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)

Two autopsy cases of neonatal argininosuccinate synthetase (ASS) deficiency demonstrating the particular histological changes of the liver are presented. Case 1 was a female infant with elevated blood ammonia and citrulline. The patient died of sepsis at nineteen days after birth. Autopsy revealed hematomas in bilateral cerebral hemispheres and a yellow liver parenchyma. Histologically, the cerebrum showed diffuse astrogliosis with Alzheimer type II cell and swollen cytoplasm. Status spongiosus and gliosis were observed in the subthalamic and pontine nuclei. The liver demonstrated fatty degeneration and wide portal space with bile duct proliferation and inflammatory cell infiltration. The ASS activities in the liver and the kidneys were not detected. Case 2 was a female infant who died of respiratory distress twenty-four days after birth. Autopsy revealed hematomas in the bilateral cerebral ventricles and a liver with yellow parenchyma. Histologically, there was destruction of arrangement in the cerebrum and cerebellum together with marked decrease of nerve cells with gliosis and phagocytosis. The liver showed mild fatty degeneration and wide portal space accompanied by bile duct proliferation and inflammatory cell infiltration. The ASS activities in the liver and kidneys were not detected.
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PMID:Neonatal type of argininosuccinate synthetase deficiency. Report of two cases with autopsy findings. 407 82

We report on a boy with ureteroceles that obstructed the bladder outlet and ureters, who presented with sepsis and hyperammonemia despite normal liver function. The hyperammonemia was most likely caused by excessive absorption of ammonia produced by Proteus mirabilis in the obstructed urinary tract.
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PMID:Hyperammonemia in a boy with obstructive ureterocele and proteus infection. 669 67

Six normal volunteers were vaccinated against typhoid-cholera. 15N-Glycine was injected the morning after vaccination. The injection was repeated three to six days and 10 days later. All subjects ate the same diet on each occasion. Excretion of 15N in urinary ammonia and total urinary excretion of nitrogen, ammonia, and creatinine were determined after each injection of isotope. Urinary excretion of 15N was used to calculate rates of whole-body protein turnover. Total urinary nitrogen and ammonia excretions showed no appreciable change on all three days. Creatinine excretion was significantly higher the day after vaccination than on the other two days (p < 0.05). Rates of protein turnover were also significantly higher on this day: a 37% increase in synthesis and 55% increase in degradation were noted. These results show that during the reaction to vaccination there was a stimulation of whole-body protein metabolism that is similar to that produced by sepsis.
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PMID:Stimulation of protein synthesis and breakdown by vaccination. 742 36

Fulminant hepatic failure is an extremely rare coma syndrome resulting from massive necrosis of liver cells. A wide variety of etiologic agents have been identified, including viruses, drugs, and other toxic agents. Treatment focuses on reducing the ammonia load presented to the liver and on preventing or controlling complications, including sepsis, bleeding, cerebral edema, renal failure, and respiratory failure. With further research and identification of the specific toxins or metabolic derangements underlying the pathophysiology of this syndrome, more effective therapeutic measures may be devised.
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PMID:Fulminant hepatic failure: a rare but often lethal coma syndrome. 743 88

Catabolic illness such as sepsis and injury induce profound changes in host amino acid metabolism, including increased hepatic amino acid uptake. Because many amino acid-dependent pathways such as gluconeogenesis and acute-phase protein synthesis are activated in the liver during severe infection, this review will focus on the control of hepatic plasma membrane amino acid transport by specific inflammatory mediators. We specifically review the role of cytokines, eicosanoids, and glucorticoids in this response. Collectively, these signaling molecules act in a concerted manner to exert local control of hepatic function including the stimulation of amino acid transport. In particular, we review the role of glutamine and its transport in the liver, as it occupies a unique role in interorgan ammonia metabolism during critical illness.
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PMID:Hepatic uptake of glutamine and other amino acids during infection and inflammation. 764 31

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26

The activity of glutaminase is high in lymphoid organs, lymphocytes and macrophages and increases in the popliteal lymph node in response to an immunological challenge. Consistent with this high activity, glutamine is utilised at a high rate by resting lymphocytes and macrophages in culture. Mitogenic stimulation of lymphocytes increases both glutaminase activity and the rate of glutamine utilisation. The major products of glutamine utilisation by lymphocytes and macrophages in culture are glutamate, aspartate, lactate and ammonia; < 25% of the glutamine used is completely oxidised. It is suggested that the high rate of glutamine utilisation by cells of the immune system serves to maintain a high intracellular concentration of intermediates of biosynthetic pathways such that optimal rates of DNA, RNA and protein synthesis can be maintained. In the absence of glutamine, lymphocytes do not proliferate in vitro; proliferation increases greatly as the glutamine concentration increases. The synthesis of interleukin-2 by lymphocytes and of interleukin-1 by macrophages is glutamine-dependent. Macrophage-mediated phagocytosis is influenced by glutamine availability. Glutamine is synthesized in skeletal muscle. Skeletal muscle and plasma glutamine levels are lowered by sepsis, injury, burns, surgery and endurance exercise and in the overtrained athlete. These observations indicate that a significant depletion of the skeletal muscle glutamine pool is characteristic of trauma and it has been suggested that the lowered plasma glutamine concentration contributes, at least in part, to the immunosuppression which accompanies such situations. Beneficial effects of the provision of glutamine or its precursors have been reported in patients following surgery, radiation treatment or bone marrow transplantation or suffering from injury, sepsis or burns.
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PMID:The proposed role of glutamine in some cells of the immune system and speculative consequences for the whole animal. 926 77

