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PubMed2000

Large goiter and multiple rib tumors.

We report an interesting case of a 47-yr-old who had a large goiter and multiple rib tumors. The patient was initially suspected of having thyroid cancer, which had metastasized on the ribs, based on imaging studies. However, laboratory tests revealed a high level of ionized calcium and parathyroid hormone (PTH). The large goiter was diagnosed as having parathyroid tumors owing to the high level of PTH in the tissue fluid. The biopsy specimen from a rib tumor was diagnosed as containing brown tumors associated with primary hyperparathyroidism (PHP). The patient also had prolactinoma and pancreatic gastrinoma. Her daughter had both prolactinoma and PHP, and her brother and her father had PHP. Thus, the patient was diagnosed as having multiple endocrine neoplasia type 1.

Adult↗
PubMed1992

[Primary hyperparathyroidism caused by a mediastinal adenoma with intermittent hypercalcemia and severe bone disease].

We report the case of a 33-year-old woman who was operated on with the diagnosis of primary hyperparathyroidism (PHP) in 1986. She had bone disease and slight hypercalcemia. Two parathyroid glands were removed with a lack of clinical improvement. Subsequently, the serum calcium levels were normal with occasional slight increases. Depressed phosphorus values and elevated alkaline phosphatases and PTH levels were also present, associated with severe bone involvement and muscular weakness. A second cervical exploration performed in 1989 disclosed only a normal parathyroid gland, which was not removed. In 1990, a thoracic CT scan showed the presence of a 1 cm mediastinal nodule close to the great vessels. A thoracotomy was performed to remove this nodule, which proved to be a parathyroid adenoma. After surgery, the patient presented with a "hungry bone" syndrome, characterized by very low levels of calcium, phosphorus and magnesium, which required enteral and parenteral calcium and magnesium supplements, plus dihydroxyvitamin D. The association of normocalcemia and intermittent hypercalcemia with severe bone disease is very rare, as is the presence of a mediastinal adenoma. This could explain the difficulty in the diagnosis in this case.

Adenoma↗
PubMed1981

Failure of ablation of a mediastinal parathyroid adenoma by repeated contrast staining.

In a patient with primary hyperparathyroidism an attempt was made to ablate a middle mediastinal parathyroid gland by forceful staining with radiographic contrast material. The gland was stained on two separate occasions, two weeks apart. Both times the serum calcium level temporarily fell to the normal range but reverted to abnormal levels. The patient ultimately required surgery for correction of hypercalcemia. The mechanism of staining and possible reasons for failure as well as potential complications are discussed.

Adenoma↗
PubMed1992

Fine-scale mapping of the gene responsible for multiple endocrine neoplasia type 1 (MEN 1).

We have constructed a high-resolution genetic linkage map in the vicinity of the gene responsible for multiple endocrine neoplasia type 1 (MEN1). The mutation causing this disease, inherited as an autosomal dominant, predisposes carriers to development of neoplastic tumors in the parathyroid, the endocrine pancreas, and the anterior lobe of the pituitary. The 12 markers on the genetic linkage map reported here span nearly 20 cM, and linkage analysis of MEN1 pedigrees has placed the MEN1 locus within the 8-cM region between D11S480 and D11S546. The markers on this map will be useful for prenatal or presymptomatic diagnosis of individuals in families that segregate a mutant allele of the MEN1 gene.

Alleles↗
PubMed1986

[Multiple endocrine adenomatosis manifested chiefly by hyperparathyroidism].

A case with multiple endocrine neoplasia was reported, including parathyroid adenoma, of the main cells of the gland, multiple small adenomas in the tail of pancreas, (cytologically and electron-microscopically determined as A cellular) and light-cellular adenoma of adrenal. The hyperfunction of parathyroid adenoma was manifested with hypercalcemia (3.75 mmol/l), and morphologically--with the multiple calcium metastases in lungs, kidneys and heart, established at necropsy. The cause for the death was the acutely advanced ischemic disease of myocardium, on the background of chronic pyelonephritis and renal insufficiency. The timely diagnosis of such morbid states is concluded to be important for the clinical practice and could lead to the saving of the patients by operative removal of the tumour.

