Hepatitis - Acute

The nurse immediately reportsany signs of acetaminophen toxicity, such as nausea, vomiting, anorexia, malaise, diaphoresis abdominal pain, confusion, liver tenderness hypotension, arrhythmias jaundice, and acute hepatic and renal failure. Early diagnoss is important because liver failure may be reversible. Toxicity is treated with gastric lavage, preferably within 4 hours of ingestion of the acetaminophen. Liver function studiesare perform ed frequently. Acetylcysteine (Mucomyst) is an antidote to acetaminophen toxicity and acts by protect-... 

Naltrexone is contraindicated in those with a hypersensitivity to the narcotic antagonists. Naltrexone is contraindicated during pregnancy (Category C). Naltrexone is used cautiously in those with a narcotic addiction in patients with cardiovascular disease, acute hepatitis, liver failure, or depression and in patients who are suicidal. Naltrexone is used cautiously during lactation. 

Laxatives are contraindicated in patients with known hypersensitivity and those with persistent abdominal pain, nausea, or vomiting of unknown cause or signs of acute appendicitis, fecal impaction, intestinal obstruction, or acute hepatitis. These dragp are used only as directed because excessive or prolonged use may cause dependence. Magnesium hydroxide is used cautiously in patients with any degree of renal impairment. Laxatives... 

McCarthy MC, He J, Hyams KC et al (1994) Acute hepatitis E infection during the 1988 floods in Khartoum, Sudan. Trans R Soc Trop Med Hyg 88 177 Shears P (1988) The Khartoum floods and diarrhoeal diseases. Lancet 2 517 Campanella N (1999) Infectious diseases and natural disasters the effects of Hurricane Mitch over Villanueva municipal area, Nicaragua. Public Health Rev 27 311-319... 

At the doses used, there is blockage of the effects of as much as 25 mg of injected heroin. Toxicity in heroin addicts is low, but some reported subtle adverse effects of naltrexone such as decreased energy (Hollister et al. 1981). Nonaddicted obese subjects have been known to develop markedly elevated transaminase levels at doses of 300 mg/day (Mitchell et al. 1987). The inference has been drawn that high doses are potentially hepatotoxic (Pfohl et al. 1986), and the drug is contraindicated in liver failure or acute hepatitis. 

HCV infection is rarefy diagnosed in the acute phase, as most acutely infected individuals are asymptomatic. Between 50% and 90% of patients develop chronic infection, however, and this warrants early therapy. After occupational exposure with a known date, treatment should not be started before the acute episode characterized by alanine aminotransferase elevation, but it should always be started within 24 weeks after the onset of symptoms. The optimal treatment schedule for acute hepatitis C is controversial. Pegylated IFN-a monotherapy at the standard dose for 24 weeks yielded SVR rates close to 100% in symptomatic patients referred to tertiary care centers (De Rosa et al. 2006 Jaeckel et al. 2001 Santantonio et al. 2005 Wiegand et al. 2006). Shorter therapy may be envisaged (Calleri et al. 2007). Combination with ribavirin is recommended if a first course of pegylated IFN-a monotherapy fails to eradicate the infection. Viral elimination appears to be independent of the HCV genotype and the HCV RNA level (Calleri et al. 2007 De Rosa et al. 2006 Jaeckel et al. 2001). 

De Rosa EG, Bargiacchi O, Audagnotto S, Garazzino S, Cariti G, Veronese L, Raiteri R, CaUeri G, Di Perri G (2006) The early HCV RNA dynamics in patients with acute hepatitis C treated with pegylated interferon-alpha2b. Antivir Ther 11 165-171 Di Bisceglie A (1997) Hepatitis D virus. Marcel Dekker, NY... 

Santantonio T, Fasano M, Sinisi E, Guastadisegni A, Casalino C, Mazzola M, FrancavUla R, Pastore G (2005) Efficacy of a 24-week course of PEG-interferon alpha-2b monotherapy in patients with acute hepatitis C after failure of spontaneous clearance. J Hepatol 42 329-333... 

The citric acid cycle is the final common pathway for the aerobic oxidation of carbohydrate, lipid, and protein because glucose, fatty acids, and most amino acids are metabolized to acetyl-CoA or intermediates of the cycle. It also has a central role in gluconeogenesis, lipogenesis, and interconversion of amino acids. Many of these processes occur in most tissues, but the hver is the only tissue in which all occur to a significant extent. The repercussions are therefore profound when, for example, large numbers of hepatic cells are damaged as in acute hepatitis or replaced by connective tissue (as in cirrhosis). Very few, if any, genetic abnormalities of citric acid cycle enzymes have been reported such ab-normahties would be incompatible with life or normal development. 

