Anatomy of Liver
Functions of the Liver
Liver Function Tests
Liver Diseases
Prevention of Liver Diseases
Liver & Special Population
Diet and Nutrition
Vaccinations for Hepatitis A & B
Useful Links
What is Organ Donation
Who Can Donate?
How to Donate?
Is Organ Donation Legal?
What is Brain Stem Death
Donor Centers
Donor Form
Volunteer Form

There are over 100 types of liver diseases, and because of more than 200 functions that the Liver plays, many can be life-threatening unless treated.
The Liver diseases have been listed down in alphabetical order. Click on the alphabet to read more about the diseases.
Drug induced liver damage Dubin-Johnson Syndrome

Drug induced liver damage

Disease condition

Many chemicals that are inhaled or swallowed can damage the liver. Among these are drugs, industrial solvents and pollutants. Almost every known drug has at one time or another been implicated as a cause of liver damage.

Chemicals which damage the liver fall onto two groups:

Predictable liver toxins - These damage the liver regularly following exposure to a certain amount of the substance.

Unpredictable liver toxins - These cause damage in only a small percentage of people exposed to them.

Type and example Pathogenesis
Acute hepatocellular injury  
Toxic necrosis (e.g., CCl4,acetaminophen) Membrane damage, some via toxic metabolite; dose-related, predictable
Hepatitis-like (e.g.,isoniazid, methyldopa)
Idiosyncrasy; ? immune, ? metabolic; unpredictable, not dose-related
Inflammatory (e.g.,chlorpromazine)
Unknown; unpredictable; periportal inflammation and cholestasis
Pure (e.g., oral contraceptives)
Exaggeration of normal hormonal effect on bile transport; ?genetic idiosyncrasy; pure cholestasis, no inflammation
Miscellaneous acute/subacute
Variable, usually unknown
Chronic liver disease  
Chronic hepatitis (e.g., isoniazid, methyldopa) Idiosyncrasy; ? immune, ? metabolic
Chronic cholestasis (e.g., chlorpromazine) Unknown; rare
Fibrosis/cirrhosis (e.g., methotrexate) Dose-related, insidious toxic metabolic damage
Tumor: adenomas (oral contraceptives) Unknown; rare

Disease Etiology:

Why is the Liver susceptible to injury by chemicals and drugs?

The reason seems to be linked to the liver's unique function of processing the chemicals and drugs which enter the blood stream. Many of these chemicals are difficult for the kidneys to excrete out of the body. The liver helps by removing these chemicals from the blood stream and changing them into products that can be readily removed through the bile or urine. In this process, unstable toxic products are sometimes produced. These can attack and injure the liver.

Analgesics (pain killers) and antipyretics (fever reducers) that contain acetaminophen are a common cause of liver inflammation. If over-the-counter medications are used, never increase the dose beyond what is recommended on the bottle / packaging.

These medications can damage the liver when taken in doses that are not much greater than the recommended therapeutic dose. If patient drinks heavily or regularly, he/she should completely avoid these medications or discuss safe doses with the treating physician.

Other problem drugs for the liver include the general anesthetic halothane, methyldopa, isoniazid (used for the treatment of tuberculosis), methotrexate, amiodarone, and HMG CoA reductase inhibitors, which are also called statins.

Some medications can interfere with the flow of bile, which can also lead to liver inflammation. These include erythromycin, oral contraceptives, chlorpromazine, and anabolic steroids. Usually, drug-related hepatitis subsides within days or weeks after the offending drug is stopped.

NSAID medications such as ibuprofen and naproxen may also cause drug-induced hepatitis.


The symptoms are similar to those of viral hepatitis, and include a yellowish skin tone (jaundice), nausea, vomiting, and white or clay-colored stools. Some patients may have no symptoms.


Diagnosis requires first and foremost a careful history of drug ingestion, including over-the-counter and illicit agents as well as prescribed medications.

Elevated liver enzymes

Enlarged liver

Abdominal tenderness - right upper quadrant

Treatment – Medical, Surgical

Acute damage usually resolves when the offending agent is withdrawn, but cases of severe acute necrosis can be fatal or result in postnecrotic scarring..

Life expectancy and Quality of Life

In cases of chronic injury, further hepatocellular damage and inflammation will generally cease when the drug is stopped, but any concomitant fibrosis will be irreversible.

Dubin-Johnson Syndrome

Disease condition

Dubin-Johnson syndrome (DJS) is a type of hereditary hyperbilirubinemia that was first described independently in 1954 by Dubin and Johnson and by Sprinz and Nelson.

Hereditary hyperbilirubinemias can be divided into conjugated and unconjugated forms. While Gilbert and Crigler-Najjar syndromes are examples of the unconjugated hyperbilirubinemias, Dubin-Johnson and Rotor syndromes represent the 2 types of familial conjugated hyperbilirubinemias.

Both types of conjugated hyperbilirubinemias have a relatively benign course, but it is important to establish the diagnosis to spare patients from undergoing multiple unnecessary procedures and to exclude other more serious causes of hyperbilirubinemia.

There is no haemolysis but conjugated bilirubin is raised due to a defect on the chromosome (10q24 affecting the CMOAT protein). There is impaired secretion of conjugated bilirubin and other non-bile salt organic anions from hepatocytes into the bile. It runs a generally benign course.

Patients with DJS tend to develop nonpruritic jaundice during their teen years.

Disease Etiology

DJS occurs in 1 case per 1300 persons of Iranian Jewish descent, primarily because of inbreeding. It is reported in Japanese. It is inherited as an autosomal recessive and consanguinity is a risk factor (if the parents are related or they may be cousins).

Subclinical cases can become evident during pregnancy or following the initiation of oral contraceptives.

A thorough family history can reveal a history of jaundice in an autosomal recessive pattern.


Although the metabolic defect is present from birth it rarely presents in infancy and usually becomes apparent in either late teens or early 20s. It has been reported from 10 weeks to 56 years.

There is recurring jaundice but no pruritus.

Despite an equal sex incidence, there is reduced penetrance in females although it may be precipitated by pregnancy or oral contraceptives due to further inhibition of bilirubin excretion.

Clinically there is often nothing to find except for jaundice although there may be hepatosplenomegaly with palpable organs and a little tenderness.


Tests that may be abnormal include:

Serum bilirubin

Urinary coproporphyrin levels (mostly coproporphyrin I in Dubin-Johnson patients versus coproporphyrin III in normal subjects)

Liver biopsy

Oral cholecystography fails to visualize the gallbladder in patients with DJS.

The patients also tend to have unique findings on hepatobiliary scans.

Treatment - Medical, Surgical

DJS is a benign disorder and does not require any specific therapy. In the past, patients were treated with phenobarbital, which was primarily used to reduce serum bilirubin levels. This is no longer recommended. Drug therapy is currently not a component of the standard of care for this syndrome.

Life expectancy and Quality of Life

Reassurance is required that no treatment is necessary, nor further investigation, once diagnosis is made. There is no reduction in life expectancy.

Once diagnosed, the patients would be informed of the disease process and its benign nature, and they should understand that no further investigative workup is required in the future.