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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lithium has proved to be a highly effective preventive measure in mood disorders and an increasing number of patients are receiving long-term lithium carbonate therapy. Among other biologically and clinically important effects of lithium, the possible induction of hyperparathyroidism was first suggested in 1973 by Garfinkel et al. About thirty other case reports have since been described, but they could simply have represented the coincidental occurrence of primary hyperparathyroidism and lithium carbonate treatment in the same patients. Eleven cross-sectional studies of calcium metabolism in patients treated with lithium carbonate have been reported. Evidence of a causal relationship of lithium to hyperparathyroidism can lead to a loss of effectiveness of lithium in controlling the affective symptoms. Interestingly, coexistence with hypothyroidism is not uncommon. Low serum phosphate, high serum chloride are also observed. Bone mineral content may decrease. In addition, several studies have shown that lithium treatment increases serum magnesium level. Unusual metabolic features are associated with hyperparathyroidism and long-term lithium treatment: low urinary calcium excretion, absence of nephrolithiasis, and normal urinary cyclic AMP excretion. Lithium inhibition of PTH sensitive adenylcyclase in the kidney would explain these features. In vitro studies suggested that lithium is a potent inhibitor of several hormone responsive adenylcyclase systems. It is possible that the tissue susceptibility to adenylcyclase inhibition in an individual may decide the nature of endocrine dysfunction seen during lithium treatment. Information about the time course with which abnormalities may develop is derived from longitudinal studies. Several months to several years are needed for lithium inducing primary hyperparathyroidism. In vitro studies provide strong evidence that lithium can induce a shift in the set-point for inhibition of PTH secretion by calcium and a direct stimulation of PTH secretion. The extent to which we can extrapolate these data to the clinical situation is discussed. In vivo data from Shen an Seely are compatible with these two mechanisms. These alterations should cause parathyroid hyperplasia. The possibility that a generalized parathyroid stimulus might lead to formation of a single adenima is not proved. Several recommendations regarding parathyroid function in patients receiving lithium have been suggested. Measurement of total calcium and serum proteins or of serum calcium ion values when available should be performed before therapy is begun. If elevated values are obtained, lithium treatment should be deferred and evaluation for hyperparathyroidism performed. Serum calcium should be monitored periodically during lithium treatment. Sustained hypercalcemia or true hyperparathyroidism require parathyroidectomy. If hypercalcemia is mild without complication and psychiatric symptoms well controlled, perhaps surgery should not be employed.
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PMID:[Hyperparathyroidism with lithium]. 808 38

Recurrent or persistent primary hyperparathyroidism (HPT) is a rare occurrence requiring generally a careful reoperation. From 1980 to 1992 a total of 192 patients underwent bilateral cervical exploration following a diagnosis of primary hyperparathyroidism. Persistent of recurrent HPT was found in 6 (3.04%) of our cases. In two patients a subtotal parathyroidectomy was performed (parathyroid hyperplasia) and hyperfunctioning parathyroid tissue was found at neck exploration. In one case an ectopic adenomatous fifth gland was found in mediastinum at reoperation. Three patients with recurrent HPT had a parathyroid carcinoma but in only two cases it was possible to identify and remove the pathologic tissue preoperatively localised in mediastinum by double-tracer scintigraphy and CT scan 6 and 15 months after first operation respectively. The third patient with parathyroid carcinoma was inoperable on account of multiple metastases both cervical and thoracic.
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PMID:[Surgical approach in the treatment of recurrent primary hyperparathyroidism]. 815 59

Surgery for primary hyperparathyroidism is successful in 95% of patients, but ectopic glands and anatomic variations in location are causes of surgical failure. The radionuclide imaging agent, technetium (Tc)-99m-sestamibi, in conjunction with subtraction iodine-123 scanning, is a new method of preoperative localization of abnormal parathyroid glands. In a study approved by the Institutional Review Board, 22 patients with primary hyperparathyroidism underwent preoperative evaluation with high-resolution ultrasonography and Tc-99m-sestamibi/I-123 radionuclide scanning for attempted localization of abnormal parathyroid glands. Results of Tc-99m-sestamibi scanning and ultrasound were correlated with surgical and pathologic findings. Of 22 patients, 16 had a solitary parathyroid adenoma, 1 had a double adenoma, and 5 had diffuse parathyroid hyperplasia. The Tc-99m-sestamibi/I-123 radionuclide scan preoperatively identified a solitary adenoma in 14 of 16 patients (sensitivity: 88%). However, when the data were analyzed retrospectively along with surgical and pathologic findings, the Tc-99m-sestamibi scan correctly localized all parathyroid adenomas for a sensitivity of 100%. The one patient with a double adenoma had a localization image consistent with two enlarged glands. All patients with diffuse parathyroid hyperplasia had Tc-99m-sestamibi imaging consistent with diffuse hyperplasia, although delineation of individual enlarged glands was not possible. High-resolution ultrasound identified 11 of 16 parathyroid adenomas (sensitivity: 69%). The patient with a double adenoma had a negative ultrasound. Ultrasound was less accurate in five patients with diffuse hyperplasia: one scan was completely negative, two scans revealed only one enlarged gland, and two scans revealed two enlarged glands. The Tc-99m-sestamibi/I-123 subtraction radionuclide scan is more sensitive than high-resolution ultrasonography for the preoperative localization of abnormal parathyroid glands. Tc-99m-sestamibi/I-123 radionuclide scanning may be more useful than ultrasonography to the surgeon in the preoperative localization of abnormal parathyroid glands.
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PMID:Prospective comparison of technetium-99m-sestamibi/iodine-123 radionuclide scan versus high-resolution ultrasonography for the preoperative localization of abnormal parathyroid glands in patients with previously unoperated primary hyperparathyroidism. 821 95

