Amyloidosis in rheumatoid arthritis treated with hormones.

Experimental evidence suggests that treatment with cortisone orACTH increases the rate of accumulation of tissue amyloid. Thus Teilum (1952) has shown that mice previously treated with casein in doses insufficient to cause amyloidosis accumulate amyloid quickly in the spleen after a small number of injections of cortisone. Latvalahti (1953) has confirmed this observation and has shown that mice given either cortisone or ACTH develop amyloidosis much more frequently when given caseinate than mice given caseinate alone. Similar studies have been made by Perasalo (1954). Widespread amyloidosis of secondary distribution is now recognized with considerable frequency in rheumatoid arthritis (Missen and Taylor, 1956; Cruickshank, 1957). For some time it has seemed possible that the incidence of amyloidosis in this disease may be rising as the result of the widespread therapeutic use of cortisone and other steroids and of ACTH. The alternative possibility, that an apparent increase in the incidence of amyloidosis may have resulted from contemporary interest in the pathological characteristics of rheumatoid arthritis, has received less attention. More than 10 years have elapsed since the introduction of cortisone therapy. It appears reasonable to examine the available records of cases of rheumatoid arthritis which have come to necropsy in this centre in an attempt to answer the question posed by the provocative experimental evidence.