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Results for “Parathyroid Neoplasms”

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PubMed1979

[Superselective parathyroid hormone determination--a reliable diagnosis of the location of endocrinological active parathyroid neoplasms].

The importance of superselective catheterization of the small jugular veins for PTH-radioimmunoassay is shown as an improvement of the preoperative localization technique. Since May 1976 in 20 patients the diagnosis of pHPT could be established. Our own experiences with the method of small vein sampling combined with the radioimmunoassay demonstrate that a reliable localization of overactive parathyroid tumours is possible.

Humans↗
PubMed2003

Parathyroid neoplasms: clinical, histopathological, and tissue microarray-based molecular analysis.

We studied 45 patients with typical and 8 with atypical parathyroid adenomas as well as 20 with parathyroid carcinomas. Clinical, pathological, and molecular analyses were conducted on all adenomas. Clinical data were analyzed for 20, histopathologic slides for 16, and tissue specimens for 8 patients with carcinoma. Molecular expression profiles were investigated by immunohistochemistry (IHC) for Ki-67, p53, mdm2, p21, Bcl-2, cyclin D1, and p27 on paraffin-embedded tissues arrayed on tissue microarrays. Trabecular growth and vascular, capsular, and soft-tissue invasion were characteristic of parathyroid carcinomas but not of typical adenomas. No adenomas recurred. Seventy-four percent of carcinomas recurred, most in the neck. Seventy-nine percent of patients with such illness died of disease after an indolent, multiply recurrent course responsive to repeated resections; the 5-year survival rate was 50%. High Ki-67 proliferative index was seen in 2% of adenomas and 25% of carcinomas, whereas p27 expression was present in 80% of adenomas and 18% of carcinomas. The molecular phenotype, p27(+)Bcl-2(+)Ki-67(-)mdm2(+), was observed in 76%, 29%, and 0% of typical and atypical adenomas and carcinomas, respectively. The complexity of molecular phenotypes increased with tumor aggressiveness. Parathyroid carcinoma is an aggressive disease with a propensity for multiple recurrences. It is characterized by capsular, vascular, and soft-tissue invasion. Recurrence portends poor outcome. Molecular markers, Ki-67 and p27, may distinguish parathyroid carcinoma from adenoma. The molecular phenotype, p27(+)Bcl-2(+)Ki-67(-)mdm2(+), appears to be unique to nonmalignant parathyroid tumors, and multimarker phenotypes are more complex in carcinomas.

Adenoma↗
PubMed2026

Single-cell and spatial transcriptomics define a progenitor subpopulation and fibroinflammatory niche at the leading edge of parathyroid carcinoma.

Parathyroid carcinoma (PC) is a rare but clinically aggressive endocrine malignancy with limited treatment options and a poorly defined tumor microenvironment (TME). To elucidate its cellular heterogeneity and spatial architecture, we integrated single-cell and spatial transcriptomic profiling with whole-exome sequencing and multiplex immunohistochemistry on eight parathyroid neoplasm specimens, including PC, parathyroid adenoma, and atypical parathyroid tumor. We identified a distinct progenitor-like endocrine subpopulation (Ca-1) enriched in CDC73-mutant PC, exhibiting stem-like properties, elevated cell cycle activity, and pronounced genomic instability. Spatial mapping revealed that Ca-1 cells preferentially localize at the leading edge, forming a fibroinflammatory niche characterized by the enrichment of inflammatory cancer-associated fibroblasts (iCAFs) and SPP1+ macrophages. Within this niche, the dipeptidyl peptidase 4 (DPP4) is selectively expressed in Ca-1 cells and iCAFs, implicating a potential paracrine axis driving stromal remodeling and immunosuppression. These findings suggest that a spatially organized ecosystem may promote PC progression through TME remodeling and highlight the DPP4-CXCL2 axis as a candidate pathway for future investigation in aggressive parathyroid neoplasms.

Humans↗
PubMed1994

p53 abnormalities in human parathyroid carcinoma.

