levels of renin mRNA from their endogenous renin gene and release approximately eightfold-more prorenin than active renin in culture. Levels of renin mRNA in As4.1 cells are decreased in a dose-dependent manner by the addition of physiological concentrations of cytokine interleukin-1 to the media. Stability of renin mRNA and initial rates of release of active renin and prorenin were not significantly altered by interleukin-1. In contrast, transcription initiated from a construct that consisted of 4.1 kilobases of renin 5' flanking sequence fused to a reporter gene (chloramphenicol acetyltransferase) was markedly inhibited by interleukin-1. On the basis of our findings, we conclude that downregulation of renin synthesis caused by interleukin-1 occurs primarily at the level of transcription and that DNA sequence or sequences mediating that effect are positioned within 4.1 kilobases upstream of the renin gene. The physiological relevance of this regulation is related to the events that occur during septic shock, characterized by hypotension, cardiovascular collapse, multiple organ failure, and high mortality. Unexpectedly, hypotension associated with septic shock does not lead to activation of the renin-angiotensin system. The hypotension in septicemia is believed to be mediated by the combined action of many modulators including cytokines, and data presented here suggest direct involvement of interleukin-1 in this process.
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PMID:Downregulation of renin gene expression by interleukin-1. 926 Sep 85


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