Jaundice alcoholic liver cirrhosis

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. 

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. " ... 

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. 

Zieve, L. Jaundice, hyperlipidemia and hemolytic anemia a heretofore unrecognized syndrome associated with alcoholic fatty liver and cirrhosis. Ann. Intern. Med. 1958 48 471—496... 

A 49-year-old man with alcoholic cirrhosis developed jaundice, fatigue, and choluria after he started to take celecoxib 200 mg/day for musculoskeletal pain (9). There were increases in transaminases, alkaline phosphatase, and bilirubin (to 547 pmol/l). Liver biopsy showed cirrhosis and marked hepatocellular cholestasis. On withdrawal of celecoxib the bilirubin began to fall very slowly 1 year later he was well, with a total bilirubin concentration of 44 pmol/l. 

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%. ... 

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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