Role of calcitonin in osteosclerosis of myeloma

To the Editor. —In the August 1979Archives(139:892-896), Driedger and Pruzanski analyzed 68 cases of plasma cell neoplasia with osteosclerotic lesions. They perfectly stressed the main clinical features—younger age at diagnosis, higher incidence of peripheral polyneuropathy, hepatosplenomegaly, and lymphadenopathy as compared with large series of myeloma in general—and the essential laboratory data in these rare forms of plasma cell neoplasia, but they did not give any positive explanation for osteosclerosis. They proposed two theoretical hypotheses, either failure of osteosclerotic activating factor production by the plasmocytes or ability of the host tissues to respond to the proliferation of myeloma cells by prompt osteoblastic activity. Recently, we reported one case of osteosclerotic myeloma with polyneuropathy and lympadenopathy, in which unexplained and marked hypercalcitoninemia (between 3,000 and 6,000 pg/mL during follow-up) was discovered. 1 In our laboratory, mean values of basal calcitonin (CT) are 180 ± 150 pg mL. 2 Although, to