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PubMed1986

[Hiob syndrome. A case report of multiple endocrine neoplasia].

It is reported on a now 48-year-old male with a multiple endocrine neoplasia (MEN I). The most impressive symptomatology issued from a relapsing organic hyperinsulinism the cause of which were multiple islet cell tumours. Up to now the hyperparathyroidism was not mastered by the removal of two adenomas of the parathyroid gland. As third fact in this clinical picture, called also Hiob syndrome, the hypophyseal manifestation developed in form of a space occupation with a hypersomatotropism, the course and final clarification of which are still open.

Acromegaly↗
PubMed1989

Association of parathyroid tumors in multiple endocrine neoplasia type 1 with loss of alleles on chromosome 11.

Familial multiple endocrine neoplasia type 1 (MEN-1) is an autosomal dominant disorder characterized by the combined occurrence of tumors of the parathyroid glands, the pancreas, and the pituitary gland. Pancreatic tumors have previously been shown to be associated with the loss of alleles on chromosome 11; we therefore looked for similar genetic alterations in specimens of parathyroid tumors, which are the most common feature of MEN-1. We obtained parathyroid tumors and peripheral-blood leukocytes from six patients with MEN-1; 18 cloned human DNA sequences from chromosome 11 were then used to identify restriction-fragment-length polymorphisms. A loss of heterozygosity was detected in parathyroid tumors from three of the six patients with MEN-1; this finding demonstrated that allelic deletions on chromosome 11 are involved in the monoclonal development of parathyroid tumors in patients with MEN-1. In addition, studies of three affected families (with 17 affected members and 51 unaffected members) established linkage with the oncogene INT2 (peak lod score, 3.30, at 0 percent recombination); the MEN-1 gene was thus mapped to the pericentromeric region of the long arm of chromosome 11 (11q13). Our location of the MEN-1 gene at 11q13 is close to the location previously reported. We conclude that a single inherited locus on chromosome 11, band q13, causes MEN-1 and that the monoclonal development of parathyroid and pancreatic tumors in patients with MEN-1 involves similar allelic deletions on chromosome 11.

Adolescent↗
PubMed1993

Rare mutations of the Gs alpha subunit gene in human endocrine tumors. Mutation detection by polymerase chain reaction-primer-introduced restriction analysis.

BACKGROUND: The Gs alpha (Gs alpha) gene can be activated to the putative oncogene gsp by specific point mutations at codons 201 or 227. Such mutations have been reported in growth hormone (GH)-secreting pituitary adenomas and thyroid tumors. To clarify the role of Gs alpha gene in human endocrine tumors, 197 tumors were screened for point mutations at codons 201 or 227 of the Gs alpha gene. METHODS: Mutations were detected by primer-introduced restriction analysis (PIRA) of the polymerase chain reaction (PCR) product of genomic DNA. RESULTS: These Gs alpha mutations were present in 4 of 53 pituitary adenomas (4 of 43 GH-secreting adenomas; 1 of these 4 was a GH- and prolactin-secreting adenoma from a patient with familial multiple endocrine neoplasia Type 1), 4 of 66 thyroid tumors (4 of 30 papillary carcinomas), and 1 of 19 adrenocortical adenomas (1 of 6 aldosterone-secreting adenomas). In contrast, none of these Gs alpha mutations were detected in parathyroid tumors, endocrine pancreatic tumors, or pheochromocytomas. CONCLUSIONS: Gs alpha mutations at these two loci may play a role in the pathogenesis of a small population of GH-secreting pituitary adenomas, papillary thyroid carcinomas, and adrenocortical adenomas, but that they are not involved in the pathogenesis of other types of endocrine tumors.

Acromegaly↗
PubMed2005

Multiple endocrine neoplasia type 1.

Multiple endocrine neoplasia-1 (MEN-1) is an autosomal dominant inherited syndrome that occurs due to inactivating mutations of the MEN1 gene locus, coding for a tumor-suppressor protein, menin. The components of MEN-1 are hyperparathyroidism due to multiple parathyroid adenomas, pancreatic neuroendocrine tumors, and pituitary adenomas, in addition to some less common neoplastic manifestations. Care of people with MEN-1 requires knowledge of the problems that may arise, and the best approaches to detect and care for the manifestations of this incurable, but manageable, disease.

Adenoma↗
PubMed1996

Loss of heterozygosity studies at the retinoblastoma and breast cancer susceptibility (BRCA2) loci in pituitary, parathyroid, pancreatic and carcinoid tumours.