Primary hyperparathyroidism (PHPT) is found not uncommonly in patients with cancer. In this report, however, we describe a patient where both humoral hypercalcaemia of malignancy and PHPT were present coincidentally. A 47-year-old man was found to have PHPT due to parathyroid hyperplasia. Serum parathyroid hormone (PTH) levels, which were elevated before parathyroidectomy, were undetectable post-operatively; however, hypercalcaemia persisted. Nephrogenous cyclic adenosine monophosphate was elevated along with this undetectable PTH, indicative of the presence of a PTH-like factor in the serum. This was confirmed by the finding of an elevated level of PTH-related protein (PTHrP) in plasma (9.1 pmol/l, normal < 2.6 pmol/l). Secondary carcinoma was identified in a lesion in the region of the manubrium sternii. This stained positively for PTHrP by immunocytochemistry and PTHrP messenger RNA was detected by in-situ hybridization. This case illustrates the value of sensitive PTH assays in distinguishing PHPT from other causes of hypercalcaemia and also shows the importance of considering primary hyperparathyroidism in the differential diagnosis of the patient with cancer and hypercalcaemia.
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PMID:Coincidental occurrence of primary hyperparathyroidism and cancer-associated hypercalcaemia in a middle-aged man. 831 76

Fifty-eight human fetal thyroid glands obtained at autopsy were systematically studied for the presence of intrathyroidal parathyroid tissue. The latter was found in 13 thyroid lobes from 12 fetuses. It was located in a subcapsular position in 9 of 58 cases and lying deep in thyroid tissue in 4 of 58. Our findings suggest that intrathyroidal parathyroid tissue is not such a rare finding and should always be considered especially for the clinical and surgical management of patients with primary hyperparathyroidism due to parathyroid hyperplasia.
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PMID:Intrathyroidal parathyroid. 847 53

Primary hyperparathyroidism is a common condition due to either a parathyroid adenoma or, less commonly, parathyroid hyperplasia, whose treatment is essentially surgical. We have, therefore, assessed the accuracy of Tc-99m pertechnetate/Tc-99m sestamibi (methoxy-isobutyl isonitrile) imaging in the localization of adenomas and hyperplastic parathyroids. The clinical records of all patients who had Tc-99m pertechnetate/Tc-99m sestamibi imaging and parathyroid surgery at this hospital were reviewed. The technique used involves standard subtraction methodology with the addition of a novel change detection algorithm to optimize localization. Of 46 patients scanned in 48 patient episodes, 36 patients had adenomas; 28 (78%) were accurately localized to the correct quadrant, and 4 were correctly lateralized. Two patients with parathyroid carcinomas had their metastases correctly localized. Thus, in 34 of 38 (89.5%) of the scans, adenomas or carcinomas were able to be anatomically localized. Six patients presented with hyperplasia; 5 were diagnosed by sestamibi scans, and 3 of these accurately localized all hyperplastic glands. Four additional patients had known hyperplasia, of which 2 were rendered normocalcemic after removal of their sestamibi-positive glands; the other 2 had small second glands detected only at surgery. In patients with unknown pathology, imaging suggested that 6 patients had hyperplasia; this was correct in 5 cases (83%). Nine of the 12 scans in patients who had had previous parathyroid surgery accurately localized the tumors, 7 in the neck and 2 outside. We suggest that sestamibi imaging can help to distinguish hyperplasia from adenomatous disease; when imaging is required, we recommend it as the imaging modality of choice in all patients with primary hyperparathyroidism, especially in reoperated patients.
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PMID:The accuracy of parathyroid gland localization in primary hyperparathyroidism using sestamibi radionuclide imaging. 855 Jul 76

