PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “parathyroid carcinoma”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources

99mTc-MIBI radio-guided surgery in primary hyperparathyroidism: a prospective study of 128 patients.

UNLABELLED: AIMS AND STUDY DESIGN: We investigated the role of an intraoperative gamma probe (IGP) technique in 128 patients with primary hyperparathyroidism (HPT). The patients were evaluated before surgery by 99mTc04/MIBI scintigraphy and neck ultrasound and then operated on by the same surgical team. The IGP technique consisted of the injection of a low dose (37 MBq) of 99mTc-MIBI in the operating room shortly before the start of surgery. Quick parathyroid hormone (QPTH) was routinely measured during the operation. RESULTS: In 94/97 patients (96.9%) with a preoperative diagnosis of solitary parathyroid adenoma (PA) minimally invasive radioguided surgery (MIRS) was successfully performed; in the other 3/97 patients (3.1%) conversion to bilateral neck exploration (BNE) was required because of the intraoperative diagnosis of parathyroid carcinoma in two cases and multiglandular disease (MGD) in one. MIRS was successfully performed also in 23 patients who had undergone previous thyroid or parathyroid surgery. In 31 patients with a preoperative diagnosis of MGD (n = 5) or concomitant nodular goiter (n = 26) the IGP technique was used during a bilateral neck exploration. Among these patients IGP was useful in localizing an ectopic parathyroid gland in the thymus in one case of MGD and a PA located deep in the neck (n = 2) or ectopic at the carotid bifurcation (n = 1) in three cases with nodular goiter. However, in several other patients with nodular goiter it was difficult for the probe to distinguish intraoperatively between thyroid nodules and PA located close to the thyroid gland. CONCLUSIONS: It can be concluded that a) in primary HPT patients with a high likelihood (according to scintigraphic and ultrasound findings) of being affected by a single PA and with a normal thyroid gland, the IGP technique appears useful in MIRS; b) a 99mTc-MIBI dose as low as 37 MBq appears to be adequate to perform MIRS; c) the measurement of QPTH is strongly recommended in HPT patients selected for MIRS to confirm the radicality of parathyroidectomy; d) MIRS can be useful also in HPT patients who underwent previous parathyroid or thyroid surgery to limit the surgical trauma of reoperation and minimize complications; e) with the exception of PAs located at ectopic sites or deep in the neck, the IGP technique does not seem to be recommendable in HPT patients with concomitant nodular goiter.

Humans↗

Medical approaches to primary hyperparathyroidism.

Medical therapy is useful in cases of acute primary hyperparathyroidism, patients with recurrent disease, and parathyroid carcinoma. Among the therapeutic agents that have been employed, oral phosphate, bisphosphonates, and estrogens have been successful. The newly described calcimimetic agents directly block secretion of parathyroid hormone from the glands and offer an important new approach to medical therapy of primary hyperparathyroidism.

Calcium↗

Continuous arteriovenous hemofiltration--a new treatment in hypercalcemic crisis.

A case of hypercalcemic crisis, with accompanying anuria, due to recurrence of a parathyroid carcinoma and unresponsive to conventional medical treatment, was treated with continuous arteriovenous hemofiltration (CAVH). A maximum of 24 mmol of calcium was removed per 24 h by CAVH and serum calcium was temporarily normalized. Rising values during continued treatment necessitated acute parathyroidectomy. CAVH may represent a new treatment in hypercalcemic crisis, unresponsive to medical treatment.

Adult↗

An ultrastructural cytochemical stain specific for neuroendocrine neoplasms.

