Obtaining a full history is usually the first port of call regarding clinical evaluation for individuals with Dubin-Johnson syndrome or other suspected causes of conjugated hyperbilirubinemia .
Wild mushrooms, environmental chemicals (e.g solvents) and drugs (potential toxins) have to be excluded carefully. Failing to appropriately diagnose toxic hepatitis often leads to hepatic failure and death.
It is equally important to elicit some of the possible risk factors for viral hepatitis. Some of these possible risk factors are: Exposure to an infected individual, multiple sexual partners, intravenous drug use and transfusion .
Accurate laboratory testing for DJS and other cases of conjugated hyperbilirubinemia is dependent on the physical examination findings and clinical history of the patient . However, all patients of this condition should be tested for:
Dubin-Johnson syndrome is a benign disorder which usually does not require any specific treatment.
The outlook is very positive for Dubin-Johnson syndrome and other conditions that lead to conjugated hyperbilirubinemia and generally the condition does not shorten the lifespan of the individual.
The condition develops as a result of reduced secretion of conjugated bilirubin into the bile and is often present in patients with hepatitis.
It can equally be seen with patients with biliary obstruction, where there is an impaired flow of bile into the intestine . The formation of bile is very sensitive and thus can be affected by various conditions like high levels of inflammatory cytokines, etc.
In the United States, conjugated hyperbilirubinemia is commonly seen among patients with other biliary or notable liver diseases. It is equally common seen in patients with sepsis, cardiogenic shock and other systemic illnesses. Dubin-Johnson syndrome however, is very rare .
Internationally, ascariasis, clonorchiasis, and other parasistic diseases commonly lead to biliary obstruction especially in lesser-developed countries. Malaria and other haemolytic differences can equally make patients susceptible to biliary obstruction due to the formation of gallstone pigments. Dubin- Johnson syndrome equally occurs rarely.
Regarding racial differences, conjugated hyperbilirubinemia will only reflect the differences noted for the underlying disease condition. No difference is recorded for Dubin Johnson syndrome. The situation is the same for sex related differences in occurrence. 
The age at which conjugated hyperbilirubinemia is reflected is also dependent on the disease state. Biliary artesia leads to conjuhated bilirubinemia within the first month of life, the occurrence is more frequent within midlife for patients with primary biliary cirrhosis or viral hepatitis to senescence as is the case with malignancies and biliary stones.
Dubin-Johnson syndrome or high levels of conjugated bilirubin often secondarily increase the level of unconjugated bilirubin.
The mechanism behind this is not clearly defined but one possible cause is the reduced hepatic clearance of unconjugated bilirubin. This is due to competition with conjugated bilirubin for excretion or uptake .
There are no guidelines for prevention of Dubin-Johnson syndrome.
Dubin-Johnson syndrome is a disorder that brings about an increase in levels of conjugated bilirubin found in the serum . When the increase occurs, there is no elevation of ALT, AST and other liver enzymes.
The syndrome is an autosomal recessive disorder. Dubin-Johnson syndrome has similarities with the Rotor syndrome as it is a defect in the ability of hepatocytes to disseminate bilirubin into the bile.
The condition is generally asymptomatic but it can be diagnosed early in infants with the aid of laboratory tests.
Before being eliminated from the body, bilirubin must be converted into a soluble conjugate since it is not soluble in water. Uridine diphosphate (UDP)-glucuronyl transferase is the compound which converts bilirubin to a mixture of monoglucuronides and diglucuronides (conjugate bilirubin) in the liver. An ATP-dependent transporter disseminates the conjugate bilirubin into the bile. Under normal conditions, this process is very efficient leading to low concentration levels of plasma unconjugated bilirubin .
Apart from the Dubin-Johnson syndrome, there are many conditions that lead to the accumulation of bilirubin in the plasma. Conditions like hemolysis which bring about an increase in the bilirubin formation or conditions like Gilbert syndrome which reduce the rate of bilirubin conjugation bring about unconjugated hyperbilirunemia.
If the disease reduces the flow of bile into the intestine or the secretion of conjugated bilirubin into the bile conjugated hyperbilirunemia sets in. This is because of the reflux of conjugates into the plasma. Hepatobiliary diseases lead to elevated conjugated bilirubin levels.
The patients need to be reassured that no treatment is required if only Dubin-Johnson syndrome is diagnosed. Again, there is typically no reduction in life expectancy .