Severe Hypercalcemia Indicating Relapse of Acute Myelocytic Leukemia after Bone Marrow Transplantation

Dr. Jesús Montoliu, Nephrology Service, Hospital Arnau de Vilanova, Rovira Roure 80, E-25006 Lleida (Spain) Sir, Hematologic malignancies, particularly multiple myeloma, are common causes of hypercalcemia. Other types of hematologic cancer where hypercalcemia can be found include Hodgkin’s and non-Hodgkin’s lym-phoma and adult T-cell leukemia caused by human T-cell lymphotropic virus type I [1-3]. The present report describes a patient with acute myelocytic leukemia that underwent bone marrow transplantation and in whom relapse of leukemia presented clinically as severe hypercalcemia. A 32-year-old man presented in May 1988 with fever, gum hypertrophy and splenomegaly. He had a total white blood cell (WBC) count of 222 × 1071, with 90% blasts, some of them with Auer rods. Hemoglobin was 128 g/l and the platelets were 48 × 1071. A bone marrow examination showed complete invasion by blast cells, and after histo-chemistry and cell markers he was diagnosed as having acute myelocytic leukemia, class Ml by the FrenchAmerican-British (FAB) classification. At that point, his serum calcium was normal (2.19 mmol/l), as well as his serum creatinine and urinary sediment. He was treated with daunoblastin, VP 16 and cytosine arabinoside with good response and apparent complete remission in the bone marrow and peripheral blood. He underwent later 2 consolidation treatments. One month after the 2nd consolidation treatment (October 1988) he was in complete remission. In early April 1989, he was found to be in relapse. A bone marrow biopsy disclosed 50% infiltration by blast cells. He was treated with cytosine arabinoside and mitroxantrone and achieved complete remission 23 days after chemotherapy. During his first relapse, serum calcium was still normal (2.2 mmol/l). In June 1989, he underwent successful bone marrow transplantation from an HLA identical brother. Throughout the period of bone marrow transplantation, he maintained normal serum calcium levels. In early December 1989, he was asymptomatic and in complete remission. His serum calcium was 2.27 mmol/l and medications consisted of low-dose ciclosporin and prednisone, 30 mg on alternate days for grade I graft versus host disease. He was readmitted to the Hospital on December 24, 1989, with a 3-day history of marked weakness, vomiting