DUBIN-JOHNSON-LIKE SYNDROME IN GOLDEN LION TAMARINS (LEONTOPITHECUS-ROSALIA ROSALIA)

On routine blood screens, persistent conjugated hyperbilirubinemia was discovered in two groups of closely related adult female golden lion tamarins (Leontopithecus rosalia rosalia, n = 8). Bromosulfophthalein (BSP) retention tests were performed on four hyperbilirubinemic and th ree control tamarins. BSP excretion was delayed in hyperbilirubinemic tamarins as compared with controls. Grossly, liver of affected tamarin s was dark brown to black, with a prominent reticulated pattern. Histo logic examination revealed abundant intrahepatic pigment, primarily in a centrilobular and midzonal distribution. Most of the pigment did no t react with Perls' Prussian blue method for iron, Hall's method for b ilirubin, or the Armed Forces Institute of Pathology acid-fast method for lipofuscin but was positive with Fontana and lipofuscin-ferric fer ricyanide reduction techniques. Liver from control golden lion tamarin s had intrahepatocellular Perls' iron-positive pigment diffusely throu ghout the lobule with a small amount of Fontana method-positive pigmen t. Ultrastructurally, hepatocytes from a hyperbilirubinemic tamarin co ntained pleomorphic electron-dense structures within lysosomes. Transp ort studies demonstrated secretion of fluorescein isothiocyanate-label ed glycocholic acid, a fluorescent bile acid analog, into bile canalic uli and no secretion of carboxydichlorofluorescein diacetate, a non-bi le acid organic anion, by liver from a hyperbilirubinemic tamarin. In contrast, control liver secreted carboxydichlorofluorescein diacetate readily into bile canaliculi. The clinicopathologic presentation of th is syndrome in golden lion tamarins is similar to that described for D ubin-Johnson syndrome of human beings.