Summary. Erythrocytosis has occasionally been associated with uterine fibromyoma and attributed to an inappropriate elaboration of erythropoietin (Ep) by the tumour. Whether Ep per se, its precursor substrate, or activator analagous to the renal erythropoietic factor (REF) is produced, has not been defined. In a 54‐yr‐old woman with erythrocytosis and uterine fibromyoma, plasma, urine and tumour extracts were examined to clarify these possible mechanisms. Preoperatively, elevated serum and urinary Ep were present with constant levels over a range of haematocrits induced by serial phlebotomy. Extracts of the tumour did not generate Ep when incubated with normal serum, nor did they contain substrate activity for known REP. Tumour extracts did, however, possess Ep activity which was abolished with anti‐Ep. The patient has remained haematologically normal more than 1 yr following surgery. The data show that the erythrocytosis associated with uterine fibromyoma is mediated through the direct production of Ep by the tumour and not by a substrate‐REF‐like mechanism as found in the normal kidney.
A method was developed for the quantitative separation of platelets from CF1 mouse whole blood. This made it possible to determine the platelet incorporation of 35S-sulfate without the necessity of doing platelet counts. Daily hypertransfusions of the mice to three to four times normal platelet levels for 4-5 days significantly reduced platelet uptake of radiosulfate to an average of about 40% of the nontransfused controls. Mice rendered thrombocytopenic 48 hr earlier by antiplatelet serum, had 2-day 35S uptakes over 2 1/2 times the controls and 6 times the hypertransfused animals. The administration of a total of 2 ml of serum, given twice daily for 3 days from a thrombocytopenic patient with Hodgkin's disease caused a highly significant 103% rise in radiosulfate incorporation when compared with saline in the hypertransfused mouse. Normal human serum from a healthy donor caused a small and insignificant rise. The serum from a patient with Hodgkin's disease caused a highly significant 63% rise in 35S incorporation when compared to the normal serum.
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