Jaundice alcoholic hepatitis

Inflammatory conditions of the liver, in particular inflammatory hepatocellular cholestasis, are one of the most frequent causes of jaundice in the clinic. The major underlying denominator of this disorder is the inhibition of transporter expression and function by proinflammatory cytokines, which are either induced systemically or within the liver. Alcoholic hepatitis accounts for up to two-thirds of patients and is the most frequent trigger, followed by idiosyncratic drug reactions, sepsis or other extrahepatic bacterial infections, some variants of viral hepatitis, and total parenteral nutrition [95, 96]. 

Older adults are particularly susceptible to a potentially fatal hepatitis when taking isoniazd, especially if they consume alcohol on a regular basis. Two other antitubercular drugs rifampin and pyrazinamide, can cause liver dysfunction in the older adult. Careful observation and monitoring for signs of liver impairment are necessary (eg, increased serum aspartate transaminase, increased serum alanine transferase, increased serum bilirubin, and jaundice). 

Acetaminophen causes few adverse reactions when used as directed on the label or recommended by the primary health care provider. Adverse reactions associated with the use of acetaminophen usually occur with chronic use or when the recommended dosage is exceeded. Adverse reactions to acetaminophen include skin eruptions, urticaria (hives), hemolytic anemia, pancytopenia (a reduction in all cellular components of the blood), hypoglycemia, jaundice (yellow discoloration of the skin), hepatotoxicily (damage to the liver), and hepatic failure (seen in chronic alcoholics taking the drug). 

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. 

A 52-year-old man with a history of heavy alcohol use took rosiglitazone for at least 30 days before developing jaundice (116). Liver histology showed cholestatic hepatitis with enlarged xanthomatous Kupffer cells and no evidence of cirrhosis. 

Adverse effects Adverse effects are a minor problem with rifampin, but can include nausea and vomiting, rash, and fever. The drug should be used judiciously in patients with hepatic failure because of the jaundice that occurs in patients with chronic liver disease, alcoholics, or in the elderly. 

Cirrhosis is often asymptomatic until complications of liver disease are present. Mrs MW may present with itching, jaundice, dark urine, pale fatty stools, abdominal pain, nausea, fatigue, bleeding - such as nose bleeds, hepatic encephalopathy, hepatomegaly, ascites, distended abdominal veins, spider angiomata, palmar erythema and asterixis. She may also present with the signs and symptoms of alcohol withdrawal, which include irritability, anxiety, tachycardia, tremor, sweating, confusion and hallucinations. 

Bilirubin. Jaundice is the clinical manifestation of hyperbilirubinaemia. A raised level of uncongugated bilirubin occurs when there is excessive breakdown of red blood cells, for example in haemolytic anaemia, or where the ability of the liver to conjugate bilirubin is compromised, for example in cirrhosis. A raised blood level of congugated bilirubin occurs in various liver and bile duct conditions. It is particularly high if the flow of bile is blocked, for example by a gallstone in the common bile duct or by a tumour in the pancreas. It can also be raised with hepatitis, liver injury or long-term alcohol abuse. 

Decompensated hepatic disease (e.g., active alcoholism, ascites, coagulopathy, hypoalbuminemia, or jaundice) should not be treated with PEG-interferon a-2b... 

In liver cirrhosis, hepatorenal syndrome is nearly always (> 80%) accompanied by ascites. HRS is most common in alcoholic cirrhosis. In some 75% of cases, hepatic encephalopathy is witnessed at the same time, and jaundice is evident in about 40% of cases. HRS occurred in 18% of all cirrhotic patients with ascites within one year and in 32% within 5 years. (21)... 

The prognosis of alcoholic liver disease is better than that for other forms of liver disease, with only 10% to 15% developing cirrhosis and a much smaller fraction developing Both hepatitis B and hepatitis C appear to accelerate the course of alcoholic liver disease. The 5-y survival rate in patients with cirrhosis, jaundice, and ascites is 40% if the patient continues drinking and 60% if the patient abstains. " ... 

Liver biopsies performed in patients with chronic HBV infection are classified as chronic persistent hepatitis, chronic active hepatitis, and cirrhosis. Histologic results do not correlate with symptoms and often patients are asymptomatic until the development of cirrhosis. " Cirrhosis is manifested by interlacing strands of fibrous tissue with nodules of regenerating cells resulting in a characteristic small and knobby-appearing liver. This form of injury is irreversible and can be exacerbated by heavy alcohol consumption and concomitant infection with HCV or HIV. Hepatic decompensation as a result of cirrhosis includes ascites, jaundice, variceal bleeding, and hepatic encephalopathy. The 5-year risk of decompensation after the development of cirrhosis is estimated to be 20%. ... 

Patients with acute hepatitis C are often asymptomatic, but they may have malaise, anorexia, and jaundice, which occur in up to 25% of cases.The mean incubation period of HCV is 50 days and viremia can be detected within 3 weeks of initial exposure. Hepatic transaminase values, specifically serum ALT, can be elevated within 4 to 12 weeks of exposure. Acute hepatitis C can be associated with severe symptoms, but fulminant disease is rare. Coinfection with HIV and a history of chronic alcohol consumption are associated with more severe disease during acute HCV infection. " An important feature of hepatitis C infection is that up to 70% of cases develop chronic hepatitis. " Of note, patients with asymptomatic acute HCV infection may be more likely to develop chronic HCV. ... 

Diphenoxylate is an opiate (schedule V) with antidiarrheal properties. It is usually dispensed with atropine and sold as Lomotil. The atropine is added to discourage the abuse of diphenoxylate by narcotic addicts who are tolerant to massive doses of narcotic but not to the CNS stimulant effects of atropine. Diphenoxylate shonld be used cautiously in patients with obstructive jaundice because of its potential for hepatic coma, and in patients with diarrhea cansed by pseudomembranous colitis because of its potential for toxic megacolon. In addition, it should be used cautiously in the treatment of diarrhea caused by poisoning or by infection by Shigella, Salmonella, and some strains of E. coli because expulsion of intestinal contents may be a protective mechanism. Diphenoxylate should be used with extreme caution in patients with impaired hepatic function, cirrhosis, advanced hepatorenal disease, or abnormal liver function test results, because the drug may precipitate hepatic coma. Because diphenoxylate is structurally related to meperidine, it may cause hypertension when combined with monoamine oxidase inhibitors. As a narcotic, it will augment the CNS depressant effects of alcohol, hypnotic-sedatives, and numerous other drugs, such as neuroleptics or antidepressants that cause sedation. 

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