Previous work from our laboratory has indicated that the uranaffin reaction, when run under specific conditions, will stain neurosecretory granules. In this ultrastructural cytochemical study, we analyzed the granule-staining properties of 13 normal, 10 abnormal (non-neoplastic), and 138 neoplastic tissues in an attempt to evaluate the specificity of the uranaffin reaction for diagnostic purposes when compared with routinely processed specimens. For the uranaffin reaction, previously fixed tissue stored in buffer was rinsed with 0.9% NaCl and reacted with a 4% aqueous solution of uranyl acetate (pH 3.9) for 48 hours. After three NaCl rinses, the tissue was dehydrated and processed for electron microscopy. The granules of normal or non-neoplastic neuroendocrine cells that stained positively with the uranaffin reaction included pancreatic islet cells, thyroid C cells, adrenal medullary cells, parathyroid chief cells, and the neuroendocrine cells of the intestine. All 42 neuroendocrine neoplasms studied possessed abundant uranaffin-positive granules and included carcinoids, oat cell carcinomas, islet cell neoplasms, medullary carcinomas of the thyroid, pheochromocytomas, carotid body paragangliomas, a pituitary adenoma, Merkel cell carcinomas, parathyroid adenomas, and a neuroblastoma. All 96 control neoplasms that were not classified as neuroendocrine in nature were negative for neurosecretory granules when studied with the uranaffin reaction and included 13 neoplasms derived from endocrine glands, 57 neoplasms from secretory epithelium, 10 of hematopoietic origin, and 16 miscellaneous neoplasms. It was determined that the uranaffin reaction is a useful ultrastructural cytochemical marker for neuroendocrine granules and helped distinguish these cytoplasmic organelles from ultrastructurally similar granules derived from non-neuroendocrine cells.

Adult↗

Parathyroidectomy via bilateral cervical exploration: a retrospective review of 866 cases.

INTRODUCTION: Parathyroidectomy via cervical exploration is an effective primary-modality treatment for hyperparathyroidism, with cure rates of greater than 95%. We retrospectively reviewed 866 consecutive parathyroidectomies performed by a single surgeon between 1960 and 1997. We attempted to describe the polymorphic variation in multiglandular disease, the anatomic locations of pathologic glands, and the operative strategy and techniques which we believed were important to minimizing morbidity and maximizing curative success. METHODS: The cases of 329 males and 537 females (age, 1-88 years) were reviewed. There were 766 operations performed: primary hyperparathyroidism (713), tertiary hyperparathyroidism (100), reoperations (53). The strategy for primary exploration includes a bilateral neck exploration, early recurrent laryngeal nerve skeletonization, and identification of at least four glands. RESULTS: Normocalcemia was achieved in 98.2% of cases after initial cervical exploration. Persistent hypercalcemia occurred in 7 patients (<1%). Nine patients (1%) suffered persistent postoperative hypocalcemia. Unilateral recurrent laryngeal nerve injury occurred in two patients (<1%). Other perioperative complications included: reoperation for hematoma, repaired carotid artery injury, unexplained dysphagia, pneumothorax, deep venous thrombosis, and aspiration pneumonia. There were two mortalities (<1%) attributable to severe, comorbid disease. Ectopic glands were found in 120 cases. The frequency of glands at these sites were as follows: mediastinal (4.9%), intrathymic (8.4%), intrathyroid (6.7%), and retroesophageal/retrotracheal (3.5%). Thyroid resections provided diagnosis of concomitant thyroid carcinoma in 8.0% of resected patients. The pathology of patients with primary hyperparathyroidism (PHPT) consisted of single adenomas (77.2%), hyperplasia (21.0%), normal glands (1%), double adenomas (<1%), and parathyroid carcinoma (<1%). The distribution of adenomas was as follows: left upper, 25.3%; left lower, 27.3%; right upper, 26.8%; right lower, 20.6%. Hyperplastic glands were found in ectopic positions as follows: intrathymic (7.5%), intrathyroid (11.3%), mediastinal (2.5%), and retroesophageal/retrotracheal (0%). The average volume difference between the largest and smallest hyperplastic gland of each case was 1.80 + 4.40 cm3. Reoperations were performed upon 53 referred patients and 7 patients after failed exploration. Normocalcemia was attained in 98.3% of cases. Glandular pathology was identified in the previous operative field in 52 patients (86.7%). Adenomas were identified in 56.0% (n = 23) and hyperplasia in 39.0% (n = 16). CONCLUSIONS: In our series, we were able to attain normocalcemia in 98.2% of cases after initial cervical exploration. We believe that identification of four glands, an exhaustive search of ectopic sites, bilateral exploration, and liberal use of biopsy and intraoperative frozen section were essential to curative success. The pathologist should identify parathyroid tissue in the specimen and differentiate the "abnormal" from "normal" gland. Morphologic criteria alone cannot be used because of polymorphic variation in hyperplasia in which pathologic glands may appear normal. Early identification of the recurrent laryngeal nerve allows for a safer neck exploration by alerting the surgeon to the location and course of the nerve. A bilateral approach does not contribute increased morbidity from recurrent laryngeal nerve injury.

