Elevated iPTH Levels Research Articles

Hypercalcemia Associated With Chronic Lymphocytic Leukemia

A patient with chronic lymphocytic leukemia (CLL) is described in whom hypercalcemia occurred in association with elevation of the peripheral lymphocyte count and expansion of total tumor mass. Hypercalcemia was ameliorated with the institution of chemotherapy for the leukemic process and subsequent fall in WBC count and decrease in total tumor burden; hypercalcemia recurred with relapse of the leukemic process. The serum immunoreactive parathyroid hormone (iPTH) concentration, when measured, was inappropriately elevated for the degree of hypercalcemia. The hypercalcemia would appear to be a direct consequence of the leukemia, and possibly involved secretion of a parathyroid hormone-like polypeptide by the CLL cells. Although a possible role for either an osteoclast-activating substance or prostaglandins was not excluded, they would not account for the elevated serum iPTH levels observed.

CONGENITAL HYPERPERATHYROIDISM /HPT/AND VITAMIN D DEFICIENCY SECONDARY TO MATERNAL HYPOPARATHYROIDISM /HoPT/

A new case of congenital HPT secondary to maternal HoPT is described. Maternal HoPT appeared 4 days after thyroidectomy performed for a cold nodular goiter during the first month of pregnancy:hypocalcemia /< 80 mg/1/and low serum immunoreactive parathyroid hormone levels /iPTH/were present. Diagnosis of neonatal HPT was based on elevated iPTH levels and evidence of long bones demineralisation and sub-periosteal resorption of the metaphyses. Plasma Ca ranged from 77to 88mg/l and plasma P from 47to 52mg/l.IV Ca load /15mg/kg/3h/ lowered the iPTH levels from 270to 100μlEq/ml /N<c50 μlEq/ml/. Low plasma levels of 25 OHD/ < 4ng/ml/were found at the age of 41days in spite of previous administration of 600u of vit.D for 12days. At the age of 3 months, 15mg of vit.D were given orally: iPTH levels which remained elevated 3weeks before /210μlEq/ml/were found to be normal 8days after this vit.D load/37 μlEq/ml/. It is suggested that in congenital HPT secondary to maternal HoPT, hyperparathyroidism increases the baby needs for vit D. This results in a state of vit D deficiency which in turn maintains a parathyroid hyperactivity. Thus high doses of Vit.D appears to be the treatment of choice in this congenital HPT.

Pseudohypoparathyroidism: Disappearance of the resistance to parathyroid extract during treatment with vitamin D

Serum immunoreactive parathyroid hormone (iPTH) levels were increased in a 15 year old girl with pseudohypoparathyroidism, hypocalcemia, hyperphosphatemia, and minimal phosphaturic and absent hypercalcemic responses to exogenous parathyroid extract (PTE). Following normalization of the serum calcium concentration with vitamin D, serum iPTH and phosphate concentrations returned to the normal range, and phosphaturia could be clearly stimulated and hypercalcemia induced by PTE. On the other hand, the urinary cyclic adenosine 3′,5′-monophosphate (cyclic AMP) excretion could not be stimulated, suggesting that in this case, there appears to be no relationship between the urinary excretion of cyclic AMP and the phosphaturic effect of PTE. The minimal phosphaturic effect and the lack of hypercalcemic effects of PTE in untreated pseudohypoparathyroidism can be explained by the secondary hyperparathyroidism causing elevated iPTH levels rather than by a defect at the level of the receptor sites. A requirement of pharmacologic amounts of vitamin D per se, however, for the responsiveness of patients with pseudohypoparathyroidism to PTE cannot be ruled out.