Oxytetracycline‐induced thrombocytopenic purpura

1 amyloidosis. Another case of amyloidosis complicating nonsecretory MM was described by Azaret al. [3]. It is interesting to speculate on the origin of the aniyloid fibrils in the absence of an overt monoclonal protein. Four of the 14 patients with nonsecretory MM reported by Preud’homme et al. [2] had Bence Jones proteins in their serum or urine at some stage of their disease. Three of the five nonexcretory myeloid patients described by Joyner et al. [4] had some monoclonal protein excretion, either at the initial or the terminal stages of their disease. Initial excretion could be the result of a very low cellular excretory rate. enabling detection of the paraprotein only when the tumor mass is maximal. Terminal excretion of monoclonal protein could also be related to alteration in tumor mass. Thus nonsecretory cells may in reality be capable of excreting secreted immunoglobulin, as suggested by the presence of surface monoclonal immunoglobulin in most cases of nonsecretory myeloma patients [2,4.5]. Preud’homme et al. [2] suggested that the inability to detect serum or urinaq immunoglobulin may be due to a chain defect that confers a susceptibility to rapid extracellular enzymatic breakdown of the immunoglobulin. The occurrence of amyloid deposits in some rare cases of nonsecretory MM, including ours, favors such a hypothesis.