Adenoma↗
PubMedDate not supplied

Successful repeat transcatheter ablation of a mediastinal parathyroid adenoma 6 years after alcohol embolization.

Recurrent hyperparathyroidism is rare following transcatheter ablation of mediastinal parathyroid adenomas. When it occurs it is usually early and resistant to further attempts at ablation. We present a patient with primary hyperparathyroidism in whom two surgical attempts at cure had been unsuccessful. Subsequently, a mediastinal adenoma was demonstrated angiographically and embolized with absolute alcohol. Hyperparathyroidism recurred 6 years later and the mediastinal adenoma was subsequently successfully ablated a second time by angiographic embolization with ionic contrast medium.

Adenoma↗
PubMed1990

[Polyneuropathy in type I multiple endocrine syndrome].

Since 1928, approximately 30 cases of peripheral polyneuropathy consecutive to hypoglycaemia caused by insulinomas or islet cell pancreatic tumours have been published. We report a case of polyneuropathy in a young woman presenting with type I multiple endocrine neoplasia syndrome including multiple insulinomas and parathyroid adenomas. The predominantly motor polyneuropathy was symmetrical and involved both the upper and lower limbs. Biopsy showed muscular atrophy and, in particular non-specific acute axonal lesions. Twelve months after surgery the clinical situation was relatively favourable with resumption of physical activities but persistence of muscular atrophy. Wether hyperparathyroidism was responsible for the neuropathy was uncertain, the subacute post-hypoglycaemia axonal damage being a more likely suspect.

Adenoma↗
PubMed2002

Cytogenetic and molecular analyses of multiple endocrine neoplasias of the MEN1 syndrome.

A pancreas carcinoid, an adrenocortical adenoma, three parathyroid adenomas and a parathyroid hyperplasia of 5 MEN1 patients were used for loss of heterozygosity (LOH) and comparative genomic hybridization (CGH) studies. The MEN1 gene is located in the region 11q13, approximately 30 kb distal to PGYM. Four tumors showed LOH on chromosome 11q13 (D11S11335, PGYM, D11S1883, FGF3, D11S937) however LOH was also found beyond 11q13. The pancreas carcinoid and adrenocortical adenoma, both from the same patient, showed LOH at marker 11q23.3 and 11q25. In the three parathyroid adenomas LOH was detected in five different markers: 11q21, 11q22.3, 11q23.2, 11q23.3 and 11q25. No LOH was found in parathyroid hyperplasia. CGH analysis showed in case of the pancreas carcinoid losses on chromosomes 1p, 2q, 3, 6, 9p, 11 and 12p. Gains were found at 4, 5, 7, 8, 13, 14, 15q, 18, 19. The parathyroid adenoma of the third patient showed losses only on chromosome 11 in the region 11p12-p15 and 11q12-q23. Our data indicate that other genes are involved in the tumorigenesis of the MEN1 syndrome. Especially the numerous allelic losses between markers 11q23 and 11q25 (D11S938 and D11S910) are a hint for further tumor suppressor genes on chromosome 11.

Adenoma↗
PubMed2002

Familial adenomatous polyposis associated with multiple endocrine neoplasia type 1-related tumors and thyroid carcinoma: a case report with clinicopathologic and molecular analyses.

