Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We encountered an unusual case of hyperparathyroidism with both hemosiderin deposits on the ribs and low intensity on T2-weighted magnetic resonance imaging (MRI) caused by a parathyroid adenoma with multiple brown tumors that mimicked metastatic bone tumor due to false positive results on computed tomography (CT) and Tc-99m sestamibi (MIBI) imaging. The patient, a middle-aged woman, had very high serum levels of calcium (14.1 mg/dl), alkaline phosphatase (9,369 IU/l) and intact-PTH (12,400 pg/ml), and a large tumor (2.5 cm in diameter) in the lower portion of the left lobe of the thyroid. Plain X-ray revealed a soft tumor in the left chest wall. On CT scan, there were multiple destructive masses in the ribs, including large intramedullary masses on both 3rd ribs. On MIBI scintigraphy, there was strong late uptake in the lower portion of the left cervical region, both 3rd ribs, and the left 7th, 8th, and 10th ribs. T2-weighted image MRI scans showed that both 3rd ribs had a low intensity with hemosiderin deposits. These findings suggested that the patient had hyperparathyroidism with multiple bone metastases due to carcinoma of the parathyroid gland. However, on pathology, the resected tumor of lower portion of the left lobe of thyroid was diagnosed as a parathyroid adenoma, and the tumors of the left 3rd and 7th ribs, as well as the right 2nd rib, were shown to be brown tumors. After resection, the patient's serum levels of calcium, alkaline phosphatase, and intact-PTH normalized. At 1.5-years follow-up, CT, MIBI, and MRI scans showed no abnormal findings. It is necessary to determine whether MRI can be used to distinguish between brown tumors and metastases caused by carcinoma of the parathyroid gland.
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PMID:Multiple brown tumors in primary hyperparathyroidism caused by an adenoma mimicking metastatic bone disease with false positive results on computed tomography and Tc-99m sestamibi imaging: MR findings. 1723 12

We report a 47-year-old women who presented to her general practitioner and our hospital with weight loss of unknown etiology. Eight years previously she had undergone a hemithyroidectomy for nodular goiter with one cold nodule. Laboratory results revealed hypercalcemia, evidence of primary hyperparathyroidism and computer tomography of the thorax showed bilateral pulmonary metastasis. After undergoing CT-guided biopsy of a metastasis, histology revealed an endocrine primary tumor with low parathyroid hormone expression. In view of the history, clinical and biochemical findings we diagnosed a recently metastasized functioning parathyroid carcinoma, which eight years previously has been labeled as a benign atypical thyroid adenoma. The patient underwent surgical resection of all detected metastases. Afterwards the serum calcium and parathyroid hormone levels normalized. Parathyroid carcinoma is an uncommon tumor. In the absence of pathognomonic diagnostic criteria a definitive pathological diagnosis of parathyroid carcinoma often is not possible. The treatment of parathyroid carcinoma is essentially surgical. Patients with parathyroid carcinoma mostly die from uncontrollable hypercalcemia rather than from other tumor-related complications.
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PMID:[Rare cause of hypercalcemia]. 1921 66

Treatment with cinacalcet and intravenous bisphosphonate has improved the previously often fatal prognosis of parathyroid cancer. We report two cases, of which one did not react to treatment and died within a short time-frame. In the other case, cinacalcet controlled serum calcium during a prolonged time period despite metastases. However, increasing doses of cinacalcet combined with more frequent intravenous bisphosphonate were necessary.
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PMID:[Management of serum calcium with cinacelet in parathyroid cancer]. 1981 29

Parathyroid cancer is an uncommon malignancy and rare cause of primary hyperparathyroidism (HPT) with a high morbidity and patient death in advanced cases usually resulting from intractable hypercalcemia. Inactivation of the HRPT2/CDC73 gene, encoding the putative tumor-suppressor protein parafibromin and discovered in the context of the hyperparathyroidism-jaw tumor (HPT-JT) syndrome, is a common, somatic event in most parathyroid cancers. Approximately 25% of patients with apparently sporadic parathyroid cancer carry germline HRPT2/CDC73 mutation. Germline DNA analysis for HRPT2/CDC73 mutation is recommended in all patients with parathyroid cancer because of the potential benefit for first-degree relatives, who should nevertheless undergo serum calcium screening. The histopathologic diagnosis of parathyroid cancer is nonspecific unless vascular, lymphatic, capsular, or soft tissue invasion is seen, or metastases are clinically evident. Immunohistochemical analysis of parathyroid tumors for loss of parafibromin expression offers promise as a diagnostic tool. En bloc tumor resection offers the highest chance of cure in patients with suspected parathyroid carcinoma. No adjuvant chemotherapy regimen has yet proven effective, and the role of local adjuvant radiotherapy is being evaluated. Metastatic disease can be palliated with surgical debulking. Medical therapy with the calcimimetic cinacalcet and bisphosphonates can ameliorate hypercalcemia in patients with inoperable disease.
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PMID:Parathyroid cancer. 2116 77

