The effect of lithium on PTH release from human parathyroid tissue was studied using a perifusion system and an immunoradiometric assay for intact human PTH. Tissue was obtained from three patients undergoing surgery for thyroid disease, three patients with secondary hyperparathyroidism due to chronic renal insufficiency, and four patients with primary hyperparathyroidism due to a parathyroid adenoma. Addition of lithium in concentrations equivalent to the therapeutic serum levels normally attained in man (1.3 mmol/L) resulted in a significant (P less than 0.05) increase in PTH release under normocalcemic (1.15 mmol/L) conditions from normal and hyperplastic tissues. The magnitude of the lithium-induced response of PTH release ranged from a 1.4- to 5.3-fold increase above basal levels (perifusion with 1.15 mmol/L calcium alone) and was comparable to the response during a low calcium (0.42 mmol/L) perifusion. Although the response to lithium was delayed compared to that of hypocalcemia, PTH returned to basal levels immediately after removal of either stimulator. In contrast, parathyroid adenomas did not respond to either lithium or hypocalcemia in a characteristic manner, but, rather, functioned in an autonomous fashion with repeated pulsatile bursts of PTH release that were not suppressible even under hypercalcemic (1.70 mmol/L) conditions. These in vitro studies suggest that lithium therapy may elevate serum PTH levels in some patients and could, thus, be responsible for hypercalcemia in them.
A 30-yr-old woman with malignant hypertension was found to have biochemical evidence of pheochromocytoma. Bilateral adrenal tumors were demonstrated on computerized tomographic scanning and confirmed at the time of surgery. Complete removal of one adrenal gland with partial removal of the other adrenal gland resulted in normalization of her blood pressure and biochemical parameters (norepinephrine and epinephrine) with preservation of adrenocortical function.
The assessment of the hypothalamic-pituitary-adrenal axis in patients with chronic renal failure (CRF) on hemodialysis is often hampered by abnormal responses to the standard 1-mg dexamethasone suppression test. Various mechanisms have been proposed to explain this lack of suppressibility. The present study was designed to look into the mechanisms possible for these findings in patients with CRF. We studied 6 patients with CRF on hemodialysis and 5 healthy subjects utilizing the 1-mg dexamethasone suppression test as well as the 50-mg hydrocortisone suppression test. Samples were assayed for dexamethasone, adrenocorticotropic hormone, corticosterone, and cortisol by both direct radioimmunoassay (RIA) and RIA after paper chromatography. Utilizing the direct cortisol RIA, 4 of 6 patients with CRF exhibited blunted dexamethasone suppression, while all 6 patients showed normal suppressibility after dexamethasone when cortisol was measured after paper chromatography. In contrast, all controls showed normal suppressibility regardless of the cortisol assay procedure used. The hydrocortisone suppression test was unreliable in the setting of CRF. Mean dexamethasone levels were similar in both groups. Plasma adrenocorticotropic hormone levels were significantly higher in the CRF patients, possibly indicative of an underlying hypothalamic-pituitary-adrenal axis abnormality. Abnormalities in dexamethasone suppression testing in patients with CRF may be explained by the overestimation of cortisol levels by direct RIA rather than by alteration of dexamethasone absorption or metabolism. Measurement of cortisol after paper chromatography is superior to direct RIA of cortisol in patients with CRF.
Parathyroid cysts are uncommon lesions of the neck leading to hypercalcemia in a significant percentage of cases. The distinction between parathyroid and thyroid cysts is difficult to make on a clinical basis alone and relies on the demonstration of elevated PTH levels in cyst fluid. We describe a case of a parathyroid cyst in which intact PTH (1-84) levels were misleadingly low while midmolecule 44-68 PTH was markedly elevated. To explain this discrepancy, we studied cyst fluid from this and two other patients using Sephadex G-75 gel chromatography. Fractions were analyzed using an immunoradiometric assay for intact hPTH (1-84) and a RIA specific for the midmolecular 44-68 region of hPTH. Immunoreactivity corresponding to hPTH (1-84) was absent in the first case but present in the remaining two. Immunoreactive peaks corresponding to PTH fragments were demonstrable in all three cyst samples. Patients with elevated hPTH (1-84) in cyst fluid were hypercalcemic; in contrast, the patient with a low cyst level of hPTH (1-84) was normocalcemic despite having markedly elevated levels of midmolecule PTH (44-68) in both serum and cyst fluid. Parathyroid cysts may thus produce fragments rather than intact PTH; reliance on an intact hPTH assay could lead to misdiagnosis. The measurement of PTH by a midmolecular assay may be preferable to the measurement of intact PTH in the evaluation of fluid from cystic neck masses.
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