We describe a sporadic case with familial adenomatous polyposis, multiple endocrine neoplasia type 1 (MEN1)-related tumors (an endocrine cell tumor of the pancreas and bilateral parathyroid tumors), and a papillary thyroid carcinoma. To clarify how mutations of the adenomatous polyposis coli ( APC ) gene and the MEN1 gene, responsible for familial adenomatous polyposis and MEN1, respectively, might have contributed to tumorigenesis in this case, we studied germline mutations in both genes and loss of heterozygosity at their genetic loci in multiple lesions. In addition, we performed immunohistochemistry for beta-catenin, associated with the function of the APC gene. A germline mutation was found in the APC gene but not in the MEN1 gene. Normal allelic loss at the APC gene locus was observed in bilateral parathyroid tumors. Immunohistochemical staining of beta-catenin demonstrated accumulation in the cytoplasm in addition to membrane staining in all analyzed tumors and a strong nuclear reaction in the endocrine cell tumor of the pancreas. The presence of normal allelic deletions of the APC gene in bilateral parathyroid tumors and nuclear staining of beta-catenin in the pancreatic tumor in addition to the germline mutations suggests that functional loss of the APC gene played an important role not only in familial adenomatous polyposis but also in the MEN1-related tumors in this case.

Adenomatous Polyposis Coli↗
PubMed1996

Surgical aspects of MEN I syndrome.

Multiple endocrine neoplasia (MEN) Type I syndrome is a rare tumor of unknown etiology with a prevalence of 0.02 to 0.2 per 1000. Some of the tumors associated with MEN I include pituitary adenomas, parathyroid adenomas, hyperplastic tissue, and pancreatic B and non-B islet cell tumors. The clinical presentation is usually secondary to the specific hyperfunction characteristic of the different endocrine glands. Hyperparathyroidism and hypercalcemia precede all other manifestations in the majority of cases. Surgery plays a major role in management, and the condition should be considered when a tumor is diagnosed along the endocrine axis of glands, especially in hyperparathyroid patients.

Adenoma↗
PubMed1981

A large functioning parathyroid lipoadenoma found in the posterior mediastinum.

A patient who was evaluated for a voice change was found to have a large posterior mediastinal mass on chest roentgenogram. Laboratory parameters suggested hyperparathyroidism. The 190-g resected tumor had the histologic features of a parathyroid lipoadenoma, that is, a diffuse mixture of parathyroid glandular elements and fat or myxoid stroma throughout. This case report emphasizes that the large size of these rare tumors may result in herniation into unusual sites, and this gives rise to a confusing clinical presentation. Ultrastructural analysis showed a uniform population of chief cells with a distribution of cellular organelles consistent with slow hormone production and release. Similarities to normal and adenomatous chief cells are discussed. The myxoid stroma surrounding the glandular elements had the ultrastructural features of loose connective tissue.

Adenoma↗
PubMed1979

[Prolactin adenoma and Wermer's syndrome. A 10-year follow-up of a case with two parathyroid tumors, as adrenal adenoma, and a malignant pancreatic tumor (author's transl)].

A man of 38 years of age was found to have a type I endocrine polyadenomatosis in 1969. He was operated upon for removal of tumor of the islets of Langerhans with lymph gland metastases, and the head of the pancreas was removed. This was followed at a later date by ablation of two parathyroid adenomas. A clinically silent adenoma of the left adrenal was not removed and a silent and enclosed pituitary tumore was discovered. There were no clinical or hormonal signs of progression of the pancreatic tumor ten years later, but hypertension and behavioural disorders had developed. Catecholamine levels were normal. Selective blood aldosterone levels were just within significant values. A massive increase in prolactin secretion (more than 100 times the normal) was noted. This could be reduced by bromocriptine, and the possible role of prolactin in the behavioural disorders present is discussed.

Adenoma↗
PubMed2002

A case of lung cancer with hypercalcemia which was incidentally complicated with primary hyperparathyroidism due to parathyroid adenoma.

