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PubMed1999

Cytogenetic and CGH studies of four neuroendocrine tumors and tumor-derived cell lines of a patient with multiple endocrine neoplasia type 1.

A malignant insulinoma (LOHG-I), a carcinoid of the lung (LOHG-L), a parathyroid adenoma (LOHG-NSA), and a fibroma (LOHG-F) were obtained from a patient with multiple endocrine neoplasia type 1 (MEN1). Long-term cultures were established. Essential neurobiological properties of the cell lines were proven immunocytochemically and by electron microscopy. Molecular analysis of the germline DNA showed a 4 bp deletion in exon 3 of the MEN1 gene. Cytogenetic and CGH analyses of the tumors/tumor cell lines revealed diploidy and balanced and unbalanced structural aberrations different for each tumor. Chromosomes 6q21, 11q and 17q were most frequently involved in clonal structural aberrations.

Adenoma↗
PubMed1998

Somatostatin-receptor scintigraphy in the management of gastroenteropancreatic tumors.

OBJECTIVE: This study evaluates the diagnostic and therapeutic implications of somatostatin-receptor scintigraphy in the management of patients with proven or high clinical suspicion of gastroenteropancreatic endocrine tumors. METHODS: Forty-one patients were studied by planar and tomographic imaging at 4 h and 24 h after 111In-pentetreotide injection. Scintigraphic findings were compared with computed tomography, and in several patients also with ultrasound, angiography, biopsy, and/or surgery, when performed. RESULTS: Among 23 patients with carcinoid tumor, three of nine primary tumors were initially identified by scintigraphy. Unsuspected mesenteric metastases found on scintigraphy in three patients led to octreotide treatment. Scintigraphic detection of multiple metastases in a patient with thyroid metastasis of bronchial carcinoid spared her an unnecessary total thyroidectomy. Among 18 patients with 19 islet-cell tumors, scintigraphy detected three of five insulinomas, whereas computed tomography identified only one. Receptor positivity in an islet-cell tumor (vipoma?) with no metastases on the scan led to surgical removal of the primary tumor. Receptor-positive metastases of gastrinoma (two of three patients), glucagonoma (two of three patients), and parathyroid hormone-related peptide-producing tumor (one patient) led to octreotide treatment. Nonvisualization of metastases of a glucovipoma led to chemotherapy. CONCLUSIONS: Somatostatin-receptor scintigraphy contributes to the management of patients with gastroenteropancreatic tumors in the following ways: 1) localization of a primary occult tumor, allowing surgical removal; 2) staging of the disease for optimal therapy-surgical excision or systemic treatment; and 3) identification of receptor status of the metastases for octreotide treatment or chemotherapy.

Adenoma, Islet Cell↗
PubMed2001

A mouse model of multiple endocrine neoplasia, type 1, develops multiple endocrine tumors.

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant cancer syndrome, characterized primarily by multiple tumors in the parathyroid glands, endocrine pancreas, and anterior pituitary. Other tumors, including gastrinoma, carcinoid, adrenal cortical tumors, angiofibroma, collagenoma, and lipoma, also occur in some patients. Individuals with MEN1 almost always have loss-of-function mutations in the MEN1 gene on chromosome 11, and endocrine tumors arising in these patients usually show somatic loss of the remaining wild-type allele. To examine the role of MEN1 in tumor formation, a mouse model was generated through homologous recombination of the mouse homolog Men1. Homozygous mice die in utero at embryonic days 11.5-12.5, whereas heterozygous mice develop features remarkably similar to those of the human disorder. As early as 9 months, pancreatic islets show a range of lesions from hyperplasia to insulin-producing islet cell tumors, and parathyroid adenomas are also frequently observed. Larger, more numerous tumors involving pancreatic islets, parathyroids, thyroid, adrenal cortex, and pituitary are seen by 16 months. All of the tumors tested to date show loss of the wild-type Men1 allele, further supporting its role as a tumor suppressor gene.

Adenoma↗
PubMed1990

Calcitonin gene-related peptide in patients with endocrine tumors.

