Additional key phrases: analytical interference; arsenazo Ill; total calciumThere are a great number of potential causes of hypercalcaemia, although the vast majority of cases have either primary hyperparathyroidism or malignancy. Here, we report two cases of pseudohypercalcaemia due to interference of IgM paraproteins with total calcium assay resulting in unnecessary investigations.
CASE HISTORY 1A 63-year-old man presented in 1992 with left basal pneumonia and septicaemia. Protein electrophoresis revealed a dense discrete and abnormal band in the gamma region. His serum IgM concentration was grossly increased at 82·8 giL (reference range 0,42-2'6) and bone marrow biopsy revealed an increase in lymphoid cells, some of which showed plasma cell characteristics of binucleate forms consistent with Waldenstrom's macroglobulinaemia. He was treated with intermittent courses of chlorambucil and prednisolone with a satisfactory response, and his IgM fell to 20 g/L. His serum calcium adjusted for albumin was normal at 2·53 rnmol/L on presentation, but increased to 2·84mmol/L in August 1993 and then to 3·55 mrnol/L in December 1994 (Fig. 1). His serum parathormone (PTH) concentrations measured on three occasions when he was hypercalcaemic were within the reference range (Chi ron Magic LitePTH =2-4, 2·5 and 2·5 pmol/L; reference range 0'9-5-4) but were inappropriate for his degree of hypercalcaemia. He had normal thyroid function, and no evidence of sarcoidosis. His parathormone related peptide was below the limit of detection and his urinary calcium excretion was normal at 5·0 mmol/24 h. Radiological examination revealed osteoporosis of his Correspondence to: Dr Rhys John. 694 thoraco-lumbar spine and hands as well as possible cystic changes in his hands. He gave a history of renal stones in 1959. In 1995 he developed multiple small bladder calculi. Selective venous catheterization of his neck region revealed no localization of increased serum PTH concentration.As no cause for his hypercalcaemia was evident, he was referred for consideration of parathyroid surgery but this was not done as he was not considered to have primary hyperparathyroidism. A possibility existed that the increased calcium was caused by binding of calcium to his IgM. His ionized calcium was accordingly measured and was found to be normal at 1·15 rnrnol/L, when his total calcium was 3·02 mmol/L, His calcium measured by atomic absorption spectrophotometry was found to be normal at 2-49 mmol/L, This alerted us to the possibility that there was an interference in the calcium measurement. His calcium had been measured by the Arsenazo III dye binding method on a Beckman CX7 analyser. When a sample with a calcium of 3·22 rnrnol/L by this method was analysed on a Hitachi 747
