Effect of glycemic control on calcium and phosphorus handling and parathyroid hormone level in patients with non-insulin-dependent diabetes mellitus.

The present study was undertaken to determine whether improvement of hyperglycemia alters calcium and phosphorus handling, parathyroid hormone (PTH) secretion and bone turnover in patients with non-insulin-dependent diabetes mellitus (NIDDM). We measured serum and urinary mineral levels, serum intact PTH and osteocalcin on admission and at discharge (38 +/- 3 days later, Means +/- SEM) in 28 patients with poorly-controlled NIDDM (63 +/- 2 years old, 13 males and 15 females). During the hospitalization period, glycemic control was markedly improved. Serum calcium levels remained unchanged, but serum phosphorus increased. Urinary calcium and phosphorus excretion decreased. Serum intact PTH decreased from mid-normal (30.0 +/- 2.2 ng/l) to low normal values (24.0 +/- 1.3 ng/l) (P < 0.01, normal values: 10-65 ng/l). Serum osteocalcin increased from 4.14 +/- 0.35 to 4.92 +/- 0.40 micrograms/l (P < 0.01, normal values: 2.5-13 micrograms/l). On admission, urinary calcium and phosphorus excretion showed a positive correlation with urinary glucose excretion. Serum calcium levels showed a negative correlation with serum intact PTH (r = -0.46, P < 0.05). Moreover, the change in serum calcium during the hospitalization was negatively correlated to the change in serum intact-PTH (r = -0.45, P < 0.05). Serum phosphorus concentrations showed a positive correlation with the renal threshold for phosphorus excretion on admission (r = 0.86, P < 0.01). These results indicate that hyperglycemia causes excess urinary calcium and phosphorus excretion in patients with NIDDM. In response to urinary calcium loss, PTH secretion is mildly stimulated. Bone formation seems to be suppressed in the hyperglycemic state in spite of increased PTH secretion.