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Hepatitis fulminant

Gastrointestinal Hepatitis, fulminant hepatic failure, nausea, vomiting, diarrhea, abdominal pain, increase in aminotransferases, increase in alkaline phosphatase... [Pg.68]

The morphological spectrum may therefore range from steatosis, acute hepatitis, fulminant course, chronic hepatitis, aggressive episodes in chronic hepatitis and liver fibrosis through to micronodular cirrhosis. Complete cirrhosis can already exist in children aged 4-5 years. The development of hepatocellular carcinoma is extremely rare (360) it is assumed that copper has a protective effect against malignant transformation. (391,393)... [Pg.612]

Depending on referral patterns the proportion of patients presenting with liver disease alone varies from 20 to 46%. Liver disease may mimic any forms of common liver conditions, ranging from asymptomatic transaminasania to acute hepatitis, fulminant hepatic failure (about one out of six patients with hepatic presentation), chronic hepatitis, and cirrhosis (about one out of three patients) with all of its complications. [Pg.465]

Bihmbin oxidase [80619-01 -8] derived from Mjrothecium verrucaria was modified with polyethyleneglycol when this conjugate was injected intravenously to jaundiced rats, the plasma bihmbin dropped to normal levels. This approach might have potential in the treatment of hyperbihmbinemia, fulminant hepatitis, and neonatal bihmbin encephalopathy (177). [Pg.312]

To date, there are no documented cases of chronic hepatitis A.1 Death associated with HAV is rare and is mostly associated with fulminant hepatitis, with which approximately 100 people die annually.1... [Pg.346]

In fulminant hepatitis with hepatic encephalopathy, patients may have asterixis and coma. [Pg.348]

Managing viral hepatitis involves both prevention and treatment. Prevention of hepatitis A and B (and indirectly for hepatitis D) can be achieved with immune globulin or vaccines. There is no specific pharmacologic treatment for acute viral hepatitis A, B, C, D, or E only supportive care is available. Individuals with mild to moderate symptoms rarely require hospitalization. Occasionally, hospitalization is required in individuals experiencing significant nausea, vomiting, diarrhea, and encephalopathy. Liver transplantation may be required in rare instances if fulminant hepatitis develops. [Pg.350]

All azole antifungals carry the potential for rash, photosensitivity, and hepatotoxicity. In general, hepatotoxicity is mild and reversible, presenting as asymptomatic increases in liver transaminases. However, fulminant hepatic failure has been reported with itraconazole. Therefore, serial monitoring of liver function... [Pg.1216]

Campo, J. V., McNabb, J., Perel, J. M. et al. (2002). Kava-induced fulminant hepatic failure. /. Am. Acad. Child Adoles. Psychiatr., 41, 631-2. [Pg.107]

There have been many sporadic reports that lipo-PGEj is effective in fulminant hepatitis, neuralgia associated with herpes zoster, multiple spinal canal stenosis, cerebral infarction, myocardial infarction, chronic renal failure, and bed sores as well as for its registered indications. [Pg.267]

Baraldi M, Zeneroli ML, Ventura E, Penne A, Pinelli G, Ricci P, Santi M Supersensitivity of benzodiazepine receptor in hepatic encephalopathy due to fulminant hepatic failure in the rat Reversal by a benzodiazepine antagonist. Clin Sci 1984 67 167-175. [Pg.94]

Glutaric acidurias Type I Primary defect of glutarate oxidation Type II Defect of electron transfer flavoprotein Type I Severe basal ganglia/cerebellar disease with macrocephaly. Onset 1-2 years Type II Fulminant neurological syndrome of the neonate. Often with renal/hepatic cysts. Usually fatal Diet low in lysine and tryptophan Supplementation with coenzyme Q, riboflavin, carnitine... [Pg.668]

Mihas, A.A., Fulminant hepatitis and lymphocyte sensitization due to propylthiouracil, Gastroenterology 70, 770, 1976... [Pg.464]

Ramirez, P., Parrilla, P., Sanchez Bueno, F., Robles, R., Pons, J.A., Bixquert, V., Nicolas, S., Nunez, R., Alegria, M. S. and Miras, M. (1994). Fulminant hepatic failure after Lepiota poisoning, J. Hepatol., 19, 51-54. [Pg.90]

Only one report of human death attributed to 1,4-dichlorobenzene exposure has been located in the literature. A 60-year-old man and his wife died within months of each other due to acute yellow atrophy of the liver (also known as massive hepatic necrosis or fulminant hepatitis) (Cotter 1953). Their home had been "saturated" with 1,4-dichlorobenzene mothball vapor for a period of about 3-4 months, but no air measurements were available. Clinical symptoms included severe headache, diarrhea, numbness, clumsiness, slurred speech, weight loss (50 pounds in 3 months in the case of the husband), and jaundice. The wife died within a year of the initial exposure however, it was not clear if 1,4-dichlorobenzene was the primary cause of death. This case study did not address whether these individuals consumed excessive amounts of alcohol or had previous medical problems, such as a chronic liver infection. [Pg.33]

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]

Harrison R, Letz G, Pasternak G, et al Fulminant hepatic failure after occupational exposure to 2-nitropropane. Ann Int Med 107 466-468... [Pg.532]

