Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Liver failure fulminant

Liver disease may decrease hepatic metabolism resulting in enhanced responses to parent chemicals however, for many compounds, metabolism is only slightly impaired in moderate to severe liver disease. Disease-induced alterations in clearance and volume of distribution often act in opposite directions with respect to their effect on half-life. Bioavailability may be markedly increased in liver disease with portal/systemic anastomosis (the connection of normally separate parts so they intercommunicate) so that orally administered chemicals bypass hepatic first-pass metabolism. Altered receptor sensitivity has been observed for some chemical substances in liver cirrhosis. When liver tissue repair is inhibited by chemical co-exposure, even an inconsequential level of liver injury may lead to fulminating liver failure from a nonlethal exposure of hepatotoxic-ants. (Several articles, as reviewed by Dybing and Spderlund 1999.)... [Pg.249]

WARNING Cases of fulminant liver failure resulting in death have occurred Uses Adjunct to carbidopa/levodopa in Parkinson Dz Action COMT inhibitor slows levodopa metabolism Dose 100 mg PO tid w/ 1st daily levodopa/carbidopa dose, then dose 6 12 h later -1- w/ renal impair Caution [C, ] Contra Hqjatic impair, w/ nonselective MAOI Disp Tabs SE Constipation, XCTOstomia, vivid dreams, hallucinations, anorexia, N/D, orthostasis, liver failure, Rhabdomyolysis Interactions T Effects OF CNS dqjressants, SSRIs, TCAs, warfarin, EtOH t risk of hypotensive crisis W/ nonselective MAOIs (phenelzine, tranylc5 promine) EMS Has been associated w/ liver failure and death may experience hallucinations concurrent EtOH use can T CNS dqjression T effects of warfarin severe D is common sevoal wks afto starting OD May cause NA and dizziness... [Pg.307]

Berkovitch, M., Pope, E., Phillips, J., and Koren, G. (1995) Pemoline-associated fulminant liver failure testing the evidence for causation. Clini Pharmacol Ther 57 696—698. [Pg.261]

Initially, the patient is asymptomatic or has mild gastrointestinal upset (nausea, vomiting). After 24-36 hours, evidence of liver injury appears, with elevated aminotransferase levels and hypoprothrombinemia. In severe cases, fulminant liver failure occurs, leading to hepatic encephalopathy and death. Renal failure may also occur. [Pg.1256]

Fulminant liver failure results from massive necrosis of liver tissue. Diminution of mental function results, and this often leads to coma. The body undergoes a buildup of toxic products, alteration of its acid balance, and a decrease in cerebral blood flow. Impaired blood coagulation and intestinal bleeding occur as well. Other malfunctions and diseases of the liver include viral infections and alcoholic hepatitis. In 1999, of the 14,707 individuals on a waiting list for transplants, 4,498 received transplants and 1,709 died while waiting. As of February 2002, 18,434 people awaited liver transplants. [Pg.32]

Fulminant liver failure results from massive necrosis of liver tissue with a concurrent buildup in toxic products, disruption of acid balance, and a decrease in cerebral blood flow. Impaired blood coagulation and intestinal bleeding result. The main physiological effect is diminution of mental function that often leads to coma. [Pg.144]

Two cases of fatal fulminant hepatic failure have been described in previously healthy women aged 30 and 32 years who presented with jaundice 4 and 5 months respectively after starting to take propylthiouracil for Graves hyperthyroidism (51). Another case of fatal fulminant liver failure with cholestatic jaundice 2 weeks after the start of treatment with propylthiouracil 100 mg tds has been described (52). [Pg.339]

Macfarlane B, Davies S, Mannan K, Sarsam R, Pariente D, Dooley J. Fatal acute fulminant liver failure due to clozapine a case report and review of clozapine-induced hepatotoxicity. Gastroenterology 1997 112(5) 1707-9. [Pg.287]

Donaldson, B.W., Gopinath, R., Wanless, I.R., Phillips, M.X, Cameron, R., Roberts, E.A., Greig, P.D., Levy, G., Biendis, L.M. The role of transjugular liver biopsy in fulminant liver failure relation to other prognostic indicators. Hepatology 1993 18 1370-1374... [Pg.163]

The expression hepatic encephalopathy (HE) is a collective term covering five clinical forms of disease (H.O. Conn, 1989) (7.) Reyc s syndrome, (2.) enzyme deficiency of the urea cycle, (i.) pseudoportosystemic encephalopathy, (4.) fulminant liver failure, and (J.) portosystemic encephalopathy. It is not known whether the pathogenic mechanisms of these various clinical forms are identical, (s. tab. 15.3)... [Pg.270]

Congenital cystic fibrosis (20) Fulminant liver failure (55)... [Pg.334]