Primary hyperparathyroidism is a rare disease of childhood. The condition is even rarer in the neonatal and infant stages. The disease, with its main manifestation-hypercalcemia-often is fatal. The authors successfully treated a 2.5-month-old boy who had primary parathyroid hyperplasia. The patient had recurrent pneumonia and failure to thrive. Blood test results showed an abnormally high level of calcium, which was resistant to medical therapy. Further investigations showed high levels of parathyroid hormone. The patient underwent neck exploration, which showed hyperplasia of the all four parathyroid glands. Total parathyroidectomy was performed, with one gland being autotransplanted to the deltoid muscle. The patient had an immediate hypocalcemic period, followed by normocalcemia. In light of the present case and others in the Literature, the authors recommended total parathyroidectomy followed by autotransplantation of a gland to an accessible muscle.
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PMID:Primary hyperparathyroidism in infancy: a case report. 870 21

Information on genetic abnormalities in primary hyperparathyroidism has accumulated gradually. Genetic alterations responsible for tumorigenesis have been identified in multiple endocrine neoplasia types 1 and 2. Point mutations in a calcium-sensing receptor gene were recently found to be responsible for familial hypocalciuric hypercalcaemia and neonatal severe hyperparathyroidism. Evidence has been provided that abnormalities of cell cycle regulation participate at tumorigenesis in parathyroid adenoma and carcinoma. Clonal analysis has shown that in renal hyperparathyroidism the parathyroid glands initially grow diffusely and polyclonally, after which foci of nodular hyperplasia are transformed to monoclonal neoplasia. Somatic changes of specific genes have been suspected of being responsible for parathyroid tumorigenesis in renal hyperparathyroidism. However, the genetic loci responsible for the frequent monoclonality largely remain to be identified, and heterogeneous genetic abnormalities may contribute to the progression of secondary parathyroid hyperplasia.
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PMID:Molecular genetics of hyperparathyroid disease. 882 31

In vivo dynamic tests of parathyroid gland function have provided useful information about the secretory behavior of parathyroids in various clinical disorders, but the limitations of this approach must be recognized when applied to studies of parathyroid gland physiology. Set point abnormalities have been documented in vivo both in primary hyperparathyroidism and in familial hypocalciuric hypercalcemia. Such findings are consistent with in vitro results obtained in studies of dispersed parathyroid cells from patients with primary hyperparathyroidism and with recently described alteration in calcium receptor expression in patients with FHH. The assessment of parathyroid gland function in patients with end-stage renal disease presents distinct methodological problems, however, because of marked variation in the degree of parathyroid gland enlargement. Neither the four parameter model originally used to describe set point abnormalities both in vitro and in vivo or alternative approaches to the assessment of PTH secretion in vivo adequately address this important issue. Results from recent in vivo studies of patients with chronic renal failure do not support the view that the set point for calcium-regulated PTH release is abnormal in secondary hyperparathyroidism or that treatment with calcitriol lowers the set point for calcium-regulated PTH release in patients with uremic secondary hyperparathyroidism. The concept of set point disturbances has strongly influenced discussions about the pathogenesis of secondary hyperparathyroidism, and it has served as a focal point for examining the therapeutic response to calcitriol in patients with this disorder. This matter requires careful reconsideration, however, in light of recent clinical findings and the development of techniques to directly assess the molecular mechanisms responsible for regulating calcium-mediated PTH release in renal failure and other disorders of mineral metabolism. Although knowledge in this area remains limited, the extent of parathyroid hyperplasia and the role of factors that influence the development of parathyroid gland enlargement may ultimately prove to be particularly important modifiers of parathyroid gland function in chronic renal failure.
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PMID:In vivo assessments of calcium-regulated parathyroid hormone release in secondary hyperparathyroidism. 894 64

A retrospective study on 22 cases of parathyroid adenoma, 9 cases of primary parathyroid hyperplasia and 14 specimens of normal suppressed glandular tissue was undertaken to determine the usefulness of proliferative index (PI) for discriminating adenoma from hyperplasia, as an adjunct to the existing histological criteria. PI was determined by avidin-biotin-complex immunostaining after high temperature microwave antigen retrieval in paraffin sections, using monoclonal MIB-1 antibody which detects paraffin resistant analogue of cell cycle-associated Ki-67 antigen. PI expressed as percentage positive cell nuclei, was 1.36 +/- 0.62 (range 0.04-2.72) in adenoma, 1.17 +/- 0.83 (0.02-1.98) in hyperplasia and 0.03 +/- 0.02 (0.00-0.06) in normal suppressed glandular tissue. While the difference between normal suppressed glandular tissue and adenoma and hyperplasia was significant (P < 0.001), that between adenoma and hyperplasia was not. We conclude that although PI could distinguish between normal suppressed glandular tissue versus glands with primary hyperparathyroidism, it failed as an additional useful parameter for discriminating between adenoma and hyperplasia, both of which have low but similar proliferative activity.
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PMID:MIB-1 proliferative index in parathyroid adenoma & hyperplasia. 918 80


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