In lung cancer patients, hypercalcemia is a fairly common metabolic problem associated with malignancy. However, the occurrence of hypercalcemia in lung cancer patients means an ominous prognostic sign. As hypercalcemia often causes early death, quick diagnosis and treatment for hypercalcemia are required. A 69-year-old woman was admitted to our hospital with anorexia caused by hypercalcemia. On admission, serum level of PTH was elevated and PTHrP was normal. From the results of CT findings and transbronchial lung biopsy, the cause of the hypercalcemia was determined as lung cancer incidentally complicated with primary hyperparathyroidism. First, serum calcium level was returned to normal through hydration with saline and bisphosphonates. Next, left hemithyroidectomy for primary hyperparathyroidism was performed. Histologically, the tumor was diagnosed as parathyroid adenoma. Fifteen days later, left lower lobectomy for primary lung cancer was performed under a video-assisted thoracoscopic approach. Histologically, the tumor was diagnosed as a moderately differentiated adenocarcinoma. Four years and three months after the operation, the patient is alive and well with no sign of recurrence. When a lung cancer patient is complicated with hypercalcemia, we need to consider that primary hyperparathyroidism is a possible cause of the hypercalcemia.

Adenocarcinoma↗
PubMed1990

Chronic toxicity and carcinogenicity of bis(tri-n-butyltin)oxide (TBTO) in the rat.

In a 106-wk toxicity and carcinogenicity study, groups of 60 male and 60 female weanling Wistar rats were fed 0, 0.5, or 50 mg bis(tri-n-butyltin)oxide (TBTO)/kg diet. In males, feed consumption was increased in all treated groups and increased water consumption occurred at 5 and 50 mg/kg. During the second year, body weight decreased in the 50-mg/kg males, while the females in that group showed no weight gain. Excess mortality was confined to the 50-mg/kg group towards the end of the study. Haematological changes, comprising anaemia, lymphocytopenia and thrombocytosis were noted mainly at the high-dose level. Also, signs of decreased kidney function and increased plasma enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) were noted. No effects on serum hormone concentrations (thyrotropin, follicle stimulating hormone, luteinizing hormone or insulin) were observed, except for a decrease in the free thyroxin:thyroxin ratio in both sexes at the high-dose level. Higher serum IgM and IgA levels were present at 50 mg/kg, while, in females, IgG was decreased. At 50 mg/kg, the ovaries, adrenals, spleen (females), heart (males), pituitary, liver and kidneys were increased in weight, but the thyroid weight was decreased in females. The total tin concentrations in liver and kidneys showed a dose relationship and, in general, the concentrations were similar after 1 and 2 yr. Non-neoplastic histological alterations after 1 yr consisted of a decrease in the cell height of the thyroid follicles in all dose groups, with a reduced number of psammoma bodies at 50 mg/kg, a decrease in splenic iron content at 5 (females only) and 50 mg/kg, and a slight bile-duct activation. After 2 yr, only the thyroid changes were still present. In addition, at 2 yr, vacuolation and pigmentation of the proximal tubular epithelium and nephrosis were enhanced at 50 mg/kg. The incidence of benign tumours of the pituitary was significantly elevated and enhanced at 0.5 and 50 mg/kg. At 50 mg/kg increases in pheochromocytomas in the adrenal medulla and in parathyroid adenomas (males) were noted, while adrenal cortical tumours were decreased (males). There was a low, non-dose-related incidence of pancreatic carcinoma. Other tumour rates were in line with control data. It is concluded that lifetime feeding of 50 mg TBTO/kg diet induces toxicity in various organ systems. An increase in some common tumours was found at the high dose, probably due to hormonal or immunological changes.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Neoplasms↗
PubMed1992

Parathyroid hormone (PTH)-related protein, PTH, and 1,25-dihydroxyvitamin D in dogs with cancer-associated hypercalcemia.