Adolescent↗

Primary hyperparathyroidism. A surgical perspective.

Primary hyperparathyroidism is a common disorder and one that can usually (approximately 95%) be successfully treated by parathyroidectomy. PTH assays have become quite accurate for confirming the diagnosis. In patients with malignancy-associated hypercalcemia, parathyroid-like protein levels are usually increased, and radioimmunoassays being developed to quantitate serum levels of this protein will make the diagnosis easier. Treatment for a parathyroid adenoma is removal of the tumor and identification of the normal parathyroid glands. Treatment for primary or secondary hyperplasia is usually subtotal parathyroidectomy. Recurrent hyperparathyroidism is uncommon, except in patients with familial hyperparathyroidism, MEN-1 parathyroid carcinoma, or renal failure and secondary hyperparathyroidism. Persistent hyperparathyroidism is more common and is usually due to surgeon inexperience, but it is also caused by ectopically situated parathyroid glands, multiple abnormal parathyroid glands, or supranumerary parathyroid glands. Preoperative localization studies using ultrasound, thallium-technetium scanning, MRI, or CT scanning are reliable in patients with solitary parathyroid adenomas, but often fail to detect all of the abnormal parathyroid tissue in patients with multiple abnormal parathyroid glands. Intraoperative use of urinary cyclic AMP assays and rapid PTH assays have recently been used experimentally during parathyroid explorations to determine whether all hyperfunctioning parathyroid tissue has been removed, but these methods are not yet reliable or fast enough to be generally accepted. Most patients with primary hyperparathyroidism who are successfully treated by parathyroidectomy experience psychological, clinical, and metabolic benefits.

Calcium↗

Modulation of the Ca2+-sensing function of parathyroid cells in vitro and in hyperparathyroidism.

When raising the extracellular Ca2+ concentration stepwise from 0.5 to 3.0 mM, bovine parathyroid cells reacted with initial transient and sustained elevations of the cytoplasmic Ca2+ concentration (Ca2+i), as well as more than 50% inhibition of parathyroid hormone (PTH) release. Human parathyroid adenoma cells and bovine cells cultured for 1 day or exposed to a low concentration of a monoclonal antiparathyroid antibody exhibited right-shifted dependencies of PTH release and Ca2+i on extracellular Ca2+ and reduced Ca2+i transients. The protein kinase C activator 12-O-tetradecanoylphorbol-13-acetate (TPA) further right-shifted the dose response relationship for Ca2+ regulated Ca2+i of the adenoma cells, whereas the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) tended to normalize it, without affecting Ca2+i of normal bovine cells. In cells from an oxyphil adenoma and a parathyroid carcinoma as well as in bovine cells cultured 4 days or exposed to a high concentration of the antiparathyroid antibody, there were no Ca2+i transients, very small increases in steady-state Ca2+i and nonsuppressible PTH release. The results suggest that reduced availability of a putative Ca2+-receptor and increased protein kinase C activity may be important factors in the decreased Ca2+ sensitivity of abnormal parathyroid cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Looking at calcimimetics impact on hypercalcemia of immobilization: hypotheses and a case study.

