Etiology Of Hyperparathyroidism Research Articles

Comparison of Parathyroid Autofluorescence Signals in Different Types of Hyperparathyroidism.

There are scant data in the literature regarding whether parathyroid autofluorescence (AF) signal patterns vary based on the etiology of hyperparathyroidism. The aim of this study was to compare AF signals of parathyroid glands across different etiologies of hyperparathyroidism. As a prospective institutional review board-approved study between 2016 and 2019, AF intensities and heterogeneity indexes (HIs) of parathyroid glands in patients who underwent parathyroidectomy using AF were calculated and compared using Chi-square, Kruskal Wallis, Mann Whitney U, and logistic regression tests. Of the total of 183 patients, 127 patients had sporadic classic primary hyperparathyroidism, 30 patients had sporadic normohormonal primary hyperparathyroidism, 10 patients had sporadic normocalcemic primary hyperparathyroidism, 12 patients had tertiary hyperparathyroidism, and 4 patients had familial primary hyperparathyroidism related to multiple endocrine neoplasia (MEN) 2A. There were no statistical differences in AF signals of abnormal parathyroid glands in classic, normohormonal or normocalcemic sporadic hyperparathyroidism. Parathyroid glands in patients with tertiary hyperparathyroidism were similar in intensity, but more homogenous compared to those in sporadic primary hyperparathyroidism. The pattern of AF exhibited by abnormal parathyroid glands was similar across different spectrums of primary hyperparathyroidism, in accordance with observations in the literature. However, parathyroid glands in tertiary hyperparathyroidism were more homogeneous, despite exhibiting a similar intensity of AF compared to those in sporadic primary hyperparathyroidism. These differences should be kept in mind when using the AF pattern as an adjunct to visual assessment in parathyroid exploration.

Abstract #708: Parathyroid Carcinoma is a Rare but Important Etiology of Hyperparathyroidism

Abstract #708: Parathyroid Carcinoma is a Rare but Important Etiology of Hyperparathyroidism

A single surgical experience with 493 directed explorations for hyperparathyroidism

Objectives: To understand and implement an effective minimally invasive surgical protocol in patients with primary hyperparathyroidism utilizing appropriate selection criteria. Methods: A retrospective review of the case report forms of 535 patients with hyperparathyroidism surgically managed at an academic tertiary care medical center between December 1996 and December 2003. Case report forms included data on pre- and postoperative biochemical profile; clinical findings; imaging results; surgical findings; pathologic findings, facility utilization; complications; and outcomes. Results: A directed exploration protocol was implemented in 493 of 535 patients surgically managed for hyperparathyroidism (HPT); 55% of patients were asymptomatic or without end organ effect at presentation. The etiology of HPT was primary in 466 patients and secondary/tertiary in 27. Single gland disease was the pathologic entity in 412 patients (3 with carcinoma), followed by diffuse hyperplasia (39) and double adenoma (15). Sestamibi scan accuracy in correctly localizing hyperfunctional parathyroid tissue was 93%. Mean IOPTH degradation was 78% (range, 59%97%). Sustained normocalcemia was achieved in 98.7% of patients following DEP. Mean follow-up interval was 28 months (range, 6–72 m), with a 6-month follow-up for all patients. Eighty-five percent of DEP operative procedures were less than 1 hour and over 90% of patients were managed in an ambulatory care setting. Conclusions: The directed exploration protocol used in this series represents a highly effective and cost-efficient approach in the surgical management of the majority of patients with hyperparathyroidism.

Hyperparathyroidism in thyrotoxicosis

The frequency of hypercalcemia in 295 patients treated for thyrotoxicosis was 2 per cent. The combination of thyrotoxicosis and hyperparathyroidism is rare and only twenty-seven well documented cases could be found in the literature. Among ninety-two patients operated on for hyperparathyroidism, ten of them had thyrotoxicosis. In the present study, data on thirty-seven patients are reported. Hypercalcemia was found in all the patients and four of them had acute hyperparathyroidism. Hypophosphatemia was recorded in 60 per cent and hypercalcuria in 75 per cent of the patients. In ten patients there were renal concretions. Skeletal roentgenograms showed abnormalities in 65 per cent of the patients. In no instance had hyperparathyroidism commenced before thyrotoxicosis. Other recent reports on the etiology of hyperparathyroidism are discussed and it is concluded that hyperparathyroidism in thyrotoxicosis is a secondary disease. If a thyrotoxic patient with hypercalcemia still has elevated calcium values when becoming euthyroid after thyrostatic treatment, an operation should be performed. Because of a high recurrence rate in such patients with adequate follow-up, “near total parathyroidectomy” is recommended.