OBJECTIVE: Allelic deletion of the retinoblastoma (Rb) gene on chromosome 13 has been reported in both pituitary and parathyroid tumours. We have investigated the roles of the Rb and the hereditary breast cancer susceptibility gene (BRCA2), which lie within 25 cM of each other on chromosome 13q12-14, in the multi-step aetiology of endocrine tumours. PATIENTS AND MEASUREMENTS: Seventy-seven endocrine tumours (43 anterior pituitary, 22 parathyroid, 7 carcinoid, and 5 pancreatic islet cell tumours) with paired leucocytes have been examined for loss of heterozygosity (LOH) at the Rb and BRCA2 loci by using specific oligonucleotide primers for the PCR amplification of microsatellite polymorphisms at three intragenic Rb markers, Rb1.20, Rbi4 and D13S153, and D13S260 which is linked to the BRCA2 locus. RESULTS: Seventy-five of the 77 tumour-leucocyte pairs were informative and LOH was detected in 1 of 16 non-functioning pituitary tumours, 1 of 8 prolactinomas, 3 of 19 parathyroid adenomas and 1 of 1 parathyroid carcinoma. All the 3 parathyroid adenomas with LOH were associated with aggressive clinical and histopathological features. Allele loss was not detected in any of the 16 somatotrophinomas, 2 corticotrophinomas, 1 gonadotrophinoma, 7 carcinoid tumours (6 bronchial, 1 metastatic intestinal) or 5 pancreatic islet cell tumours that were informative. CONCLUSIONS: These results demonstrate that allelic deletions of the 13q12-14 region occur in some pituitary adenomas and 16% of parathyroid adenomas. The extensive loss, which involves both the Rb gene and the BRCA2 locus, suggests that tumour suppressor genes in this region other than Rb or BRCA2 may be involved in the development and progression of some endocrine tumours.

BRCA2 Protein↗
PubMed1998

The ectopic parathyroid adenoma: a cost justification for routine preoperative localization with technetium Tc 99m sestamibi scan.

OBJECTIVES: To evaluate the cumulative costs of failure to identify the ectopic parathyroid adenoma when exploration without preoperative localization is performed and to compare these costs with the expenses of routine preoperative localization in every patient. DESIGN: A consecutive series of 59 patients with primary hyperparathyroidism studied with preoperative scans using technetium Tc 99m sestamibi and ultrasound was submitted to a cost analysis. A subset of 5 cases of ectopic adenomas, presumed to be unidentifiable on routine surgery, was similarly analyzed. SETTING: Academic tertiary referral center. METHODS: The operative, anesthesia, hospitalization, imaging, and physician reimbursement costs of a failed exploration are compared with the costs of preoperative technetium Tc 99m sestamibi and ultrasound scans in every patient. RESULTS: Two cases of mediastinal parathyroid adenomas in this consecutive series of 59 patients were given a theoretical cost, including hospitalization, physician reimbursement, and anesthesia fees. These costs were based on a failed cervical exploration and extracted from the record of an actual patient who underwent such a process at the University of Vermont, Burlington, in 1995. In addition, the records of 2 patients with intrathyroidal adenomas were submitted to the same theoretical cost analysis with the exception that these patients were assumed to have adenomas that could be discovered after prolonged cervical exploration and thyroid lobectomy. The net management and imaging costs for 4 cases of ectopic parathyroid adenomas undergoing theoretical failed exploration are compared with the cost of obtaining routine technetium Tc 99m sestamibi and ultrasound scans for each of the 59 patients. CONCLUSION: The added cost of protracted or failed cervical exploration nearly neutralized the costs of a routine preoperative localization with technetium Tc 99m sestamibi and ultrasound scans.

Adenoma↗
PubMed1984

An unusual variant of multiple endocrine neoplasia syndrome: a case report.

A case of multiple endocrine neoplasia syndrome (MEN) in a 57-year-old woman with multiple endocrine tumours involving the pancreas, parathyroid and thyroid glands is reported. An unusual feature was the presence of collision tumours in the pituitary and adrenal. In the pituitary there were adenomas and a meningioma whereas in the adrenal there was a carcinoma along with a myelolipoma. Such collision tumours in the pituitary and adrenal as components of MEN syndrome have not been previously described.

Adenoma↗
PubMed1995

[Screening of multiple endocrine neoplasias type 1. Reflexions of the Study Group on Multiple Endocrine Neoplasias type 1].

The "Groupe d'Etude des Néoplasies Endocriniennes Multiples de type 1 (GENEM 1)" is a French group involved in a comprehensive multicentre study of Multiple Endocrine Neoplasia type 1 syndrome (NEM 1). The objectives of this group are to define diagnostic and therapeutic protocols and to carry out genetic research on NEM1. The first aim of physicians is to recognize the syndrome and to determine the appropriate screening especially into two circumstances: 1 degree In case of isolated and sporadic glandular disease -i-e-parathyroid glands, endocrine pancreas, antehypophysis, adrenal glands and neuroendocrine tumors? 2 degrees In case of very high probability of NEM 1 syndrome? This paper answers these two questions, based on the analysis of the first 150 cases collected by the GENEM 1.