For the treatment of secondary hyperparathyroidism (HPTH-II) in dialysis patients and hypercalcemia in patients with parathyroid carcinoma. Calcimimetics are a new class of drugs approved in the European Community and the United States by the Food and Drug Administration that were designed to suppress parathyroid hormone (PTH) levels with a simultaneous reduction in serum calcium and phosphorus levels, and calcium phosphorus product (Ca x P). Hypocalcemia is a frequent finding during the correction phase of the HPTH-II with calcimimetics. By contrast, the appearance of a hypercalcemia has yet to be described. In this paper, we report a case of severe hypercalcemia of immobilization in a 40-year-old hemodialyzed woman treated by cinacalcet HCl for a severe HPTH-II (PTH>1,000 pg/mL). A kidney transplantation recipient 1983 to 1995, she was diagnosed with Charcot-Marie Tooth disease in 1991. She had multiple orthopedic interventions for kidney-related osteoarticular problems probably favored by the kidney graft and the immunosuppressive treatment. While she was receiving the maximum dose of 180 mg/day of cinacalcet HCl and PTH at 443 pg/mL, she needed to be hospitalized for a right hip prothesis. Two weeks after the intervention she developed a symptomatic hypercalcemia of 3.57 mmol/L which was resistant to several measures including lowering the calcium concentration in the dialysate, withdrawing all vitamin D and calcium supplementation and the administration of calcitonin. Her serum calcium level was finally stabilized in the 2.37-2.95 mmol/L by administration of a single intravenous dose of pamidronate. This observation illustrates that the pharmacological activation of the parathyroid CaR and other putative CaR on bone cells by calcimimetics did not protect against the occurrence of hypercalcemia of immobilization favored by a severe HPTH-II in a hemodialysis patient.

Adult↗

Significance of the parathyroid hormone-related protein expression in breast carcinoma.

BACKGROUND: Parathyroid hormone-related protein (PTHrP) is produced by various neoplasms and is known to be a causative factor of hypercalcemia of malignancy. It has also been suggested to act as a cytokine for tumor progression. The purpose of this study was to clarify the significance of PTHrP expression in breast carcinoma. METHODS: PTHrP expression was examined in 177 surgically resected breast carcinoma specimens by immunohistochemistry using a monoclonal antibody against the for PTHrP, The relationship of PTHrP expression with clinicopathological factors was analyzed and the clinical courses of the patients are reported. RESULTS: Positive PTHrP staining was detected in 113 ( 64%) of the breast tumors. Among the positive cases, 36 (32%) of the tumors clearly showed strong expression. When the PTHrP expression was divided into three categories, a significant positive relationship was found between PTHrP expression and histological grade of tumor. PTHrP expression was also significantly related to bone metastasis but the staining degree of PTHrP was not. The patients with positive PTHrP tended to have poor outcome in proportion to the staining degree. Univariate analysis demonstrated a significantly shorter overall survival for patients expressing PTHrP, and in multivariate analysis showed that PTHrP status and nodal status were associated with a significantly shorter overall survival. CONCLUSION: Our results suggest that PTHrP expression is not only correlated with bone metastasis but is also related to the progression of breast carcinoma, and that overexpression of PTHrP may be a potential prognostic factor for human breast carcinoma.

Adult↗

Epidermal growth factor receptors in parathyroid tumors.

Hyperparathyroidism is caused by parathyroid adenomas, hyperplastic parathyroid glands, or rarely parathyroid carcinoma. Membrane receptors to epidermal growth factor (EGF), a growth-stimulating polypeptide, have been shown in other endocrine tissues such as thyroid, breast, and ovary, but not in parathyroid glands. Therefore we studied abnormal parathyroid glands from fourteen patients for the presence of EGF receptors. The binding of radioiodine-labeled EGF to the crude membrane fractions was studied using competitive inhibition with unlabeled EGF. In ten patients with solitary parathyroid adenomas, seven adenomas had no EGF binding, three had low affinity EGF binding with dissociation constants (Kd) of 28 to 148 nM and maximal specific binding (Bmax) of 285 to 1944 fmole/mg protein. In two patients with multiple adenomas, a high affinity EGF binding with Kd of 0.28 to 2.8 nM and Bmax of 6.7 to 43 fmole/mg protein was found. In one patient with hyperplastic parathyroid glands secondary to renal failure, a high affinity EGF binding with Kd of 1.7 nM and Bmax of 18 fmole/mg protein was found. In one patient with persistent hyperparathyroidism following a successful renal transplant (tertiary hyperparathyroidism), a low affinity EGF binding with Kd of 25 nM and Bmax of 219 fmole/mg protein was found. The binding of EGF did not correlate with the preoperative serum calcium or PTH levels. Thus, hyperplastic parathyroid glands (either primary or secondary) have high affinity EGF receptors whereas solitary parathyroid adenomas do not.

Adenoma↗

The expression of parathyroid hormone messenger RNA in normal and abnormal parathyroid tissue.

