Parathyroid Carcinoma

Department of Endocrinology and Metabolism, University of Pisa, Pisa, Italy.
Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research (Impact Factor: 6.83). 01/2009; 23(12):1869-80. DOI: 10.1359/jbmr.081018
Source: PubMed


The best opportunity to cure parathyroid carcinoma is to diagnose it before or at the time of parathyroid surgery and for the tumor to be completely removed at the time of the initial operation. Because the diagnosis is often not clear at the time of presentation, recent attempts to distinguish between benign and malignant disease both by genetic and immunohistological analyses are promising. The disease is indolent but progressive. Attempts to remove local recurrences and distant metastases can provide short- and long-term control. Other therapeutic approaches with chemotherapy and radiotherapy are not helpful. Available medical therapy targets the consequence of the disease (hypercalcemia) rather than the disease itself.

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Available from: Shonni J Silverberg, Jun 03, 2015

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Article: Parathyroid Carcinoma

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    • "Parathyroid carcinoma is a rare malignancy, affecting less than 1% of patients with primary hyperparathyroidism [1, 2]. It is usually associated with severe clinical presentations with markedly elevated levels of serum calcium >14 mg/dL and parathyroid hormone (PTH) levels from >5 to 10 times the upper normal limit [3]. Therefore, almost all the patients are symptomatic at the time of presentation [4]. "
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    ABSTRACT: Background. Fine-needle aspiration (FNA) can cause misdiagnosis of cytomorphological findings between parathyroid and thyroid lesions. Case Presentation. A 31-year-old man presented with a palpable neck mass on the right thyroid lobe. FNA cytology was reported as intrathyroidal lymphoid hyperplasia. After 5 years, repeated FNA was done on the enlarged nodule with result of Hürthle cell lesion. Prior to right lobectomy, laboratories revealed elevated serum calcium and parathyroid hormone (PTH). Careful history taking revealed chronic knee pain and ossifying fibroma at the maxilla. Ultrasonography showed a 2.8 cm mass inferior to right thyroid lobe. Pathology from en bloc resection was parathyroid carcinoma and immunohistochemical study revealed positivity for PTH. Genetic analysis found somatic mutation of CDC73 gene in exon1 (c.70delG) which caused premature stop codon in amino acid 26 (p.Glu24Lysfs*2). The final diagnosis was hyperparathyroidism-jaw tumor syndrome. Conclusions. FNA cytology of parathyroid can mimic thyroid lesion. It is important to consider and correlate the entire information from clinical history, laboratory, imaging, and FNA.
    Case Reports in Endocrinology 08/2014; 2014:680876. DOI:10.1155/2014/680876
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    • "In this study, 10 of 11 patients with PC had a parathyroid mass larger than 3.0 cm, and ROC analysis showed that the sensitivity and specificity for PC was 90.9% and 92.1%, respectively. This result is in agreement with previous findings that PC are usually larger than 3 cm and may be palpable (23). Interestingly, the median tumor size at the time of diagnosis in 286 cases of PC treated in the USA from 1985 to 1995 was approximately 3.3 cm (8). "
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    ABSTRACT: This study was conducted to review the clinical characteristics of parathyroid carcinoma (PC) and to evaluate potential preoperative predictive factors for PC in patients with primary hyperparathyroidism (PHPT). We performed a retrospective review of electronic medical records of 194 patients with pathologically confirmed PHPT in affiliated teaching hospitals of Seoul National University from January 2000 to March 2011. Adenoma was diagnosed in 171 patients, hyperplasia in 12, and carcinoma in 11. Several biochemical measurements were higher in patients with PC than in patients with benign disease, including serum total calcium (P < 0.001), intact parathyroid hormone (P = 0.003), and alkaline phosphatase (ALP) (P < 0.001). Tumors were larger in PC than in benign disease (P < 0.001). Multivariate analysis revealed that serum ALP level (P < 0.001) and tumor size were associated with PC (P = 0.03). Tumor size and serum ALP level were evaluated as preoperative predictive factors for PC using ROC analyses: a tumor size of 3.0 cm (sensitivity 90.9%, specificity 92.1%) and serum ALP level of 285 IU/L (83.3%, 97.0%) had predictive value for the diagnosis of PC in patients with PHPT. In conclusion, elevated serum ALP and a large parathyroid mass at the time of diagnosis can be helpful to predict PC in patients with PHPT.
    Journal of Korean medical science 08/2012; 27(8):890-5. DOI:10.3346/jkms.2012.27.8.890 · 1.27 Impact Factor
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    ABSTRACT: Primary hyperparathyroidism (PHPT) is one of the most frequent endocrinological disorders. In PHPT, there is abnormal regulation of parathyroid hormone (PTH) by calcium, which translates into inappropriately high PTH secretion for the level of calcemia. Most patients with PHPT have increased serum PTH levels, with increases in serum calcium, especially ionic calcium. The incidence of PHPT rises with age, the mean age at diagnosis being 55 years. This disorder affects mainly women with a female-to-male ratio of approximately 3:1. Most (80-85%) of cases are produced by chief cell parathyroid adenomas. The factors involved in the genesis of PHPT are largely unknown. Gene mutations affecting oncogenes (cyclin D1, RET) or tumor suppressor genes (MEN1, HRPT2) are found in a minority of cases. These mutations are especially important in familial forms of PHPT, such as multiple endocrine neoplasia syndrome (MEN1, MEN2A). No mutations affecting the calcium-sensing receptor (CaSR) or vitamin D receptor (VDR) gene have been found. In parathyroid adenomas and hyperplasias, there may be abnormal Wnt signalling, with mutations of the coreceptor LRP5 gene and β-catenin accumulation. Expression of the Klotho protein, which intervenes in serum calcium regulation, is reduced. Low levels of 25(OH) vitamin D frequently coexist, although whether vitamin D deficiency plays a pathogenic role in PHPT is unknown.
    Endocrinología y Nutrición 04/2009; 56. DOI:10.1016/S1575-0922(09)70849-6
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