Adenoma↗
PubMedDate not supplied

Contrast MRI in multiple endocrine neoplasia type 1 (MEN) associated with renal cell carcinoma.

The radiologic work-up of a patient with multiple endocrine neoplasia type 1 (MEN 1) syndrome and multiple endocrine nodules, with coincidental renal cell carcinoma, is described. Parathyroid adenoma was differentiated from multiple thyroid nodules by gadolinium-enhanced MRI. Adrenal enlargement due to a nonfunctioning adenoma and a renal cell carcinoma next to a simple renal cortical cyst were identified by typical signal intensities on T1- (pre- and post-Gd-DPTA) and T2-weighted images. Insulinoma was visualized only retrospectively.

Adenoma↗
PubMed1979

[Pathology of endocrine polyneoplasms (polyadenomatoses) (author's transl)].

The term "endocrine polyadenomatoses" includes two types of pathological entities in which there are an association of at least two endocrine tumors having no physiological relationships, and hereditary familial characteristics: Wermer's syndrome (Type I): pancreatic endocrine tumor, pituitary adenoma, and hyperplasia or adenoma of the parathyroids. Sipple' syndrome (Type II): medullary thyroid cancer, one of two pheochromocytomas, and parathyroid hyperplasia. The multifocal character of the pancreatic D-cell lesions in the first type, and the bilateral nature of the thyroid and adrenal lesions in the second type are particular features of each of them. Apart from some parathyroid lesions, for which the origin is still debatable, these endocrine tumors enter into the framework of the apudomes and are derived therefore from the neural crest. The association of other tumoral varieties of the APUD (carcinoid) type with nervous tissue tumors, and with dysmorphic anomalies suggests that these syndromes are the expression of a dysgenesis affecting more or less completely, structures derived from the neural crest.

Adrenal Gland Neoplasms↗
PubMed1984

[Percutaneous transcatheter ablation of parathyroid gland tumors by alcohol injection and contrast media infusion].

An attempt to obliterate the parathyroid glands by a catheter technique has been made in three patients with primary hyperparathyroidism. Two mediastinal tumours were defunctionalized with alcohol, and followup for 11 and 13 months showed that it had been successful. One cervical parathyroid tumour was over-injected with contrast medium, but there was a recurrence after 14 months, as indicated by rising serum calcium and parathormone levels. In selected cases the method may be an alternative to surgery, particularly in patients where previous surgery had been unsuccessful or if there is a high operative risk.

Adenoma↗
PubMed1976

Diagnosis and surgical treatment of mediastinal parathyroid tumors.

Experience and problems in the localization, diagnosis and surgical treatment of mediastinal parathyroid tumors are reported. Arteriography, pneumomediastinum and, especially, selective blood withdrawal with assay of parathyroid hormone, have proven valuable to the authors. Scintigram, intravital staining methods and venography are less productive. Retrosternal parathyroid tumors that can be removed from a Kocher incision should not, for practical reasons, be classified with the mediastinal tumors. The authors recommend the one-phase operation. If, after an intensive search of the neck and behind the sternum, no tumor has been found, it is advisable to incise the sternum step by step and revise the anterior mediastinum in the same session.

Angiography↗
PubMed1995

Multiple endocrine neoplasia type 1 presenting as insulinoma, gastrinoma, and postbulbar duodenal ulcers: report of a case.

We report herein the unusual case of a 55-year-old man with multiple endocrine neoplasia type 1 presenting as hyperparathyroidism, hyperpituitarism, insulinoma, and gastrinoma with postbulbar duodenal ulcers. The patient was referred to our hospital for further investigations of nephrolithiasis, acromegaly, and hematemesis. Laboratory studies showed high serum levels of calcium, parathyroid hormone, growth hormone, insulin, gastrin, and prolactin. Computed tomography of the cranial cavity demonstrated an enlargement of the serra turcica and swelling of two parathyroid glands in the neck. Computed tomography and angiography of the abdomen also showed a mass in the head of the pancreas. Endoscopy demonstrated reflux esophagitis, erosive gastritis, and multiple postbulbar duodenal ulcers. We diagnosed this patient as having multiple endocrine neoplasia type 1, with concomitant lesions of the pituitary gland, parathyroid glands, and islet cells of the pancreas. Following excision of the two enlarged parathyroid glands, his serum calcium and parathyroid hormone levels fell to within the normal range. Thereafter, a total gastrectomy was performed to alleviate the frequent bleeding from the upper gastrointestinal tract. However, resection of the pancreatic mass could not be performed owing to severe inflammation around the duodenum, probably induced by the postbulbar duodenal ulcers.