The distribution and expression of preproparathyroid hormone (PTH) mRNA were investigated in parathyroid tissue from 57 parathyroidectomy specimens. PTH mRNA was detected by in situ hybridization using digoxigenin-labelled oligonucleotide probes. Cell morphology was seen to correlate with PTH mRNA expression. Strong expression of PTH mRNA was confined to cells which on haematoxylin and eosin staining had large vesicular nuclei. These included both vacuolated and non-vacuolated cells. Chief cells with small dark nuclei and scanty cytoplasm had little or no expression. In both adenoma and chief cell hyperplasia, the striking difference from normal was the greatly increased proportion of cells expressing PTH mRNA. In adenomas, the rim of uninvolved parathyroid tissue showed PTH mRNA expression similar to that of normal parathyroid. In hyperplasia, there was frequently concordance of staining within individual nodules. The findings establish morphological criteria for activity of parathyroid tissue and support current concepts of the different pathogenesis of hyperplasia and adenoma. The expression of PTH mRNA in oxyphil change and parathyroid carcinoma was also investigated.

Humans↗

Deletion of 11q23 and cyclin D1 overexpression are frequent aberrations in parathyroid adenomas.

Hyperparathyroidism may result from parathyroid hyperplasia or adenoma, or rarely from parathyroid carcinoma. Pericentromeric inversion of chromosome 11 that results in activation of the P:RAD1/cyclin D1 gene and tumor suppressor gene loss have been described as genetic abnormalities in the evolution of parathyroid neoplasms. We studied tissue samples taken from primary parathyroid hyperplasia, parathyroid adenoma, and histologically normal parathyroid tissue by comparative genomic hybridization, fluorescent in situ hybridization, and immunohistochemistry for cyclin D1. DNA copy number changes were infrequent in primary hyperplasia (4 of 24, 17%), but common in adenomas (10 of 16, 63%; P: = 0.0059). The most common change was deletion of the entire chromosome 11 or a part of it, with a minimal common region at 11q23. This change was present in five (31%) adenomas and two (8%) primary hyperplasias. Fluorescent in situ hybridization confirmed the presence of both MEN1 alleles located at 11q13 despite deletion of 11q23 in all three cases studied. Cyclin D1 was overexpressed in six (40%) of the 15 adenomas studied, whereas none of the 27 hyperplasias (P: = 0.0010) nor the five histologically normal tissue samples overexpressed cyclin D1. Either DNA copy number loss or cyclin D1 overexpression was present in 13 (81%) of the 16 adenomas. We conclude that DNA copy number loss and cyclin D1 overexpression are common in parathyroid adenomas. The region 11q23 is frequently lost in parathyroid adenomas and occasionally in parathyroid hyperplasias, and this suggests the possibility that a tumor suppressor gene that is important in their pathogenesis is present on 11q23.

Adenoma↗

Familial isolated hyperparathyroidism: a distinct genetic entity with an increased risk of parathyroid cancer.

Familial isolated hyperparathyroidism (FIHP) is a rare heritable disorder characterized by hypercalcemia, inappropriately high PTH levels, and isolated parathyroid tumors with no evidence of hyperfunction of any other endocrine tissues. To establish whether FIHP exists as a distinct disease entity or represents a variant of any of the known multiple endocrine neoplasia (MEN) syndromes, we tested 19 members of a large, well characterized family with FIHP in which the disease is transmitted through 4 generations in an autosomal dominant fashion. Fourteen DNA markers at 10 polymorphic loci closely linked to the MEN1 locus on the long arm of chromosome 11 and 5 markers close to the MEN2A gene on chromosome 10 were tested using Southern blot analysis and polymerase chain reaction-based techniques. Additionally, two polymorphic markers (Mir1 and Mir2) within the prepro-PTH gene on the short arm of chromosome 11 were analyzed using denaturant gradient gel electrophoresis. Linkage was clearly excluded between FIHP and the MEN1 and MEN2A loci as well as to the PTH gene. Comparison of constitutional and tumor genotypes showed that constitutional heterozygosity was retained for markers in the MEN1 and MEN2A regions as well as to the PTH gene in 4 tumors from 3 affected members. In 1 individual, a parathyroid carcinoma was found after recurrence of hypercalcemia. We, therefore, propose that autosomal dominant FIHP can occur as a genetically and clinically distinct entity with an increased risk of malignant transformation of parathyroid tumors.

