LAUSR

Donor plasma, whether collected from a unit of whole blood or via apheresis can be of many hues. Typically it appears yellow-gold, but can appear green, cream, red, and brown for varying reasons. While few of the reasons for discoloration would cause patient harm, the units are frequently discarded for failing visual inspection. The plasma unit pictured demonstrates a yellow-brown discoloration, most commonly due to icterus (high bilirubin content in the blood). Blood collected from this eligible 29year-old donor tested negative for viral disease markers and the donor reported feeling well and healthy on the day of donation. Hyperbilirubinemia in a healthy person may be due to subclinical hemolysis or inherited disorders of bilirubin metabolism. Less common causes include hepatic injury or biliary tract disease, which can be ruled out by liver enzyme testing. This donor met eligibility requirements, making hemolysis unlikely and focusing our differential on inherited causes of hyperbilirubinemia. Inherited hyperbilirubinemias are categorized as either conjugated (Dubin–Johnson or Rotor syndrome), or unconjugated (Crigler–Najjar or Gilbert’s syndrome). The type of bilirubin that has accumulated in this donor’s blood is unknown. However, one can hypothesize the cause of his icterus based off the clinical picture and disease prevalence. Dubin–Johnson and Rotor syndrome are both rare. If apparent, jaundice will occur shortly after birth or in childhood in Rotor syndrome, and may occur in otherwise healthy young adults in Dubin–Johnson syndrome. Crigler–Najjar syndrome is rare (estimated prevalence of 0.6 per million) and occurs in infancy or early childhood (type I), or later in life with jaundice and neurological symptoms (type II). The clinical picture of Gilbert’s syndrome is typically that of a normal young adult and may at times include jaundice. Gilbert’s syndrome is the most prevalent of the inherited hyperbilirubinemias, and is estimated to be found in 10-15% of the Western population. Because of the donor’s age and clinical picture, Gilbert’s syndrome is the primary working diagnosis. Further work-up with laboratory and molecular testing would be required to establish a definitive diagnosis. Gilbert’s Syndrome is an inherited condition characterized by transient, mild jaundice due to reduced bilirubin conjugation in the absence of overt hemolysis and liver disease. Impaired conjugation of bilirubin is due to a mutation in the promoter region of the gene coding for the enzyme, UDPglucuronosyltransferase (UGT1A1), which is responsible for