The plasma level of calcitonin gene-related peptide (CGRP) was measured by RIA in 41 patients with endocrine tumors [22 medullary thyroid carcinomas (MTC), seven parathyroid adenomas, four benign insulinomas, five carcinoids, and three pheochromocytomas]. Of the 22 patients with MTC, all five preoperative patients had elevated CGRP levels. The correlation between CGRP and calcitonin levels was significant (P less than .001) in 22 patients with MTC. Six of 19 patients with endocrine tumors other than MTC showed elevated CGRP levels. Immunohistochemical study showed that tumor tissues from all 22 cases of MTC and seven from other endocrine tumors contained immunoreactive CGRP. CGRP reactivity was found in only small numbers of tumor cells. Thus, although CGRP appeared to be a useful additional marker for MTC, the role of CGRP in the pathophysiology of endocrine tumors was not elucidated.

Adenoma↗
PubMed1993

Ablation of mediastinal parathyroid adenomas by superselective embolization of the internal mammary artery with alcohol.

Two young patients (20 and 21 years) had recurrent hyperparathyroidism following neck exploration. Non-invasive investigations failed to localize a parathyroid adenoma. In both cases selective catheterization of the internal mammary arteries combined with digital angiography demonstrated hypervascular mediastinal adenomas. Using a coaxial catheterization technique (Tracker 18 and 10), both branch arteries of the internal mammary supplying the adenoma were selectively catheterized. In one case absolute alcohol and the other a mixture of Lipiodol and absolute alcohol were used to effect the ablation. The procedures were uneventful and serum calcium levels have subsequently returned to within normal limits. The follow-up in these two cases extends to 2 1/2 years in one and 10 months in the other case.

Adenoma↗
PubMed1999

Dendritic cell immunotherapy induces antitumour response in parathyroid carcinoma and neuroendocrine pancreas carcinoma.

Parathyroid carcinomas and neuroendocrine carcinomas of the pancreas are rare malignancies in humans. Because of their low radio- and chemosensibility, they fail to respond to conventional therapy. We therefore tested a dendritic cell immunotherapy in an attempt to control the tumour growth in two patients. Studies on mice and humans have demonstrated the potent capacity of dendritic cells to induce specific antitumour immunity. Mature dendritic cells were generated from peripheral blood monocytes in the presence of granulocyte/macrophage colony-stimulating factor, interleukin 4 and tumour necrosis factor alpha. Dendritic cells were either loaded with parathyroid hormone (PTH) or with (pancreas) tumour-derived lysate (TL), respectively, and were delivered by subcutaneous injections. All immunizations were well tolerated with no side effects, and were administered on an outpatient basis. After repeated vaccinations, specific in vivo immune response was demonstrated by positive delayed-type hypersensitivity (DTH) toward PTH or TL, demonstrating the efficient generation of antigen-specific memory T-cells. DTH reactivity was accompanied by a significant decrease of tumour markers in both patients. This approach might be generally applicable to other advanced, radio- and chemotherapy-resistant endocrine malignancies.

Biomarkers, Tumor↗
PubMedDate not supplied

[Vicissitudes of the surgery of primary hyperparathyroidism].

The difficult and disappointing cases encountered in patients who were operated upon for hyperparathyroidism between 1960 and 1987 have been studied. Ninety two patients underwent negative cervicotomy. Among the 12 patients who underwent a second operation, 4 were found to have cervical adenomas and in 6 others mediastinal adenomas were discovered by sternotomy. Most of the other cases were diagnostic errors. The present frequency of negative surgical operations is very low: 2 to 3 per cent of the cases; errors of diagnosis are exceptional, and the unusual sites of adenomas are better known. Seventeen patients were reoperated upon for persistent or recurrent hypercalcaemia despite excision of a 1st parathyroid lesion; 3 cancers which had been mistaken for adenomas at the 1st operation; 6 had a 2nd adenoma which had passed unnoticed during an exploration that was probably too limited and as hypercalcaemia persisted all 6 were reoperated upon with success at different intervals; finally, 8 patients had undiagnosed primary hyperplasia (as part of polyadenomatosis in 5 cases). Recurrences were observed, often after a long period, up to 3 to 5 years. Hypercalcaemia was corrected by the 2nd operation in only 5 out of 8 cases. In retrospect, it was found that the pathological examination could not always determine if the lesion was malignant or distinguish between adenoma and glandular hyperplasia.