Alberti-Flor, J.J., Hernandez, M.E., Ferrer, J.P., Howell, S., Jeffers, L. Fulminant liver failure and pancreatitis associated with the use of sulfamethoxazole-trimethoprim. Amer. X Gastroenterol. 1989 84 1577-1579... [Pg.388]

Pernambuco, J.R.B., Langley, P.G., Hughes, R.D., Izumi, S., Williams, R. Activation of the fibrinolytic system in patients with fulminant liver failure. Hepatology 1993 18 1350-1356... [Pg.389]

HPV B19 causes erythema infectiosum in children. It may also lead to acute hepatitis. Aplastic anaemia is found in adults with simultaneous, potentially massive liver cell necroses and fulminant liver failure. HPV B19 can be detected in the liver tissue using PCR. (80)... [Pg.467]

Tab. 29.5 Diagnostic measures in suspected fulminant liver failure... Tab. 29.5 Diagnostic measures in suspected fulminant liver failure...
Ghobrial, M., Busuttil, R.W. Fulminant liver failure dueto usnic acid for weight loss (case report). Amer. J. Gastroenterol. 2004 99 950-952... [Pg.560]

Sallie, R., Katsiyiannakis, L., Baldwin, D., Davies, S., O Grady, X, Mowat, A., Mieli-Vergani, G., Williams, R. Failure of simple biochemical index to reliably differentiate fulminant Wilson s disease from other causes of fulminant liver failure. Hepatology 1992 16 1206-1211... [Pg.633]

In another study, only four of 11 241 patients treated with interferon alfa died of fulminant liver failure (16). [Pg.1808]

Yoshida EM, Rasmussen SL, Steinbrecher UP, Erb SR, Scudamore CH, Chung SW, Oger JJ, Hashimoto SA. Fulminant liver failure during interferon beta treatment of multiple sclerosis. Neurology 2001 56(10) 1416. [Pg.1837]

Two cases of serious or fatal toxicity have been described in two infants who had been treated with herbal tea containing pennyroyal oil (4). One infant developed fulminant liver failure with cerebral edema and necrosis the other infant developed hepatic dysfunction and a severe epileptic encephalopathy. [Pg.1986]

Kraft M, Spahn TW, Menzel J, Senninger N, Dietl KH, Herbst H, Domschke W, Lerch MM. Fulminantes Leberversagen nach Einnahme des planzlichen Antidepressivums Kava-Kava. [Fulminant liver failure after administration of the herbal antidepressant Kava-Kava.] Dtsch Med Wochenschr 2001 126(36) 970-2. [Pg.2839]

Fulminant liver failure developed in a 39-year-old woman after she had taken topiramate for about 4 months, in addition to carbamazepine. The condition occurred after she increased the dosage of topiramate to 300 mg/day, and was preceded for a few days by tiredness and somnolence (50). She made an uncomplicated recovery after hver transplantation. Histological examination showed centrilobular necrosis, compatible with drug-induced fulminant liver failure. [Pg.3451]

There have been several reports of hepatotoxicity attributed to herbal medicines containing L. tridentata leaves (1,2). Of 18 reports of illnesses associated with the ingestion of chaparral, there was evidence of hepatotoxicity in 13 cases (3). The presentation was characterized by jaundice with a marked increase in serum hver enzymes at 3-52 weeks after ingestion, and it resolved 1-17 weeks after withdrawal. The predominant pattern of liver damage was cholestatic in four cases there was progression to cirrhosis and in two there was acute fulminant liver failure that required liver transplantation. [Pg.3733]

In contrast, type II hepatotoxicity is associated with massive centrilobular liver cell necrosis that can lead to fulminant liver failure. Type II hepatotoxicity is characterized by fever, jaundice, and very high serum transaminase levels. It may be immune-medi-ated and is thought to occur in genetically predisposed individuals. The incidence of type II hepatotoxicity 1 35 000 with one exposure to halothane and... [Pg.131]

Porta G, Gayotto L, Alvarez F. Anti-liver-kidney microsome antibody-positive autoimmune hepatitis presenting as fulminant liver failure. J Pediatr Gastroenterol Nutr 1990 11 138-40. [Pg.1840]


See other pages where Liver failure fulminant is mentioned: [Pg.544]    [Pg.286]    [Pg.307]    [Pg.426]    [Pg.206]    [Pg.68]    [Pg.567]    [Pg.263]    [Pg.271]    [Pg.403]    [Pg.449]    [Pg.541]    [Pg.550]    [Pg.566]    [Pg.570]    [Pg.696]    [Pg.817]    [Pg.818]    [Pg.828]    [Pg.379]    [Pg.3021]    [Pg.603]   
See also in sourсe #XX -- [ Pg.271 , Pg.378 , Pg.416 , Pg.421 , Pg.432 , Pg.449 , Pg.466 , Pg.467 , Pg.550 , Pg.613 ]




SEARCH



Fulminant

Fulminates

Fulminating

Liver failure

© 2024 chempedia.info