Etiology of hyperparathyroidism and bone disease during chronic hemodialysis. 3. Evaluation of parathyroid suppressibility.

Parathyroid function was assessed by calcium infusions (4-8 h) in 16 patients with chronic renal insufficiency being treated by long-term hemodialysis. The concentrations of two immunoreactive species of parathyroid hormone in plasma (iPTH-9, mol wt 9500; iPTH-7, mol wt 7000) were estimated by radioimmunoassays utilizing two relatively specific antisera. Control values of the smaller species, iPTH-7, were uniformly high, whereas values of iPTH-9 were normal in 12 of 19 studies. Response of iPTH-7 to calcium infusions was variable, with significant decreases occurring only five times in 27 infusions. Concentrations of iPTH-9, however, decreased during every calcium infusion. In contrast to these acute responses, five of six patients studied during periods of dialysis against both low (< 6 mg/100 ml) and high (7-8 mg/100 ml) calcium concentrations in the dialyzate showed a decrease in values of iPTH-7 during the period of dialysis against the higher calcium concentration. It is concluded that plasma concentrations of iPTH-9 reflect primarily the moment-to-moment secretory status of the parathyroid glands, while concentrations of iPTH-7 reflect more closely chronic parathyroid functional status. It is further concluded that the failure of iPTH-7 to decrease during induced hypercalcemia should not be equated with autonomy of parathyroid gland function.

Etiology of hyperparathyroidism and bone disease during chronic hemodialysis. I. Association of bone disease with potentially etiologic factors.

The present study was prompted by the observation that, in patients with chronic renal failure being followed at this center, renal osteodystrophy developed almost exclusively in those who were treated by chronic hemodialysis at home rather than in our center. A systematic comparison was made between the 10 patients with roentgenographic evidence of the bone disease and 18 patients without demonstrable bone disease. The two groups were similar in age, sex, nature of renal disease, and duration of dialysis. The mean duration of kidney disease was almost 2 yr longer in the patients without bone disease than in those with bone disease. Other significant differences related to where the hemodialysis was performed and to the calcium concentration in the dialysate (6.0-7.4 mg/100 ml in the hospital and 4.9-5.6 mg/100 ml at home). If the unknown factors related to where the dialysis was performed were of no consequence, the major factor contributing to the production of bone disease observed in these patients was the use of a dialysate with a calcium concentration less than 5.7 mg/100 ml.

Etiology of hyperparathyroidism and bone disease during chronic hemodialysis. II. Factors affecting serum immunoreactive parathyroid hormone.

Plasma concentration of immunoreactive parathyroid hormone (IPTH) was measured in 18 patients who had been on a hemodialysis program for longer than 6 months. A negative correlation was found between the predialysis plasma concentration of IPTH and the mean concentration of calcium in the dialysate previously used: plasma concentrations of IPTH were higher in patients dialyzed against a calcium concentration between 4.9 and 5.6 mg/100 ml than in patients dialyzed against a calcium concentration of 6.0 mg/100 ml or more. Plasma concentrations of IPTH also were higher in patients with bone disease than in patients without bone disease. Furthermore, a positive correlation was found between predialysis plasma concentrations of IPTH and calcium, and between mean predialysis concentration of IPTH and phosphate. To obviate the possibility that individual differences in susceptibility could have accounted for the observed effects of plasma phosphate and of dialysate calcium, a 2 x 2 factorial study was conducted in seven of these patients to examine the independent effects of perturbation of each of these factors. It was observed that plasma concentration of IPTH was lowest with the combination of high dialysate calcium and low plasma phosphate, highest with the combination of low dialysate calcium and high plasma phosphate, and intermediate with the two other combinations. It is concluded that both dialysate calcium and plasma phosphate are important determinants of parathyroid function in these patients.