Adenoma↗
PubMed1996

[New etiopathogenic, clinical and therapeutic findings in multiple endocrine neoplasia type 1].

Multiple Endocrine Neoplasia type 1 (MEN 1) syndrome comprises tumors or hyperplasia of different glands, including parathyroid, pituitary, adrenal cortex and the gastroenteropancreatic system. The vast majority of MEN 1 are found in familial clusters, although a few cases are sporadic. Hypercalcemia and/or nephrocalcinosis are the first and most common clinical manifestation in familial MEN 1 syndrome, followed by islet cell tumors (especially those secreting gastrin or insulin) and pituitary dysfunction due to either functioning or non-functioning microadenomas. Genetic studies indicate that familial MEN 1 syndrome is inherited through a dominant gene with incomplete penetrance and variable expression. The diagnosis of MEN 1 syndrome is mainly based on the careful assessment of the clinical history, symptoms physical evaluation along with the assay of serum electrolytes (i.e., calcium, phosphorus, etc.) and hormonal substances (i.e., gastrin, insulin, pancreatic polypeptide, prolactin, adrenocorticotropic hormone, etc.). In addition, several provocative tests have been used to identify endocrine tumors (particularly those of the gastroenteropancreatic system) and imaging techniques play a crucial role for the diagnostic approach in MEN 1 syndrome. Even though in the long term, the prognosis of MEN 1 syndrome is unfavourable. Recently, however, many therapeutic strategies, including both surgical and pharmacological options, have been developed to reduce the size of the neoplasm and control symptoms associated with hormone oversecretion.

Antineoplastic Agents, Hormonal↗
PubMedDate not supplied

[Recurrent brown tumors as initial manifestation of primary hyperparathyroidism. An unusual presentation].

Primary hyperparathyroidism is a rather frequent pathology characterised by hypersecretion of parathormone (PTH) which is caused by adenomas in 85% of all cases. At clinical onset, the most common symptoms are hypercalcemia-related (pain due to kidney stones, polyuria, gastrointestinal and neurological disorders) while rarer symptoms are due to brown tumors, expansive lesions often found in fibro-cystic osteitis. A case in which the patient showed recurrent mandibular brown tumors as initial clinical symptoms of primary hyperparathyroidism is described. This patient was examined for hypercalcemia, and a tumor mass at the left inferior mandibular branch was found. The patient had undergone surgical removal of a tumor in the left mandibular some years before, which was diagnosed as osteoclastoma. Primary hyperparathyroidism was diagnosed during recovery, and surgical removal of the parathyroid adenoma and mandibular tumor was performed. A histological diagnosis of large cell brown tumor was made. A microscopic observation of brown tumors which are made up of large multinuclear osteoclastic cells can often be confused with other large cell tumors during diagnosis. It is therefore necessary to exclude the presence of hyperparathyroidism with ionised calcium and, in cases of high values, intact PTH (iPTH), before performing a histological diagnosis of a large cell bone tumor. Throughout the course of primary hyperparathyroidism, brown tumors might appear in the absence of other specific symptoms and localize at the level of a single bone segment.

Adenoma↗
PubMedDate not supplied

Primary hyperparathyroidism and multiple endocrine neoplasia (MEN).

In about 80% of the cases, primary hyperparathyroidism (pHPT) is caused by a single parathyroid adenoma. However, the disease may be complicated by involvement of more than one parathyroid gland or by the combination with other endocrine tumors (syndrome of multiple endocrine neoplasia = MEN). This presentation deals with our experience in such conditions. During 11 years, 98 cases of pHPT were seen (90 in Ulm from 1968 to 1979, 8 since then in Heidelberg). In 9 patients, 2 to 4 parathyroids were in hyperfunction. A recurrence of pHPT was diagnosed after symptomfree intervals of 2 - 13 years in 5 patients. Data are presented of 4 patients suffering from MEN type I (Wermer syndrome): 3 had Zollinger-Ellison syndrome and pHPT, and the 4th insulinoma and pHPT. Whereas pHPT is the most frequent endocrinopathy in MEN type I, it is rarely seen in MEN type II, the Sipple syndrome (combination of medullary thyroid carcinoma, MTC, and pheochromocytoma). Among 20 own cases with MTC and 10 others with pheochromocytoma, no pHPT was observed. The common basis for the development of MEN syndromes is Pearse's concept of the diffuse neuroendocrine system (DNES).

