Cholestatic hepatitis

Cholestatic hepatitis

Description, Causes and Risk Factors:

Def: Jaundice with bile stasis in inflamed intrahepatic bile ducts; usually due to toxic effects of a drug.

Cholestatic hepatitis occurs when the tiny channels that carry bile from liver cells become inflamed and blocked. This means bile cannot flow from the liver to the gallbladder. This condition may occur because of gallstones or another blockage in the system, or it may be a rare complication of hepatitis A.

Cholestatic hepatitis

The mechanism of intrahepatic cholestasis in acute viral hepatitis is not clear. Recent in vitro and animal studies on lymphocyte cultures of patients with alcoholic hepatitis and acute viral hepatitis suggest that cellular or humoral immune phenomena might be involved in the pathogenesis. The other proposed mechanism is from interruption in continuity of bile flow secondary to periportal spotty necrosis. The lympholytic action of corticosteroids may be the reason for their efficacy in cholestasis due to hepatitis A infection.

In the US, approximately 2000 cases of acute liver failure occur annually and drugs account for over 50% of them. Drugs account for 2-5% of cases of patients hospitalized with jaundice and approximately 10% of all cases of acute hepatitis.

Risk Factors:

    Liver disease: In general, patients with chronic liver disease are not uniformly at increased risk of hepatic injury. Although the total cytochrome P-450 is reduced, some may be affected more than others. The modification of doses in persons with liver disease should be based on the knowledge of the specific enzyme involved in the metabolism. Patients with HIV infection who are co-infected with hepatitis B or C virus are at increased risk for hepatotoxic effects when treated with antiretroviral therapy. Similarly, patients with cirrhosis are at increased risk of decompensation by toxic drugs.

  • Genetic factors: A unique gene encodes each P-450 protein. Genetic differences in the P-450 enzymes can result in abnormal reactions to drugs, including idiosyncratic reactions.

  • Other comorbidities: Persons with AIDS, persons who are malnourished, and persons who are fasting may be susceptible to drug reactions because of low glutathione stores.

  • Drug formulation: Long-acting drugs may cause more injury than shorter-acting drugs.

Cholestatic hepatitis goes away on its own in almost all cases. There is no treatment other than rest, a balanced diet, and avoiding alcohol. The illness can last weeks or months, but a return to normal health is expected.


Symptoms may include:


  • Fatigue.

  • Anorexia.

  • Weakness.

  • Abdominal discomfort.

  • Diarrhea.

  • Low-grade fever.



  • Hepatomegaly.

  • Splenomegaly.

  • Xanthoma.


The responsibility of the surgeon in thisdisease is threefold. First, he must beaware of the occasional appearance of thistype of frustrating obstructive jaundice inwhich no gross obstruction exists. Second,at some stage of the disease he must conduct a thorough surgical exploration of thebiliary ductsystem and perform a biopsyof the liver to establish the diagnosis firmly.Third, he must consider the treatment ofthe disease. External biliary drainage hasbeen repeatedly recommended as a therapeutic measure, usually as a palliativeprocedure to relieve itching, but some surgeons have suggested that prolonged biliary drainage may aid in the cure of thedisease.

Chemical determination may include:

    Increased bilirubin.

  • Elevated alkaline phosphatase.

  • Elevated total cholesterol.

  • Elevated total lipids.

  • Hepatocellular function, normal or abnormal.


The primary goal of therapeutic management in this disease is to return the patient to as active and as normal a life as possible during the prolonged course of his illness. Bed rest, except during periods of acute exacerbations of the disease, is generally not indicated. Unrestricted activity has not been detrimental. A diet low in fat, but not fat free, will diminish the steatorrhea and diarrhea. The prime consideration is to maintain a diet with an adequate caloric intake. The fat-soluble vitamins A, D and K should be given parenterally to prevent night blindness and bone pain and to elevate the prothrombin time.

Steroids: Reduction of serum bilirubin and some regression of symptoms have been reported to follow the administration of steroids to patients with acute hepatitis and to certain patients with extrahepatic obstructive jaundice. Reports of the effect of these drugs in patients with Cholestatic hepatitis have been conflicting.

Cholestyramine: More encouraging has been the effect of the basic anion exchange resin, cholestyramine,' which is believed to bind bile salts in the intestine, thereby eliminating bilirubin in the feces and removing it from the enterohepatic circulation.

Side effects of medicine: Positive.

No specific antidote is available for the vast majority of hepatotoxic agents. Emergency liver transplantation has increasing utility in the setting of drug-induced fulminant hepatic injury. Considering early liver transplantation is important.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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