Circulating N-terminal PTH-related protein (PTHrP), N-terminal PTH, and 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were measured in normal dogs and dogs with cancer-associated hypercalcemia (CAH), parathyroid adenomas, and miscellaneous tumors. PTHrP was undetectable (less than 1.8 pM) in normal dogs and increased in dogs with CAH due to adenocarcinomas derived from apocrine glands of the anal sac (44.9 +/- 27 pM), lymphoma (8.3 +/- 4.4 pM), and miscellaneous carcinomas (13.3 +/- 11.4 pM). The PTHrP concentration decreased in dogs with lymphoma and anal sac adenocarcinomas after successful treatment of CAH. The PTHrP concentration had a significant linear correlation with total serum calcium in dogs with anal sac adenocarcinomas and hypercalcemia, but not in dogs with lymphoma and hypercalcemia. Serum N-terminal PTH concentrations were usually in the normal range (12-34 pg/ml) for all groups of dogs except dogs with parathyroid adenomas (83 +/- 38 pg/ml). The serum PTH concentration increased after successful treatment of CAH. Serum 1,25-(OH)2D concentrations were decreased, normal, or increased in dogs with CAH, and 1,25-(OH)2D levels decreased after treatment of CAH. In summary, circulating concentrations of PTHrP are consistently increased in dogs with CAH, and PTHrP appears to play an important role in the induction of hypercalcemia.

Adenoma↗
PubMed1981

A human parathyroid carcinoma that produces parathyroid hormone: long term maintenance in tissue culture.

Parathyroid carcinoma cells from a pulmonary metastasis of a patient with a serum Ca of 17 mg/dl and an immunoreactive parathyroid hormone (PTH) of 6.4 ng eq bovine (b) PTH/ml (normal 40--400 pg/ml) have been maintained in tissue culture for more than 2 1/2 years. The cells secrete PTH into the culture media that 1) during immunoassay dilutes in parallel to human hyperparathyroid serum, 2) has a molecular weight similar to intact highly purified bPTH, and 3) stimulates bone resorption in a manner that is equivalent and additive to synthetic bPTH-(1--34).

Adult↗
PubMed1994

[Multiple endocrine neoplasia type I. Review and presentation of the study group of multiple endocrine neoplasia type I (GENEM I)].

Multiple endocrine neoplasia type I, also known as Wermer's syndrome, is characterized by the presence of functioning or nonfunctioning tumors or hyperplasia of the parathyroid glands, pancreatic islet cells and pituitary gland. MEN I syndrome may be either familial or sporadic. MEN I locus has recently been mapped to chromosome 11, and further characterization of the abnormal gene appears imminent. The GENEM I, a multidisciplinary study group is in the process of formation. Pathologists have to specify the morphological criteria of hyperplasia vs tumor. Further characterization of the gene and its product requires the application of molecular biology methods to the pathologic tissues of these patients.

Adrenal Gland Neoplasms↗
PubMed2003

[Primary hyperparathyroidism, adrenal tumors and neuroendocrine tumors of the pancreas--clinical diagnosis and imaging requirements].

INTRODUCTION: Diseases of the parathyroids, the adrenals and of neuroendocrine tumors of the pancreas are primarily diagnosed by clinical and endocrinological evaluation. The requirements concerning various imaging techniques and their relative importance in localization strategies of the different tumors are complex. MATERIALS AND METHODS: Current literature search, using PubMed. RESULTS: Evaluation of primary hyperparathyroidism requires bone densitometry by DXA and search for nephrolithiasis by ultrasound or native CT examination. While ultrasound of the thyroid and parathyroids seems useful before any parathyroid surgery, more extensive preoperative localization strategies (sestamibi scintigraphy, MRI) should be restricted to minimal invasive parathyroid surgery or reoperations. For adrenal tumors CT and MRI are of similar diagnostic value. Imaging of pheochromocytomas should be completed by MIBG scintigraphy. Each adrenal incidentaloma requires an endocrinological work-up. A fine-needle aspiration or core needle biopsy of an adrenal tumor is rarely indicated. Before adrenal biopsy a pheochromocytoma has to be excluded. Successful localization strategies for neuroendocrine tumors of the pancreas include somatostatin receptor scintigraphy, endoscopic ultrasound and MRI. DISCUSSION: Specific localization strategies have been established for the aforementioned tumors. The continuous progress of different imaging techniques requires a regular reevaluation of these localization strategies.

Adenoma↗