Two cell cycle regulators have been implicated in the pathogenesis of parathyroid neoplasms: rearrangement/overexpression of the PRAD1/cyclin D1 gene in parathyroid adenomas and inactivation of the retinoblastoma tumor suppressor gene in parathyroid carcinomas. We examined parathyroid tumors for evidence of molecular genetic abnormalities in another cell cycle regulator, the p53 tumor suppressor gene. Allelic loss of the p53 gene was observed in parathyroid carcinomas from 2 of 6 genetically informative patients. Moreover, 2 of 9 patients' parathyroid carcinomas had nuclear p53 protein detectable by immunohistochemical analysis, a finding that often reflects mutational stabilization of the p53 protein. Of these two p53-immunopositive carcinomas, 1 had p53 allelic loss and 1 was genetically uninformative. In contrast, none of 20 informative parathyroid adenomas exhibited p53 allelic loss; 1 of 19 adenomas had a focal region of nuclear p53 protein staining. Single strand conformation polymorphism analysis of exons 5-9 of the p53 gene did not reveal mutations in any parathyroid neoplasm, suggesting that such mutations in parathyroid tumors may lie outside of these conserved regions. The finding of both p53 allelic loss and abnormal p53 protein expression in parathyroid carcinomas implicates p53 in the pathogenesis of a subset of these tumors.

Adenoma↗
PubMed1994

Use of preoperative fine-needle aspiration in patients undergoing reoperation for primary hyperparathyroidism.

BACKGROUND: Neck reexploration for primary hyperparathyroidism has a lower success rate and greater morbidity than initial exploration because of scarring and distortion of tissue planes and the possibility of a parathyroid neoplasm located in an ectopic or unusual position. Although the use of standard noninvasive imaging studies for reoperative parathyroid surgical procedure is well accepted, the use of invasive studies to localize parathyroid neoplasms, particularly percutaneous aspiration of potential lesions, is controversial. In this report we analyze the results and morbidity in patients undergoing fine-needle aspiration before neck reexploration. METHODS: From 1982 to 1993, 255 patients underwent reexploration for persistent or recurrent hyperparathyroidism at the National Institutes of Health. Of these 255 patients 42 underwent 44 preoperative fine-needle aspirations by ultrasonography or computed tomography guidance in an attempt to localize a parathyroid neoplasm. The aspirated contents were then analyzed for parathyroid hormone content. RESULTS: Of the 44 aspirations 26 (59%) were true positives with no false positives. Of 18 negative fine-needle aspirations, 11 (25%) were false negatives, and seven (16%) were true negatives. The specificity and sensitivity of percutaneous fine-needle aspiration were 100% and 70%, respectively. CONCLUSIONS: Percutaneous fine-needle aspiration for parathyroid hormone is a safe, well-tolerated technique that is highly specific and allows a directed surgical resection avoiding further invasive workup when the aspirate is positive.

Adult↗
PubMedDate not supplied

[Cervico-mediastinal hematoma secondary to extracapsular hemorrhage of parathyroid carcinoma. Clinical case and review of the literature].

Extracapsular parathyroid haemorrhage is a rare but ominous occurrence, which may cause cervico-mediastinal haematoma and a severe calcaemia imbalance. We identified only 23 cases reported in the literature and these were always secondary to adenoma, hyperplasia or cysts, and never to carcinoma. We describe a case of a 56-year-old man who was admitted to our Institute because of the sudden development of an anterior neck swelling, together with dysphagia, dyspnoea and hoarseness. Physical examination revealed a large ecchymosis extending from the anterior neck to the upper chest, while the early symptoms had disappeared. Laboratory studies, ultrasonography and 99mtTC-Sestamibi scintiscan demonstrated the presence of primary parathyroidism due to a right inferior parathyroid neoplasm. At operation, the parathyroid was excised en bloc with the right thyroid lobe because they were joined together by an extensive fibrous reaction. Histological examination showed a well-differentiated parathyroid carcinoma with evidence of recent haemorrhage. To the best of our knowledge this is the first case of extracapsular haemorrhage due to a parathyroid carcinoma. In summary, although parathyroid haemorrhage is a rare condition, it should always be suspected when a painful mass or diffuse swelling suddenly occurs in the anterior neck, with or without ecchymosis, especially when serum calcium and phosphorus are abnormal.

Carcinoma, Papillary↗
PubMed2000

Update on the management of parathyroid tumors.

Parathyroid tumors are virtually always benign with an estimated incidence of parathyroid carcinoma causing hyperparathyroidism in only .017% of cases. Virtually all parathyroid neoplasms, including the rare parathyroid carcinoma, are functional and discussion of the management of parathyroid tumors is tantamount to the discussion of primary hyperparathyroidism. The biochemical diagnostic criteria with rare exception is definitive, and the key issue with this functional benign endocrine neoplasm is when to recommend operation and how to ensure optimal results in this curable disease. Patients symptomatic with nephrolithiasis, significant osteoporosis, bone pain, and in some cases constitutional symptoms should undergo a surgical therapy. Also, patients with markedly abnormal laboratory values including a calcium 12.0 mg/dL, or 24-hr urinary calcium >400 mg/day should be treated surgically. The sestamibi nuclear medicine scan has become the best tool available for imaging of abnormal parathyroid glands. This study is positive between 60% and 90% of initial operations and in between 40% and 70% of reoperations. For multi-gland parathyroid disease or hyperplasia, the sensitivity of this test is decreased. Understanding of the ectopic locations of parathyroid adenoma is of utmost importance in the conduct of the parathyroidectomy. For the rare patients with parathyroid carcinoma, aggressive surgical resection with en bloc removal of any adjacent invading structures is the best chance for cure leading to 10-year survival rates of 49%.