Hepatic Nicotinic acid hepatotoxicity (including cholestatic jaundice) has occurred. Cases of severe hepatic toxicity, including fulminant hepatic necrosis, have occurred in patients who have substituted sustained-release nicotinic acid products for immediate-release nicotinic acid at equivalent doses. Monitor ALT prior to treatment, every 6 to 12 weeks during the first year, and periodically thereafter (approximately 6-month intervals). [Pg.9]

A few cases of fulminant hepatitis with fatal outcome have been reported the relationship to acarbose is unclear. [Pg.288]

Potentially fatal reactions to sulfonamides Fatalities have occurred, although rarely, as a result of severe reactions to sulfonamides (eg, zonisamide), including Stevens-Johnson syndrome, toxic epidermal necrolysis, fulminant hepatic necrosis, agranulocytosis, aplastic anemia, and other blood dyscrasias. [Pg.1215]

Adverse reactions may include acneiform eruptions allergic dermatitis arthropathy multiple cases of cholestatic and fulminant hepatitis drowsiness fatigue headache hepatotoxicity resembling viral or alcoholic hepatitis impotence metallic or garlic-like aftertaste peripheral neuropathy polyneuritis optic or retrobulbar neuritis restlessness occasional skin eruptions. [Pg.1325]

Visual disturbances If treatment continues beyond 28 days, the effect of voriconazole on visual function is not known. If treatment continues beyond 28 days, monitor visual function including visual acuity, visual field, and color perception. Hepatic toxicity There have been uncommon cases of serious hepatic reactions during treatment with voriconazole (eg, clinical hepatitis, cholestasis, and fulminant hepatic failure, including fatalities). Liver dysfunction usually has been reversible on discontinuation of therapy. [Pg.1676]

Severe, life-threatening, and, in some cases, fatal hepatotoxicity, including fulminant and cholestatic hepatitis, hepatic necrosis, and hepatic failure, has been reported in patients treated with nevirapine (see Warnings). [Pg.1886]

Especially with sulfinpyrazone and benzbromarone gastrointestinal disturbances can occur. The most frequent adverse reaction of probenecid is allergic dermatitis. Treatment with benzarone or benzbromarone can be associated with fulminant hepatic injury. [Pg.443]

Arai M, Yokosuka O, Fujiwara K, Kojima H, Kanda T, Hirasawa H et al. Fulminant hepatic failure associated with benzbromarone treatment a case report. J Gastroenterol Hepatol 2002 17(5) 625-6. [Pg.671]

Entacapone is indicated in combination with lev-odopa in patients with motility fluctuations (more than 1 hour gain in the 9-10 hour on phase). Marketing approval was awarded for entacapone just after tolcapone, a central and peripheral COMTI, was withdrawn from the market because of fulminant hepatitis. [Pg.693]

Assal F, Spahr L, Hadengue A, et al. Tolcapone and fulminant hepatitis. Lancet 1998 352 958. [Pg.1239]

In the study of N. A. Gorchakova et al, Enterosgel was used for the treatment of fulminant hepatitis in rats caused by administration of tetrachloromethane [25], It was noted that enterosorption hampered hpid peroxidation in hver tissue of experimental animals, elevated activity of enzymes of the antioxidant pool and decreased activity of serum transaminases, which indicates better preservation of hepatocyte membranes. O.R. Grek et al, used multiple administrations of CCl in combination with drinking of 5% ethanol for modeling of chronic hepatitis in rats. They demonstrated a stable positive effect of Enterosgel administration on activity of serum transaminases and alkaline phosphatase, as well as the rate of hepatic metabolism of xenobiotics [26]. [Pg.208]

SERT. However, trazodone has rarely been associated with inducing priapism. The effects of both nefazodone and trazodone since tx-blocking agents result in a dose-related orthostatic hypotension in some patients. Nefazodone has been associated with hepatotoxicity, including rare fatalities and cases of fulminant hepatic failure requiring transplantation. The rate of serious hepatoxicity with nefazodone has been estimated at 1 in 250,000 to 1 in 300,000 patient-years of nefazodone treatment. [Pg.667]

Telithromycin Oral unaffected by efflux-mediated resistance so is active versus many erythromycin-resistant strains of pneumococci rare cases of fulminant hepatic failure ... [Pg.1014]

Nevirapine NNRTI 200 mg bid. Adjust dose in hepatic insufficiency Dose-escalate from 200 mg daily over 14 days to decrease frequency of rash Rash, hepatitis (occasionally fulminant), nausea, headache See footnote 4 for contraindicated medications... [Pg.1075]


See other pages where Hepatitis fulminant is mentioned: [Pg.1807]    [Pg.745]    [Pg.1807]    [Pg.745]    [Pg.347]    [Pg.544]    [Pg.1457]    [Pg.136]    [Pg.90]    [Pg.136]    [Pg.629]    [Pg.18]    [Pg.33]    [Pg.531]    [Pg.99]    [Pg.12]    [Pg.65]   
See also in sourсe #XX -- [ Pg.739 ]




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Fulminant

Fulminant hepatic failure, metabolic

Fulminant hepatic failure, metabolic encephalopathies

Fulminates

Fulminating

Hepatic failure, fulminant/acute

Viral hepatitis fulminant

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