TY - JOUR
T1 - Immobilization hypercalcaemia due to low bone formation and responding to intravenous sodium sulphate
AU - Evans, Richard A.
AU - Lawrence, Peter J.
AU - Thanakrishnan, Govindasamy
AU - Hills, Ellen
AU - Wong, Stanley Y.P.
AU - Dunstan, Colin R.
PY - 1986/1/1
Y1 - 1986/1/1
N2 - A young man developed acute renal failure and hypercalcaemia following severe burns. The hypercalcaemia was initially controlled by haemodialysis, but it persisted after return of renal function. Plasma PTH was inappropriately elevated, but the nephrogenous cyclic adenosine monophosphate level was low; thus the PTH was probably not biologically active, and may have been artefactually elevated by the moderate renal impairment. Bone histology, showed a normal resorbing surface, but a zero forming surface, implying that the bone dissolution leading to hypercalcaemia resulted from a failure of bone formation. Because of widespread infection and impaired renal function, the hypercalcaemia could not be treated by corticosteroid drugs, mithramycin or phosphate, and there was no response to salmon calcitonin. He was therefore treated with intravenous sodium sulphate, which increased urinary calcium excretion and reduced the plasma calcium. Sodium sulphate still has a role in the treatment of patients with hypercalcaemia.
AB - A young man developed acute renal failure and hypercalcaemia following severe burns. The hypercalcaemia was initially controlled by haemodialysis, but it persisted after return of renal function. Plasma PTH was inappropriately elevated, but the nephrogenous cyclic adenosine monophosphate level was low; thus the PTH was probably not biologically active, and may have been artefactually elevated by the moderate renal impairment. Bone histology, showed a normal resorbing surface, but a zero forming surface, implying that the bone dissolution leading to hypercalcaemia resulted from a failure of bone formation. Because of widespread infection and impaired renal function, the hypercalcaemia could not be treated by corticosteroid drugs, mithramycin or phosphate, and there was no response to salmon calcitonin. He was therefore treated with intravenous sodium sulphate, which increased urinary calcium excretion and reduced the plasma calcium. Sodium sulphate still has a role in the treatment of patients with hypercalcaemia.
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U2 - 10.1136/pgmj.62.727.395
DO - 10.1136/pgmj.62.727.395
M3 - Article
AN - SCOPUS:0022616895
VL - 62
SP - 395
EP - 398
JO - Postgraduate Medical Journal
JF - Postgraduate Medical Journal
SN - 0032-5473
IS - 727
ER -