Adult↗
PubMed1988

Neurofibromatosis associated with somatostatinoma: a report of two patients.

Two patients with neurofibromatosis and somatostatinoma are described, one patient in addition having a parathyroid adenoma diagnosed post mortem. The other patient had a partial somatostatinoma syndrome with diabetes, abdominal pain and cholelithiasis. The tumour was diagnosed preoperatively and metabolic studies demonstrated mild diabetes mellitus apparently due to suppression of insulin secretion by somatostatin, since oral glucose tolerance returned to normal post-operatively despite hemipancreatectomy. The tumour also secreted gastrin. There are now 18 reported cases of neurofibromatosis and duodenal carcinoid tumours which makes a genuine association between these two conditions very likely. With the present two cases, seven of the carcinoid tumours in this group have been positively identified as somatostatinomas. The histological finding of psammoma bodies is important in the diagnosis of duodenal somatostatinomas.

Adenoma↗
PubMed1993

Localization of abnormal parathyroid glands of the mediastinum with MR imaging.

PURPOSE: To determine the sensitivity of magnetic resonance (MR) imaging for preoperative localization of abnormal parathyroid glands in the mediastinum and to compare the sensitivity of MR imaging with those of scintigraphy and ultrasonography (US). MATERIALS AND METHODS: The prospective sensitivity of MR imaging was compared with those of thallium-technetium scintigraphy and US in 25 patients in whom the abnormal gland was located in the mediastinum at surgery. RESULTS: MR imaging had a much higher sensitivity (22 of 25 cases [88%]) than did scintigraphy (11 of 19 cases [58%]) or US (three of 24 cases [12%]). The most common locations for the mediastinal gland were intrathymic (eight of 25 cases) and paraesophageal (six of 25 cases) sites. CONCLUSION: MR imaging should be considered the modality of choice for preoperative localization in this group of patients.

Adenoma↗
PubMed1996

Ectopic parathyroid adenoma with severe hungry bone syndrome: a case report.

The presentation rate of ectopic mediastinal parathyroid adenoma is about 5 approximately 22%. Ectopic parathyroid adenoma is a common etiology of failed parathyroid surgery as well as a diagnostic challenge to clinicians. We reported a case of ectopic mediastinal parathyroid adenoma. A 20-year-old girl presented with arthralgia for 2 years before hyperparathyroidism was diagnosed. Parathyroid ultrasonography failed to find the lesion, but a vivid uptake in the superior mediastinum was discovered by thallium-201 (Tl-201) and technetium-99m-sestamibi (Tc-99m-MIBI) images. Removal of the ectopic adenoma resulted in severe Hungry bone syndrome, which required a large amount of calcium and phosphorous supply. Later, the patient suffered from bilateral femoral neck fracture due to marked osteoporosis. Bone mineral density study revealed marked increase of fracture risk. Although bone disorder is rare in cases of hyperparathyroidism nowadays, it still should be considered in patients with arthritis of unknown etiology like our case. Early diagnosis and treatment can reduce the morbidity.

Adenoma↗
PubMed2000

Growth hormone overproduction in a patient with multiple endocrine neoplasia type I.

In a 69-year-old woman with a complicated history of multiple endocrine neoplasia type I (MEN 1), growth hormone overproduction was found without clinical features of acromegaly. Zollinger-Ellison syndrome was diagnosed at the age of 36 years. Total gastrectomy and partial pancreatectomy were performed. Two years later hypercalcaemia occurred, hyperparathyroidism was suspected and three hyperplastic parathyroid glands were removed. In 1994 the plasma gastrin level was elevated and a computerized tomography of the abdomen revealed a 1.5-cm large pancreatic tumour. Screening of the pituitary functions was unremarkable and a magnetic resonance scan of the pituitary gland showed no abnormalities. In 1995 type II diabetes mellitus was diagnosed. In 1997 basal plasma growth hormone levels were raised and plasma IGF-I levels were alternately high and normal. The patient had no clinical signs of acromegaly, but glucose tolerance testing resulted in a paradoxical rise in growth hormone concentration compatible with the diagnosis of growth hormone overproduction. Magnetic resonance imaging of the pituitary gland revealed a microadenoma.

