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)

Intrahepatic cholestasis is a frequent, however unresolved complication of total parenteral nutrition in infancy. A frequency of 10-50% is reported. The concentration of serum bile acids seems to be a sensitive indicator for a beginning cholestasis. As typical histological alterations of the liver are considered: inflammatory portal reaction, fibrosis and proliferation of bile ducts. As important components of the obviously multifactorial etiology are considered: lacking oral alimentation, fetal bile acid synthetic pathways, amino acid toxicity, hypoalbuminemia, sepsis and substrate excess.
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PMID:[Cholestasis in total parenteral nutrition--a review]. 310 Aug 61

Intrahepatic cholestasis is a frequent, however, unresolved complication of total parenteral nutrition in infancy. A frequency of 10-50% is reported. The concentration of serum bile acids seems to be a sensitive indicator for a beginning cholestasis. As typical histological alterations of the liver are considered: inflammatory portal reaction, fibrosis and proliferation of bile ducts. As important components of the obviously multifactorial etiology are considered: lacking oral alimentation, fetal bile acid synthetic pathways, amino acid toxicity, hypoalbuminemia, sepsis and substrate excess.
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PMID:[Cholestasis in total parenteral nutrition. A review]. 310 11

Intrahepatic cholestasis in the setting of extrahepatic bacterial infection has been attributed to the effects of endotoxin and cytokines such as tumor necrosis factor-alpha (TNF-alpha) on bile acid transport. To define the mechanism of sepsis-associated cholestasis, taurocholate transport was examined in basolateral (bLPM) and canalicular (cLPM) rat liver plasma membrane vesicles derived from control and endotoxin [lipopolysaccharide (LPS)]-treated animals and in plasma membrane vesicles prepared after TNF-alpha treatment. Na(+)-dependent [3H]taurocholate uptake and both membrane-potential-dependent and ATP-dependent [3H]taurocholate transport were reduced in bLPM and cLPM vesicles, respectively, after LPS treatment. In membrane vesicles from TNF-alpha-treated animals, Na(+)-dependent [3H]taurocholate uptake was also reduced. Northern blot hybridization, using cDNA probes for the putative sinusoidal bile acid transporter (Ntcp) and canalicular ecto-adenosinetriphosphatase, demonstrated decreased mRNA levels after LPS and TNF-alpha treatment. Immunoblot analysis of membrane extracts from LPS-treated animals revealed decreased levels of these putative bile acid transporters. Impaired bile acid transport at the sinusoidal and canalicular membrane domains by these and other mediators of the inflammatory response may account for sepsis-associated cholestasis.
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PMID:Effect of endotoxin on bile acid transport in rat liver: a potential model for sepsis-associated cholestasis. 876 Jan 17

Intrahepatic cholestasis is characterized by a decrease in bile flow in the absence of overt bile duct obstruction, resulting in the accumulation of bile constituents in the liver and blood. Various etiological factors have been incriminated including drugs, total parenteral nutrition, sepsis, pregnancy, graft-versus-host disease and systemic disorders such as sarcoidosis, amyloidosis and Hodgkin's disease. The pathogenesis of cholestasis is unclear and several mechanisms have been hypothesized, without convincing evidence that any of these play a role in clinical cholestasis. Despite the uncertainty about the pathophysiology of intrahepatic cholestasis, several forms of therapy have been employed. Ursodeoxycholic acid may relieve pruritus and lethargy, and in some cases may modify disease progression. If cholestasis persists, supportive therapy is important to maintain optimal physical and nutritional well-being. In patients with advanced liver disease associated with hepatocellular failure, liver transplantation is the only viable option.
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PMID:Intrahepatic cholestatic syndromes: pathogenesis, clinical features and management. 1043 57

Listeriosis is an infection produced by Listeria monocytogenes. It is infrequent and affects people at extreme ages, pregnant women, immunocompromised people and, occasionally, healthy people. Its incidence has increased in recent years and shows a certain tendency to seasonality, increasing in summer. It can appear sporadically or as outbreaks. In pregnant women the infection is most frequently produced in the third trimester and the symptoms are usually light. Nonetheless, the infection of the fetus is severe, and can produce miscarriages, fetal deaths, corioamnionitis and premature births with the newborn infected, manifested in the form of granulomatosis infantiseptica with abscesses and scattered granulomas or at a later stage , as meningitis or sepsis. Intrahepatic cholestasis is a reversible form of cholestasis, its cause is unknown, it is specific to pregnancy and is more frequent in multiparous women, in the third trimester and rarely before the 26th week. It disappears following childbirth and is the second cause of jaundice in pregnancy, after hepatitis. The diagnosis of cholestasis is basically clinical. It appears as palmoplantar pruritus but can also produce nausea, vomiting and abdominal discomfort localized in the right hypochondrium. Given that listeriosis and cholestasis can have a shared symptomology, the possibility of listeriosis must be borne in mind in order for early implementation of the mechanisms of diagnostic confirmation (cultivation of sterile fluids or tissues: blood, neonatal CSF, amniotic liquid or placenta) and specific treatment. We present a case of cholestasis and listeriosis in the third trimester with a good maternofetal result.
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PMID:[Cholestasis and listeriosis in the third trimester of pregnancy]. 2440 73