Glutamine, described as a "conditionally essential" amino acid for critically ill patients, has not been routinely added to parenteral amino acid formulations for critically ill neonates and is provided in only small quantities by the enteral route when enteral intake is low. We conducted a blinded, randomized study of enteral glutamine supplementation in 68 very low birth weight neonates randomly assigned to receive glutamine-supplemented premature formula versus premature formula alone between days 3 and 30 of life. Primary end points consisted of hospital-acquired sepsis, tolerance to subsequent enteral feedings (days with no oral intake), and duration of hospital stay. Hospital acquired sepsis was 30% (control group) and 11% (glutamine group). Logistic regression with birth weight as a covariate showed that: (1) feeding group was significant (p = 0.048) in determining the probability of developing proven sepsis over the course of hospitalization and (2) the estimated odds of developing sepsis were 3.8 times higher for infants in the control group than for those treated with glutamine. Glutamine-supplemented infants had better tolerance to enteral feedings as measured by percent of days on which feedings needed to be withheld (mean percentage of 8.8 vs 23.8, p = 0.007). Analysis of T cells demonstrated a blunting of the rise in HLA-DR+ and CD16 subsets in glutamine-supplemented infants. There were no differences in growth; in serum ammonia, urea, liver transaminase, or prealbumin concentrations; or in mean hospital stay. This study provides evidence for decreased morbidity in very-low-birth-weight neonates who receive enteral glutamine supplementation.
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PMID:Enteral glutamine supplementation for very low birth weight infants decreases morbidity. 940 48

During sepsis, the lung responds by exporting increased amounts of the amino acid glutamine. This response is accompanied by increased enzymatic activity of glutamine synthetase (GS), which catalyzes the synthesis of glutamine from glutamate and ammonia. It is also known that GS expression in the rat lung can be induced by glucocorticoid hormones. To determine whether the septic response and the response to glucocorticoids are related, we have characterized the induction of GS expression during lipopolysaccharide (LPS)-induced endotoxemia in normal, neutropenic, and adrenalectomized rats. Normal rats exhibited a time- and dose-dependent induction of GS mRNA levels after a single intraperitoneal dose of LPS. Responses to LPS were maximal at doses of 0.1 mg/kg body wt and above. A single 10 mg/kg body wt dose of LPS led to a rapid, transient sevenfold increase in GS mRNA (P < or = 0.1) and a twofold increase in GS protein level 8 h postinjection. Induction of lung GS mRNA 4 h after LPS injection was approximately fivefold in neutropenic (P < or = 0.1) and fourfold in nonneutropenic control rats (P < or = 0.1), suggesting that infiltrating neutrophils or neutrophil-derived factors are not required for GS induction. In response to high-dose, short-term endotoxemia, adrenalectomized rat lung GS mRNA increased twofold (P < or = 0.02) compared with sixfold in sham-operated control rats (P < or = 0.02). However, in response to low-dose, long-term endotoxemia, adrenalectomized rat lung GS mRNA increased threefold (P < or = 0.02) compared with fourfold in sham-operated control rats (P < or = 0.02). Adrenalectomy did not affect the elevation of lung GS mRNA levels in response to dexamethasone. In addition, GS mRNA was induced four- and sixfold in rat microvascular pulmonary endothelial cells exposed to plasma from control and septic rats, respectively. The addition of a glucocorticoid antagonist, RU-38486, completely blocked GS gene induction in the presence of control plasma but only attenuated the response to plasma from septic animals by 30%. These results suggest that GS gene induction during sepsis is only partially mediated by adrenal-derived glucocorticoid hormones.
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PMID:Glutamine synthetase gene expression in the lungs of endotoxin-treated and adrenalectomized rats. 943 73

Low perfusion of the liver due to hypovolaemia and sepsis-induced pathological distribution of blood volume can lead to severe liver disturbances. Damage to the liver as shock organ is manifold and affects other functions. Increased serum levels of ammonia and zerebral symptoms with disturbances of neurotransmission are responsible for the development of encephalopathia. Based on a case report, the differential diagnosis of Leigh-Syndrome as a mitochondric encephalopathy with uniform morphologic form is discussed. Long lasting parenteral nutrition, sepsis, metabolic imbalance and disturbance of the electrolyte balance can influence the extent of the mitochondric encephalopathy.
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PMID:[Hepatotoxic encephalopathy versus Leigh syndrome--a case report]. 961 64


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