Hypercalcaemia in the accelerated phase of chronic myelogenous leukaemia: no relationship to the phenotype of the blast cells.
2 patients with chronic myelogenous leukaemia developed hypercalcaemia and severe myelofibrosis in the terminal phases of their disease. Hormonal studies excluded the hypercalcaemia being caused by primary hyperparathyroidism or ectopic parathyroid hormone secretion. Its development was unrelated to the phenotype of the blast cells, as assessed by conventional cytochemistry and immunological surface typing. The finding of increased urinary cAMP excretion in 1 of the patients suggests a circulating, nonparathyroid humoral bone resorbing factor with partial biological PTH-activity to be one of the pathogenetic mechanisms responsible for the occurrence of hypercalcaemia in patients with chronic myelogenous leukaemia.
D000328:Adult; D001856:Bone Marrow Examination; D003520:Cyclophosphamide / Q000627:therapeutic use; D003561:Cytarabine / Q000627:therapeutic use; D003630:Daunorubicin / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006918:Hydroxyurea / Q000627:therapeutic use; D006934:Hypercalcemia / Q000188:drug therapy / Q000209:etiology*; D007951:Leukemia, Myeloid / Q000150:complications* / Q000473:pathology; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D010641:Phenotype; D055728:Primary Myelofibrosis / Q000209:etiology
D003561:Cytarabine; D003520:Cyclophosphamide; D006918:Hydroxyurea; D008727:Methotrexate; D003630:Daunorubicin