Priest RJ, Horn RC. 1965. Trichloroethylene intoxication A case of acute hepatic necrosis possibly due to this agent. Arch Environ Health 11 361-365. 

Woolf GM et al. (1994) Acute hepatitis associated with the Chinese herbal product jin bu huan. Ann Int Med 121(10) 729-735... 

Add protein back in 20 g increments every 3-5 d once acute hepatic encephalopathy improves and until protein caloric goal is achieved (usually 0.8-1 g/kg/d)... 

In acute hepatic encephalopathy, temporary protein restriction to decrease the rate of ammonia production can... 

Household contacts with acute hepatitis B with open cuts Health care providers in contact with contaminated needles Patients undergoing dialysis Hepatitis C... 

Only 10% to 15% of patients have acute hepatitis C that resolves without any further sequelae.10 In more than 85% of cases, hepatitis C develops into a chronic disease. Approximately 70% of chronic HCV cases progress to mild, moderate, or severe hepatitis. While the natural history of the progression to cirrhosis is not clear, it is estimated that 10% to 20% of cases may take up to 20 to 40 years from the time of exposure to advance from fibrosis to cirrhosis.10 Fifteen to twenty percent of patients infected with HCV develop complications associated with cirrhosis. Once cirrhosis is confirmed, the rate of developing hepatocellular carcinoma increases to 1% to 4% per year.10 The estimated death rate from HCV infection is 1.8 deaths per 100,000 persons per year.12,15... 

Hepatitis E is associated with more than 50% of the acute hepatitis cases in endemic areas (Afghanistan, Bangladesh, Burma, China, India, Indonesia, Kazakhstan, Kyrgyzstan, Malaysia, Mongolia, Nepal, Pakistan, Tajikistan, Turkmenistan, Uzbekistan, Mexico, the Middle East, Northern Africa, and sub-Saharan Africa). The virus is primarily transmitted by the fecal-oral route. Transmission of HEV is more prominent in underdeveloped countries where sanitation is poor. 

At present, only acute cases of hepatitis E have been documented. There are no vaccines available to prevent hepatitis E however, a recombinant hepatitis E vaccine is undergoing Phase II/III study to determine its efficacy in preventing hepatitis E infections.49 Supportive care is the only treatment available for acute hepatitis E infection.19... 

Acute hepatic necrosis (e.g., chronic or acute hepatitis B or C)... 

Levi M, Guchelaar HJ, Woerdenbag HJ, Zhu YP. Acute hepatitis in a patient using a Chinese herbal tea—a case report. Pharm World Sci 1998 20 43-44. 

Mas A, Rodes J, Sunyer L, Rodrigo L, Planas R, Vargas V, Castells L, Rodriguez-Martinez D, Fernandez-Rodriguez C, Coll I, Pardo A Comparison of rifaximin and lactitol in the treatment of acute hepatic encephalopathy Results of a randomized, double-blind, doubledummy, controlled clinical trial. J Hepatol 2003 38 51-58. 

The disease exhibits three phases incubation (averaging 28 days, with a range of 15 to 50 days), acute hepatitis (generally lasting 2 months), and convalescence. Most patients have full clinical and biochemical recovery within 12 weeks. Nearly all individuals will have clinical resolution within 6 months of the infection. HAV does not lead to chronic infections. 

Nausea Vomiting Insomnia Headache Acute hepatic failure ... 

Valproic add Cl upset Acute hepatic failure Polycystic ovary-like syndrome... 

However, the high values of SDH activity in acute hepatitis make possible the differentiation of this disease from others (W21). The high level is found to be reduced within 2 weeks, thus representing convalescence. 

Decreased BUN level is usually indicative of acute hepatic dysfunction and excessive dehydration,... 

Alcoholic cirrhosis or cirrhosis caused by acute hepatitis can lead to decreased Lp(a) concentrations (F6, M14). 

Brown BR Jr., Sipes IG, Sagalyn AM. 1974b. Mechanisms of acute hepatic toxicity Chloroform, halothane, and glutathione. Anesthesiology 41 554-561. 

Symptoms for the first four deficiencies include anorexia, vomiting and lethargy, from which patients may progress to irreversible coma (acute hepatic coma) and death. If infants survive, but remain undiagnosed and untreated for some time, they become mentally handicapped. In arginase... 

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