Adenoma↗
PubMed2006

A case of hyperparathyroidism-jaw tumour syndrome found in the treatment of an ossifying fibroma in the maxillary bone.

Hyperparathyroidism-jaw tumour (HPT-JT) syndrome is characterized by parathyroid tumours as well as by ossifying fibromas of the mandible and maxilla, renal cysts, or Wilms' tumours. Recently, the gene responsible for HPT-JT syndrome has been identified as the HRPT2 tumour suppressor gene. In an 18-year-old male, a tumour in the maxilla was first diagnosed as an ossifying fibroma. During biochemical screening before surgery, the patient received a diagnosis of primary hyperparathyroidism. Neck computed tomography scanning showed a parathyroid tumour. Surgical excisions to remove the jaw tumour and parathyroid adenoma were performed. The postoperative course has been uneventful and a follow up at 2 years revealed no evidence of recurrence. The HRPT2 germline mutation of 39delC was detected in the proband, but not in his unaffected parents. These results suggested that the germline mutation occurred de novo.

Adenoma↗
PubMed1997

Differential loss of heterozygosity in familial, sporadic, and uremic hyperparathyroidism.

Various genetic loci harboring oncogenes, tumor suppressor genes, and genes for calcium receptors have been implicated in the development of parathyroid tumors. We have carried out loss of heterozygosity (LOH) studies in chromosomes 1p, 1q, 3q, 6q, 11q, 13q, 15q, and X in a total of 89 benign parathyroid tumors. Of these, 28 were sporadic parathyroid adenomas from patients with no family history of the disease, 41 were secondary parathyroid tumors, 5 were from patients with a history of previous irradiation to the neck, 12 were from patients with a family history of hyperparathyroidism, and 3 were parathyroid tumors related to multiple endocrine neoplasia type 1 (MEN1). In addition, we determined the chromosomal localization of a second putative calcium-sensing receptor, CaS, for inclusion in the LOH studies. Based on analysis of somatic cell hybrids and fluorescent in situ hybridization to metaphase chromsomes, the gene for CaS was mapped to chromosomal region 2q21-q22. The following results were obtained from the LOH studies: (1) out of the 24 tumors that showed LOH, only 4 had more than one chromosomal region involved, (2) in the tumors from uremic patients, LOH of chromosome 3q was detected in a subset of the tumors, (3) LOH of the MEN1 region at 11q13 was the most common abnormality found in both MEN1-related and sporadic parathyroid tumours but was not a feature of the other forms of parathyroid tumors, (4) LOH in 1p and 6q was not as frequent as previously reported, and (5) tumor suppressor genes in 1q and X might have played a role, particularly on the X chromosome, in the case of familial parathyroid adenomas. We therefore conclude that the tumorigenesis of familial, sporadic, and uremic hyperparathyroidism involves different genetic triggers in a non-progressive pattern.

Adenoma↗
PubMed1981

Persistent and recurrent hyperparathyroidism.

Twenty-six patients with persistent or recurrent primary hyperparathyroidism after an initial cervical exploration are presented. Failure of the first operation was related in part to an ectopic location of the abnormal parathyroid tissue (in 58 percent), and to a discrepancy in the histologic diagnosis between the frozen-section analysis at the time of operation and the final pathologic interpretation (in 55 percent). Before secondary operation, selective venous sampling for parathormone levels and arteriography were accurate in localizing the lesion in 88 and 71 percent of cases, respectively. A plan for intraoperative management of these difficult problems is suggested.

Adenoma↗
PubMedDate not supplied

Clinical highlights from the National Cancer Data Base, 2000.

The National Cancer Data Base (NCDB) is the empirical data collection and analysis arm of the American College of Surgeons Commission on Cancer, and is supported in part by the American Cancer Society. The NCDB collects oncology patient demographic information, diagnostic and treatment information, and outcomes data from a broad spectrum of hospital-based cancer registries throughout the US, ranging from large research and teaching facilities to small community hospitals. Through this unique network, data are aggregated and reported back to participating hospitals to allow individual facilities to evaluate local patient care practices and outcomes. This article highlights the principal findings of articles published in 1999 and early 2000 that used NCDB data as the empirical basis of their analyses. Included among these are articles on breast cancer, gastric carcinoma, head and neck cancers, leukemia, liver carcinoma, lung cancer, parathyroid tumors, prostate carcinoma, small bowel adenocarcinoma, testicular malignancies, and vulvar melanoma. These articles are based on cases diagnosed between 1985 and 1996. The NCDB has accrued more than 6.4 million cancer cases for this time period. Sufficient numbers of rare cancers are reported to the NCDB to permit some types of clinical evaluation not possible using other data sources.

Adult↗