Adult↗
PubMed2000

Three Cases of Primary Hyperparathyroidism (PHP) with Prior Failed Surgery Where Culprit Lesions Were Identified by 11C-Methionine Positron Emission Tomography (PET) and Accurately Localized with PET-MRI Coregistration.

This report describes 3 cases of primary hyperparathyroidism (PHP) in which presurgical localization of the culprit lesions was essential. In 2 cases, the initial parathyroid surgery had failed to restore normal levels of either parathyroid hormone (PTH) or calcium (Ca(++)). In each of these cases experienced surgeons performed the initial parathyroid explorations. In one of these 2 cases, a positive 99mTc sestamibi (MIBI) scan was obtained prior to the initial surgery. 11C-methionine-positron emission tomography (PET) scans and magnetic resonance imaging (MRI) studies were performed prior to repeat surgical exploration with these data coregistered (the digital data sets from each modality were spatially aligned). In each case, the 11C-methionine-PET studies identified metabolically active tumors whose anatomic locations were accurately determined on the PET coregistration. The third case had previously undergone a thyroidectomy and modified right radical neck dissection for removal of a thyroid cancer and regional lymph node metastases. Following the diagnosis of PHP, MIBI, thallium, and ultrasound studies were performed and were all negative. 11C-methionine-PET and MRI were performed identifying a parathyroid adenoma in the prior surgical field. In these 3 cases culprit lesions were readily located at surgery, excised and confirmed as parathyroid neoplasms. This 11C-methionine PET-MRI coregistration technique appears to be effective at localizing parathyroid neoplasms in high risk patients with PHP in the setting of initially failed surgery or when PHP occurs following previous regional neck surgery.

Journal Article↗
PubMed1981

Surgical resection of metastatic parathyroid carcinoma.

The incidence of parathyroid carcinoma is no more than 0.5 to 3% of parathyroid neoplasms and can often be cured by an adequate initial surgical excision. If the carcinoma has already spread outside the capsule or is implanted at surgery, the chance of local recurrence is high, but is best managed by surgical resection of any recurrence. Distant metastases occur less frequently, but the associated hypercalcemia is poorly controlled by hormonal, chemotherapy, or radiation therapy. Though the chance for cure is small, a review of previously reported cases and our own experience leads us to encourage an aggressive search for metastases, and if possible, surgical resection. If not curative, this approach will often allow prolonged palliation of the effect of hypercalcemia.

Adenocarcinoma↗
PubMed2001

Parathyroid carcinoma.

Although parathyroid neoplasms are common and cause primary hyperparathyroidism, parathyroid carcinoma is a rare entity. At times it can be difficult to diagnose. Patients with parathyroid carcinoma usually present with profound symptoms of hyperparathyroidism and highly elevated serum calcium and parathyroid hormone (PTH) levels. At the time of neck exploration, a large, gray-white, locally invasive tumor is commonly encountered. The course of patients with parathyroid carcinoma is variable; unfortunately, more than 50% have persistent or recurrent disease due to regional or distant disease. Surgical resection is the principal treatment for patients with parathyroid carcinoma. The optimal surgical treatment is en bloc tumor resection with ipsilateral thyroid lobectomy when the diagnosis is suspected and until it is proven otherwise. Patients who have persistent or recurrent parathyroid carcinoma should have localizing studies to identify loco-regional or distant tumor sites. Reoperation in patients with localized parathyroid carcinoma is recommended because it relieves symptoms of hypercalcemia, and it normalizes serum calcium and PTH levels in most patients. For patients who have unresectable parathyroid carcinoma, a protocol-based treatment with chemotherapy and external radiotherapy should be considered. Additionally, second-generation bisphosphonates and the NPS R-568 calcimimetic agent may be useful in normalizing the serum calcium and improving symptoms of hypercalcemia. However, they do not treat the tumor and are rarely effective in the long term.

Adenocarcinoma↗
PubMed2001

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↗