Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With over 2 000 articles published on thyroid cancer between January 1, 2006 and September 10, 2007 it is difficult to offer an updated and complete review on this malignancy. Thus, I elected to summarize papers published in 2007 on topics frequently overlooked in other reviews or books, and papers that are likely to be followed by interesting developments. Papers include: 1) the accuracy and currency of websites on thyroid cancer; 2) the detection of the V600E BRAF mutation in very small papillary thyroid cancers that are detected histologically; 3) the relationship between thyroid cancer and Hashimoto's thyroiditis or hepatitis C virus, an association that appears to be nonrandom; 4) the not negligible frequency of coexistence of thyroid cancer with primary hyperparathyroidism; 5) the value of ultrasound elastography of thyroid nodules in distinguishing malignant form benign lesions; 6) the value of percutaneous ethanol injection in the treatment of thyroid or nodal recurrences of thyroid cancer; 7) the relatively benign course of intrathyroid metastases from renal cell carcinoma; 8) the exceedingly rare thyroid paraganglioma, though the rate of reports has increased recently; and 9) the increase in serum calcitonin caused by chronic alcoholism, an increase that cannot be reversed by three weeks of alcohol weaning.
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PMID:Update on thyroid cancer. 1849 Dec 51

Carney Complex (CNC) and Multiple Endocrine Neoplasia type 1 (MEN1) are forms of multiple endocrine neoplasia of dominant autosomal inheritance. Diagnosis of CNC occurs when two major criteria (lentiginoses, primary pigmented nodular adrenocortical disease, cardiac and cutaneous myxomas, acromegaly, testicular neoplasias, thyroid cancer) are observed and/or a major criterion associated with a supplementary criterion (affected relative, PRKAR1A gene mutation) occurs. On the other hand, diagnosis for MEN1 occurs through detection of two or more tumors located at the pituitary gland, parathyroid and/or pancreatic cells. The present case describes a 55 year-old male patient, diagnosed with acromegaly, primary hyperparathyroidism and papillary thyroid cancer, exhibiting components that meet the diagnostic criteria of both conditions described. Despite the occurrence of only one sporadic association or the acromegaly per se being responsible for the papillary cancer, new molecular mechanisms may not be ruled out.
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PMID:Possible association between Carney complex and multiple endocrine neoplasia type 1 phenotypes. 1916 94

A 51-year-old female patient presented with atypical chest pain, laryngo-oesophageal reflux, increased levels of serum calcium and parathyroid hormone. Ultrasonography showed a multinodular goiter with a prominent solid nodule in the lower left thyroid lobe and a solid hypoechoic nodule outside this area.Tc99m-sestamibi parathyroid scintigraphy was performed to investigate a primary hyperparathyroidism, revealing an area with increased uptake in the lower left thyroid lobe and another area with marked uptake lower than this level. Thyroid scintigraphy with 99mTc showed a cold nodule of the left lower pole. FNA of the thyroid nodule was positive for papillary carcinoma later verified by postoperative histopathology.This case underlines the need for a clinical high index of suspicion for synchronous hyperparathyroidism and thyroid cancer.
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PMID:Synchronous parathyroid adenoma and thyroid papillary carcinoma: a case report. 2006 98

Patient with primary hyperparathyroidism and papillary thyroid cancer was presented. The female patient, 45 years old, because of papillary thyroid cancer was treated in the typical way by total strumectomy with lymphadenectomy following by 1131 therapy and L-thyroxine suppressive therapy. After 9 years, during one of control routine examinations, the serum levels of calcium and parathormone were increased (Ca2+: 1.449 mmol/l; Ca: 2.91 mmol/l; PTH: 256 pg/ml). Primary hyperparathyroidism was diagnosed and the patient underwent the surgery in the anterior cervical region with removal of parathyroid adenoma, histopathologically confirmed. Serum PTH level together with calcium levels decreased into the normal range. The coexistence of primary hyperparathyroidism and thyroid non-medullary cancer was already reported, but in this case the time of the onset was delayed. Due to the fact that patients after the treatment of thyroid non-medullary cancer, especially after of the neck radiation or radioactive iodine therapy, are more exposed to develop hyperparathyroidism, complete and wide examinations, even many years after treatment of thyroid cancer, are needed.
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PMID:[Primary hyperparathyroidism in patient with thyroid papillary cancer--case report]. 2129 88

