A 56-yr-old woman with long-standing rheumatoid arthritis exhibited jaundice, pruritus and abdominal discomfort after 8 yr of periodic gold sodium thiomalate injections amounting to a cumulative dose in excess of 2.5 gm. Histopathological examination of the liver biopsy specimen showed submassive loss of parenchyma, collapse of reticulin and mixed cellular inflammatory infiltrates. Macrophages contained dark granules, which displayed the characteristics of aurosomes when examined by transmission electron microscopy and electron microprobe analysis. It is likely that hepatocellular injury occurred when the lysosomal storage capacity for gold was exceeded. (&PATOLOGY 1991;14:422-425.)
The liver is only rarely affected by gold-salt toxicity. This is manifested in several forms of injury, which in some instances have caused death (1-4). The most common form of gold-induced liver injury is reversible cholestasis, which occurs early after initiation of therapy (1,2,5-8). This form of hepatic injury is not dose related and is often associated with skin rashes and eosinophilia. Its tendency to recur with rechallenge by the same drug suggests that the reaction is the consequence of hypersensitivity. Another type of gold-induced hepatic toxicity is dose related and occurs late in the course of therapy, without biochemical o r structural evidence of cholestasis. Generally, gradual improvement of liver chemistries follows discontinuation of therapy, although rarely this form of toxicity is associated with fatal, submassive hepatic necrosis (3, 4). In this report we describe a case of hepatotoxicity (from which the patient recovered) after prolonged gold-salt therapy for rheumatoid arthritis.
CASE REPORT
A 56-yr-old housewife had rheumatoid arthritis involving multiple joints and causing severe deformities of the hands,