Hypernephroma and amyloidosis.

T^HE etiology of amyloidosis remains obscure, .*. but it is now generally agreed that immuno¬ logical mechanisms are involved in its pathogenesis and that the primary and secondary forms of the disease, and myelomatosis, derive from the same etiological factors and may be variants of the same condition.15 The secondary form develops most frequently in association with suppurative condi¬ tions,6 probably as a result of hyperimmunization with bacterial products; in such cases, removal of the exciting cause results in regression or dis¬ appearance of the amyloidosis. Also, secondary amyloidosis may be associated with neoplastic dis¬ ease,7 when it seems likely that an immunological relationship between tumour and host may give rise to antibody formation to tumour antigens which affect neoplastic growth, and spread and ultimately lead to the deposition of amyloid ma¬ terial in various tissues.8 Amyloidosis can be produced experimentally by protein feeding, and may be influenced by many other factors, in¬ cluding diet, environment,9 sex and breed.10 It develops in many chronic conditions, notably rheumatoid arthritis and leprosy. The relatively small number of cases of malignant tumour with concomitant amyloidosis may be due chiefly to the shortened survival times of most of these pa¬ tients. However, although documented reports of spontaneous regression or delayed development of carcinoma are now quite numerous, few of them refer to amyloidosis. The case presented here poses many questions in regard to the origin and development of amy¬ loidosis, and the relationship of its immunological mechanisms to those of neoplasia. The outstanding feature was the development of what appeared to be massive metastatic deposits, and later their com¬ plete clearing at a time when, probably, amyloid disease was beginning to develop. Did antitumour antibodies from the primary hypernephroma give rise to amyloidosis and/or affect the secondary neoplastic process? The evidence is uncertain, but