Concomitant papillary thyroid cancer and parathyroid adenoma is rare. We report a 55 years old female with papillary cancer admitted for surgery. Preoperative laboratory findings revealed hypercalcemia and then primary hyperparathyroidism. Thyroidectomy, neck dissection and excision of parathyroid adenoma were performed. Histological examination revealed parathyroid adenoma. Serum calcium returned to normal range after surgery. We recommend preoperative check of calcium in patients with thyroid cancer.
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PMID:Papillary thyroid carcinoma associated with parathyroid adenoma. 2283 91

Although the pathological relationship between parathyroid and thyroid diseases is common, an association between parathyroid adenoma and thyroid cancer is rare. Concomitant thyroid cancer in patients with primary hyperparathyroidism (pHPT) has been reported at varying frequencies. WE present here a 23-year-old man who had papillary thyroid carcinoma in the right thyroid lobe and a parathyroid adenoma in the left thyroid lobe, which were confirmed surgically.
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PMID:Concurrent papillary thyroid cancer and parathyroid adenoma as a rare condition: a case report. 2293 12

Multiple endocrine neoplasia type 2 (MEN2) is an autosomal-dominant cancer syndrome characterized by variable penetrance of medullary thyroid carcinoma(MTC), pheochromocytoma (PHEO), and primary hyperparathyroidism (PHPT). MEN2 consists of two clinical subtypes, MEN2A and MEN2B. Familial medullary thyroid cancer is now viewed as a phenotypic variant of MEN2A with decreased penetrance for PHEO and PHPT rather than a distinct entity. All subtypes are caused by gain-of-function mutations of the RET proto-oncogene. Genotype-phenotype correlations exist that help predict the presence of other associated endocrine neoplasms as well as the timing of thyroid cancer development. Recognition of the clinical entity in individuals and families at risk of harboring a germline RET mutation is crucial for the management and prevention of associated malignancies. Recent guidelines released by the American Thyroid Association regarding the management of MTC will be summarized in this chapter.
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PMID:Multiple endocrine neoplasia type 2. 2365 68

Primary hyperparathyroidism is a very rare complication following radioactive iodine therapy. There is typically a latency period of more than a decade following radiation exposure and, therefore, it is observed almost exclusively in adults. Consequently, pediatricians are not aware of the association. We present a case of primary hyperparathyroidism due to a solitary parathyroid adenoma occurring in an adolescent male two years following radioactive iodine treatment for papillary thyroid carcinoma. Periodic screening of serum calcium following ablative doses of radioactive iodine for thyroid cancer may be justified even in adolescents.
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PMID:Hyperparathyroidism two years after radioactive iodine therapy in an adolescent male. 2459 49

Epigenetics alterations are involved in tumorigenesis and have been identified in endocrine neoplasia. In particular, DNA methylation, microRNAs deregulations and histone methylation impairment are detected in tumors of the parathyroid glands. Parathyroid tumors are the second most common endocrine neoplasia following thyroid cancer in women, and it is associated with primary hyperparathyroidism, a disease sustained by PTH hypersecretion. Despite the hallmark of global promoter hypomethylations was not detectable in parathyroid tumors, increase of hypermethylation in specific CpG islands was detected in the progression from benign to malignant parathyroid tumors. Furthermore, deregulation of a panel of embryonic-related microRNAs (miRNAs) was documented in parathyroid tumors compared with normal glands. Impaired expression of the histone methyltransferases EZH2, BMI1, and RIZ1 have been described in parathyroid tumors. Moreover, histone methyltransferases have been shown to be modulated by the oncosuppressors HIC1, MEN1, and HRPT2/CDC73 gene products that characterize tumorigenesis of parathyroid adenomas and carcinomas, respectively. The epigenetic scenario in parathyroid tumors have just began to be decoded but emerging data highlight the involvement of an embryonic gene signature in parathyroid tumor development.
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PMID:Epigenetic alterations in human parathyroid tumors. 2572 13

Concurrent thyroid carcinoma and parathyroid adenoma is rare, they can and do coexist. We present here a 63-year old man who had bilateral papillary thyroid carcinoma and a parathyroid adenoma in the right thyroid lobe. Thyroid cancer was confirmed surgically. After the operation, the patient was found hypercalcemie and hypophosphatemia along with an elevated parathyroid hormone (PTH), indicating primary hyperparathyroidism. Also, the parathyroid 99mTc-MIBI scan demonstrated parathyroid adenoma in the right lower pole of the thyroid. The abnormal parathyroid tissue was carried out, and then serum calcium and PTH levels decreased to normal ranges.
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PMID:[Bilateral papillary thyroid carcinoma concurrent with parathyroid adenoma: one case report]. 2621 Nov 70


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