A case was a 67-year-old man, who presented an inferior limb lassitude approximately in January 2009. We noted a thyroid gland mass by examination and referred for a further checkup. Biochemical examination of blood showed hypercalcemia, a high iPTH level of 2,190. The cervical echography evidence showed a mass image of the border regular in the back of inferior pole of left thyroid gland. It also revealed a mass image with the calcification in the inferior pole of left lobe of thyroid gland at the same time. We performed aspiration biopsy cytology for a thyroid gland mass, and it was class IIIa. We also performed parathyroidectomy and left lobe of thyroid gland ablative surgery because of a diagnosis of the hyperparathyroidism confirmed a primary parathyroid adenoma. Preoperative pathological diagnosis was adenoma. However, histopathology laboratory findings showed it to be of adenocarcinoma of the parathyroid, which metastasized into the thyroid. Many times parathyroid cancer preoperative diagnosis is inconclusive. So we are reporting our experience with parathyroid cancer metastases to the thyroid for reference.
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PMID:[Experience of parathyroid cancer which required a differentiation from adenoma]. 2122 61

Parathyroid carcinoma (PTC) is a rare malignant disease that is usually hyperfunctioning, which produces an excess of parathyroid hormone. Hyperparathyroidism causes bone metabolism disorders, as osteopenia and sometimes brown tumors. Brown tumors are benign but locally aggressive bone lesions, whose differential diagnosis with metastases or other primary malignancies may be complicated. (99m)Tc-Sestamibi scan is the usual procedure for the detection of parathyroid pathology, with a sensitivity of 85-100% and specificity close to 100% in parathyroid adenomas, it having similar percentages in the detection of PTC. We present the case of a patient diagnosed of a malignant hyperparathyroidism associated with bone lesions in which the (99m)Tc-Sestamibi scan showed a false negative result in the detection of parathyroid condition. However, (18)F-FDG-PET/CT detected the PTC and helped in the differential diagnosis of associated bone lesions, which were finally confirmed as brown tumors.
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PMID:[False negative of the scintigraphy with 99mTc-sestamibi in parathyroid carcinoma with associated brown tumors. Contributions of the 18F-FDG-PET/CT]. 2134 24

Parathyroid carcinoma is a rare disease, which accounts for less than 1% of all case of primary hyperparathyroidism and is usually not detected until the time of surgery or thereafter. For most patients preoperative staging is not available. A radical excision remains the standard management; the place of adjuvant radiotherapy is not well established yet. Local recurrence and/or the metastases are unfortunately frequent. The present paper presents an up to date review of the literature illustrated by three clinical cases.
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PMID:Parathyroid carcinoma: a review with three illustrative cases. 2204 38

Parathyroid carcinoma is a rare disease in pediatric patients. We present a case of a 13-year-old girl who presented to the Thyroid Department for an asymptomatic palpable neck mass for 1 year. The high levels of calcium, ionized calcium, and parathyroid hormone level along with parathyroid scintigraphy studies suggested primary hyperparathyroidism. Parathyroid carcinoma was confirmed by biopsy and pathologic examination after resection. Six months postoperatively, persistent hypercalcemia and multiple lung metastases were found on computed tomography. Bilateral lung wedge resection was performed. En bloc resection for primary parathyroid carcinoma and aggressive resection of metastatic disease is the most effective treatment to control hypercalcemia.
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PMID:Parathyroid carcinoma with lung metastasis in a thirteen-year-old girl. 2270 2

Parathyroid carcinoma is a malignant neoplasm affecting 0.5% to 5.0% of all patients with primary hyperparathyroidism. Since it was first described by De Quervain in 1904 to this day, it continues to defy diagnosis and treatment because of its rarity, overlapping features with benign parathyroid disease, and lack of distinct characteristics. En bloc surgical extirpation of the tumor with clear margins remains the best curative treatment. Although prolonged survival is possible with recurrent or metastatic disease, cure is rarely achievable. Efficacy of adjuvant therapies, such as radiotherapy and chemotherapy, in management of persistent, recurrent, or metastatic disease has been disappointing.
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PMID:Parathyroid carcinoma: challenges in diagnosis and treatment. 2311 78

Parathyroid cancer is a rare, clinically aggressive cause of primary hyperparathyroidism, and whether these malignancies generally evolve from pre-existing benign adenomas or arise de novo is unclear. Furthermore, while inactivation of the CDC73 (HRPT2) tumor suppressor gene, encoding parafibromin, is a major contributor, other genes essential to parathyroid carcinogenesis remain unknown. We sought to identify genomic regions potentially harboring such oncogenes or tumor suppressor genes, and to gain insight into the origins and molecular relationship of malignant versus benign parathyroid tumors. We performed genome-wide copy-number and loss of heterozygosity analysis using Affymetrix 50K SNP mapping arrays and/or comparative genomic hybridization on 16 primary parathyroid carcinomas, local recurrences or distant metastases, and matched normal controls, from 10 individuals. Recurrent regions of allelic loss were observed on chromosomes 1p, 3, and 13q suggesting that key parathyroid tumor suppressor genes are located in these chromosomal locations. Recurrent allelic gains were seen on chromosomes 1q and 16, suggesting the presence of parathyroid oncogenes on these chromosomes. Importantly, the most common alteration in benign parathyroid adenomas, loss of 11q, was not found as a recurrent change in the malignant parathyroid tissues. Molecular allelotyping using highly polymorphic microsatellite markers provided further confirmation that the prevalence of 11q loss is markedly and significantly lower in carcinomas as compared with adenomas. Our observations provide molecular support for the concept that sporadic parathyroid cancer usually arises de novo, rather than evolving from a pre-existing typical benign adenoma. Furthermore, these results help direct future investigation to ultimately determine which of the candidate genes in these chromosomal locations make significant contributions to the molecular pathogenesis of parathyroid cancer.
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PMID:Allelic imbalance in sporadic parathyroid carcinoma and evidence for its de novo origins. 2343 13


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