Adolescent↗

Multiple endocrine neoplasia type 2-associated RET proto-oncogene mutations do not contribute to the pathogenesis of sporadic parathyroid tumors.

BACKGROUND: Parathyroid disease occurs sporadically or as part of hereditary multiple endocrine neoplasia (MEN) syndrome. The aim of this study was to evaluate the possible role of the RET proto-oncogene not only in hereditary MEN 2-associated hyperparathyroidism but also in different forms of sporadic hyperparathyroidism. METHODS: We investigated 22 patients with parathyroid disease whose family history and results of laboratory and clinical examinations excluded MEN 2 syndrome. DNA extractions of histologically confirmed tumor tissue of patients with primary hyperparathyroidism (n = 18), renal hyperparathyroidism (n = 2), and parathyroid carcinoma (n = 2) were performed. Using solid phase DNA sequencing, mutation analysis of polymerase chain reaction amplified products focused on exons 10, 11, and 16 of the RET proto-oncogene. Parathyroid tissue from four patients with known MEN 2A served as positive controls. RESULTS: No mutations of the codons 609, 611, 618, 620, 634, and 918 were found in the sporadic parathyroid tumors analyzed. DNA sequencing revealed heterozygous mutations in codon 634 of the RET proto-oncogene in four parathyroid glands from four patients with MEN 2A. CONCLUSIONS: Mutations of the RET proto-oncogene contributing to MEN 2 syndromes are absent in sporadic parathyroid tumors. Our data in conjunction with the literature suggest at least three different modes of tumorigenesis in parathyroid disease.

Adenoma↗

Parathyroid hormone and calcitonin in serum of patients with mammary carcinoma.

Immunoreactive parathyroid hormone and calcitonin in serum were measured in 34 normocalcemic patients with mammary carcinoma. The mean value of parathyroid hormone was significantly higher in 26 patients with bone metastases than in 8 patients without (p less than 0.025). One patient with bone metastases had slightly raised calcitonin in serum. No difference as to parathyroid hormone values between the groups of previously irradiated and non-irradiated patients was found. A possible explanation of the normocalcemic hyperparathyroidism is presented.

Adult↗

[Therapeutic agents for disorders of bone and calcium metabolism. The calcimimetic cinacalcet HCl].

Calcimimetics drug such as cinacalcet suppress the secretion of parathyroid hormone by sensitizing parathyroid calcium receptors to extracellular ionized calcium. Standard treatment for secondary hyperparathyroidism is associated with the risk of hypercalcemia, but cinacalcet don't induce elevation of serum calcium. And some studies were reported the use of cinacalcet not only to manage primary hyperparathyroidism, but also secondary hyperparathyroidism in nondialyzed stage, renal transplant patients and parathyroid carcinoma.

Cinacalcet↗

Hyperparathyroidism.

Primary hyperparathyroidism is the most prevalent cause of hypercalcemia. Although renal stone disease and osteitis fibrosis were prominent complications of this disorder in the past, the advent of biochemical screening has resulted in earlier detection. This has changed the clinical presentation of primary hyperparathyroidism, so that as many as 80% of patients do not have any sign or symptom that can be attributed solely to the disease. Improvement in assays for PTH has allowed for accurate bio-chemical diagnosis in over 90% of cases. Neck exploration is the treatment of choice for any patient who presents with signs, symptoms, or complications of hypercalcemia or hyperparathyroidism. Medical therapy is indicated in patients who either cannot undergo surgery because of medical contraindication, failed prior neck surgery, unresectable parathyroid carcinoma or simply refuse surgery. Medical therapy is not optimal, although sex steroid replacement therapy in the postmenopausal woman has met with some success. Calcitonin, phosphate, and bisphosphonates may be used, but their long-term efficacy is not clear. Recent studies have suggested that a large proportion of patients with asymptomatic primary hyperparathyroidism do not demonstrate progression of disease in terms of renal dysfunction, bone disease, or biochemical changes in calcium or PTH. Guidelines have been established for medical follow-up of such patients. If any such patient develops signs or symptoms during medical follow-up, surgery is then indicated.

Calcitonin↗