Jaundice acute liver failure

Hepatotoxicity Severe hepatic reactions, including acute liver failure, jaundice, hepatitis, and cholestasis, have been reported rarely in postmarketing data in patients receiving infliximab. Autoimmune hepatitis has been diagnosed in some of... 

Hepatitis A is common, particularly in areas of poor sanitation, and is transmitted by food or drink contaminated by a sulferer/carrier. Clinical symptoms include jaundice, and are usually mild. A full recovery is normally recorded. Hepatitis B is transmitted via infected blood. Symptoms of acute hepatitis B include fever, chill, weakness and jaundice. Most sufferers recover from such infection, although acute liver failure and death sometimes occur 5-10% of sufferers go on to develop chronic hepatitis B. Acute hepatitis C is usually mild and asymptomatic. However, up to 90% of infected persons go on to develop a chronic form of the condition. Hepatitis D is unusual in that it requires the presence of hepatitis B in order to replicate. It thus occurs in some persons concomitantly infected with hepatitis B virus. Its clinical symptoms are usually severe, and can occur in acute or chronic form. 

A 52-year-old man with a 10-day history of fatigue and jaundice had been taking nefazodone (300 mg/day) for depression for about 6 weeks. Biochemical investigations showed acute liver failure. Infective hepatitis and immune disorders were excluded. He failed to respond to medical treatment, and hepatic transplantation was performed. Histological examination of the liver showed parenchymal necrosis, particularly in centrilobular areas, together with lymphocytic infiltration (10). 

Organisms other than the viruses discussed earlier can cause acute liver infections, such as Leptospira icterohaemorrhagia, which causes Weil s disease, fungal infections caused by Candida species or aspergillosis, and schistosomiasis caused by trematodes. A number of systemic infections may also affect the liver, leading to jaundice, abnormal liver function tests or even acute liver failure. Table 3.6 lists some of the infective organisms that have been associated with liver disease. 

Acute liver failure (ALF) is defined as an acute clinical picture with jaundice due to a most severe disorder in the liver function and/or massive liver cell necrosis which, without any pre-existing liver disease, culminates in hepatic coma (= endogenous coma) within 8 weeks. Potentially, the condition is fully reversible (C. Trey et al., 1970). In addition, coagulopathy must also be present (D.F. Schafer et al., 1989). 

Clinically, there are three different courses of disease following the onset of jaundice .) fulminant or hyperacute liver failure (= occurrence of hepatic encephalopathy in the 1 week), (2.) acute liver failure (= occurrence of hepatic encephalopathy between the and 4 week), and (5.) subacute liver failure (= occurrence of hepatic encephalopathy between the 5 and 8 week). Surprisingly, however, it could be shown that 30-40% of the hyperacute forms survived in spite of the development of hepatic coma and cerebral oedema. As opposed to this, the subacute forms displayed a survival rate of only 10-20%, despite a lower frequency of cerebral oedema and better liver function, (s. tab. 20.1)... 

Complications The following complications have been reported (i.) cholangitis, (2.) obstructive jaundice, (i.) intrahepatic cholelithiasis, (4.) sepsis, (J.) portal hypertension (oesophageal varices, portal vein thrombosis, chronic Budd-Chiari syndrome, etc.), (6.) thrombosis of the inferior vena cava, (7.) amyloidosis, (8.) immune complex-associated glomerulonephritis, (9.) metastases, (10.) acute on chronic liver insufficiency or acute liver failure, and (11.) bronchobiliary fistula. 

A severe cholestatic syndrome (H. Ballard et al., 1961) can be observed in patients suffering from alcoholic fatty liver, (s. fig. 28.16) The clinical picture may correspond to that of obstructive jaundice and cause great problems in differential diagnosis, particularly because such patients may not have been known before to be suffering from alcohol-induced liver disease. Extremely severe forms to the point of acute liver failure have been observed. 

Acute reversible cytolytic or cholestatic jaundice can also occur after low-dose cyclophosphamide in adults and children (SED-13,1122) (SEDA-19,347) (SEDA-20, 342) (SEDA-21, 386). Acute liver failure required liver transplantation in one patient (21). Although glucocorticoids... 

A 48-year-old woman with normal liver function took venlafaxine 75 mg/day and trazodone 200 mg/day for depression and 4 months later developed increasing jaundice and encephalopathy. She had markedly raised transaminases and bilimbin. There were no other explanations for her hepatic failure, and she received an urgent liver transplantation. The pathology showed severe acute hepatitis compatible with toxic acute liver failure. She recovered fully, and had normal liver function tests 1 year later. 

There has been a review of eight patients who developed liver injury after taking Hydroxycut all were hospitalized, and three required liver transplantation [59 ]. Nine other cases with adequate clinical information were obtained from the FDA MedWatch database, including one fatal case of acute liver failure. The usual symptoms were jaundice, fatigue, nausea, vomiting, and abdominal pain. Most patients had hepatocellular liver damage. 

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-... 

Hepatic 7 (acute hepatic failure with jaundice, enlarged liver, and greatly increased serum bilirubin) ... 

A 43-year-old woman was admitted to hospital in December feeling unwell with a two-week history of urinary symptoms. She had decompensated cirrhosis of her liver on ultrasound and was taking pentoxifylline (oxpentifylline, Trental), co-amoxiclav, omeprazole and thiamine. She was jaundiced and confused with respiratory failure limiting speech to partial sentences. There was a marked deterioration in liver function overnight and she went into acute renal failure. 

A 7-year-old boy with Duchenne muscular dystrophy and attention deficit hyperactivity disorder (ADHD) developed acute hepatic failure, with features of autoimmune hepatitis (2). The only medications he had taken were pemoline (56 mg/day) and cjrproheptadine (2 mg/day). Pemoline was withdrawn after 8 months as the presumed cause of his raised transaminases. Two weeks later he developed an altered mental state, jaundice, and encephalopathy. The histological features of the liver and his autoimmune antibody panel were consistent with autoimmune hepatitis. He was treated with corticosteroids and azathioprine and recovered. 

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. 

Hepatic Effects. Icterus, jaundice, abdominal pain, liver failure, acute toxic hepatitis, and elevated serum liver enzymes were among the effects reported in four individuals who repeatedly ingested chaparral capsules (160-1,500 mg chaparral/day) over a period ranging from 6 weeks to 10 months. 

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