sodium-bicarbonate and Hyperparathyroidism

We have developed a new test for estimating the secretory capacity of parathyroid hormone (PTH) from the parathyroid gland. Sodium bicarbonate solution [8.4% (w/v); 35 ml/m(2) body surface area] was infused for 2 min, and blood samples for the determination of plasma ionized calcium, plasma PTH (intact, midregion, carboxy-terminus) and related parameters were serially obtained. In 8 healthy volunteers, the mean (+/-SE) plasma ionized calcium fell promptly and significantly (from 1.21 +/- 0.01 to 1.11 +/- 0.01 mmol/L) after the sodium bicarbonate infusion. The mean (+/-SE) plasma intact PTH increased promptly and significantly, by more than four fold (42.3 +/- 4.2 to 182.4 +/- 34.7 pg/ml), and then gradually returned to basal levels. In patients with partial hypoparathyroidism who have detectable basal plasma levels of PTH, the absolute increment in PTH levels was much less, and in the plasma obtained from patients with complete hypoparathyroidism, absolutely no response was observed. Plasma obtained from patients diagnosed with primary hyperparathyroidism (parathyroid adenoma or hyperplasia) has high basal PTH levels. The response to the sodium bicarbonate infusion in these patients was markedly blunted (less than a two-fold increase in all cases examined). No significant adverse effects were observed during the procedure. Therefore, the sodium bicarbonate infusion test is a simple and sensitive method to stimulate PTH release, and is clinically useful for evaluating parathyroid gland function.

Topics: Adult; Aged; Calcium; Case-Control Studies; Female; Humans; Hyperparathyroidism; Infusions, Intravenous; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Sensitivity and Specificity; Sodium Bicarbonate

To test the hypothesis that alterations in acid base or calcium concentration may affect proinsulin processing or the insulin secretion mechanism.. Changes in proinsulin secretion or cleavage were assessed by measuring serum intact proinsulin and immunoreactive insulin concentrations in three models of acid base and calcium disturbance: (1) subacute changes in acid base status in six volunteers who received oral placebo, ammonium chloride, or sodium bicarbonate for three five day periods; (2) acute changes in calcium concentration in eight subjects who received 25 mmol oral calcium; (3) chronic changes in calcium concentration in seven patients with primary hyperparathyroidism and five with pseudohypoparathyroidism.. Acid base changes were confirmed by rises in serum bicarbonate concentrations (p < 0.01). No changes in serum insulin, intact proinsulin, or the proinsulin:insulin molar ratio were found. Serum calcium concentrations increased (2.49 v 2.38 mmol/l; p < 0.05) and parathyroid hormone concentrations decreased (1.1 v 1.9 pmol/l; p < 0.01) two hours after acute calcium loading. There were no significant differences in serum glucose, insulin, or intact proinsulin concentrations. Fasting proinsulin concentrations were significantly lower in the hyperparathyroid group (1.1 v 2.1 pmol/l; p < 0.05) and increased significantly after parathyroidectomy (2.1 v 1.1 pmol/l; p < 0.05).. The results indicate that subacute acid base changes do not affect proinsulin cleavage. Although acute calcium loading has no demonstrable effect, chronic hypercalcaemia may influence the mechanism of insulin secretion.

Topics: Acid-Base Equilibrium; Adult; Ammonium Chloride; Blood Glucose; Calcium; Fasting; Humans; Hyperparathyroidism; Insulin; Male; Proinsulin; Pseudohypoparathyroidism; Sodium Bicarbonate

The case is described of a 29-year-old man with renal failure and recurrent hyperparathyroidism who 3 weeks postparathyroidectomy developed hypocalcemic tetany because he was taking one-half the prescribed dose of calcitriol. He interpreted his symptoms as those of potassium intoxication and self-administered almost 1,500 mEq sodium bicarbonate. The increase in plasma sodium and osmolarity led to increased fluid intake, and at presentation he had an ionized calcium of 0.50 mmol/L, K 5.3 mmol/L, Na 148 mmol/L, total CO2 52.6 mmol/L, pO2 51.2 mm Hg, and pH of 7.61. He had gained 7 kg in weight. All abnormalities were corrected by dialysis, using initially a calcium-free dialyzate with extra calcium infused. The case illustrates the effect of alkalosis in reducing the amount of calcium that exists in ionized form, and it is suggested that complexing of calcium as calcium bicarbonate together with the pH change contributed to the decrease in ionized calcium. It is also an example of the hazards of treating patients who devise their own therapeutic regimens.

Topics: Adult; Alkalosis; Calcitriol; Calcium; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Male; Parathyroidectomy; Postoperative Complications; Renal Dialysis; Self Medication; Sodium Bicarbonate; Tetany

Three siblings with neonatal familial hyperparathyroidism diagnosed at age 4 months, 2 months, and 5 days, respectively, were treated. Hypercalciuria, nephrocalcinosis, and renal tubular acidosis were present in each child. In all three, there were higher responses of serum parathyroid hormone to serum calcium and higher elevation of serum calcium with oral calcium loading. The metabolism of vitamin D and calcitonin seemed to be intact. Hypercalcemia associated with the abnormal response of parathyroid hormone secretion disappeared when the children passed the age of approximately 2 years, although renal tubular acidosis and nephrocalcinosis remained. An autosomal recessive inheritance seems likely.

Topics: Acidosis, Renal Tubular; Bicarbonates; Calcinosis; Calcium; Calcium, Dietary; Chromosome Aberrations; Chromosome Disorders; Female; Humans; Hypercalcemia; Hyperparathyroidism; Infant, Newborn; Kidney Diseases; Male; Parathyroid Hormone; Sodium; Sodium Bicarbonate; Vitamin D