Adenoma↗
PubMed1992

Clinical features of multiple endocrine neoplasia type 1 and type 2.

The term 'Multiple Endocrine Neoplasia' (MEN) denotes a genetically determined syndrome characterized by the independent appearance of benign or malignant changes of several endocrine organs as well as occasional changes of neural, muscular and connective tissue. Three different forms have been identified: MEN 1 (Werner's syndrome) includes parathyroid hyperplasia in combination with pancreatic islet cell and pituitary tumours; MEN 2a (Sipple's syndrome) includes medullary thyroid carcinoma in association with phaeochromocytoma and parathyroid hyperplasia; MEN 2b includes medullary thyroid carcinoma, phaeochromocytoma and mucosal neuromas. MEN syndrome is transmitted as an autosomal dominant trait with a high degree of penetrance. The changes in the individual glands appear to be causally and temporally independent of each other. A spectrum of pathological changes exist in the affected glands which range from hyperplasia to adenoma to carcinoma. The pathological process is almost always multicentric, often resulting in bilateral disease of organs. The appearance of an endocrine tumour known to be associated with MEN should alert the physician to the possibility of a MEN syndrome. When the possibility of such a syndrome exists, screening and long-term observation should be initiated to diagnose a carcinoma in its earliest stage, or before the development of clinical manifestations of hormone excess.

Adenoma, Islet Cell↗
PubMed1986

Improved diagnosis of primary hyperparathyroidism by defining the inverse relationship between serum immunoreactive parathyroid hormone and calcium.

Serum concentrations of immunoreactive parathyroid hormone (iPTH) measured with a mid-region specific radioimmunoassay and total calcium were correlated in 300 healthy subjects and 158 patients with surgically verified primary hyperparathyroidism (HPT). All the healthy individuals could be separated from the patients by a monoexponential declining curve in which iPTH at concentrations of 0.60 micrograms/l and 0.33 micrograms/l corresponded to calcium concentrations of 2.20 mmol/l and 2.60 mmol/l, respectively. In 22 patients more than one sample was analysed and serum iPTH and calcium were inversely correlated. In contrast, three patients with parathyroid carcinoma showed no reciprocal fluctuations between serum iPTH and calcium. Of 75 patients with hypercalcaemia due to malignant diseases (metastatic mammary carcinoma, bronchial carcinoma, renal carcinoma, myelomatosis), 62 had a normal iPTH/calcium relationship. Two patients with myelomatosis had a temporary elevation of serum iPTH and calcium due to renal impairment. One patient with bronchial carcinoma probably had ectopic production of iPTH. The remaining 10 patients (six mammary carcinomas and four bronchial carcinomas) were found in the pathological iPTH/calcium range. In conclusion, we have demonstrated that an inverse relationship exists between serum iPTH and calcium in patients with non-malignant, primary HPT. Evaluation of iPTH and calcium in the same serum sample gave a correct diagnosis in more than 90% of patients with primary HPT.

Adult↗
PubMed2000

Multiple endocrine neoplasia type 1: from bedside to benchside.

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by the combined occurrence of parathyroid, pancreatic endocrine, and anterior pituitary tumors. MEN1 has two characteristics; a hormone excess and a sometimes lethal outcome due to malignant tumors. The recent identification of the MEN1 gene has opened the door to a much deeper understanding of this syndrome. Germline MEN1 mutations have been identified in most MEN1 families. They were not found, however, in families with familial pituitary tumors. Thus, studies with the MEN1 gene helped to establish that mutation of some other gene(s) is likely causative of the MEN1 phenocopy. These recent advances provide for the identification of mutant MEN1 gene carriers who are at a high risk of developing MEN1. The protein encoded by the MEN1 gene has been shown to function in the regulation of JunD-activated transcription but much still remains to be elucidated.

Genes, Tumor Suppressor↗
PubMed1990

Chromogranin A as a marker of neuroendocrine histogenesis of tumours: an immunoelectron microscopic study with considerations about the influence of fixation and embedding media on immunolabelling.

The ultrastructural localization of chromogranin A (Chr A) was studied in eleven neoplasias of the diffuse neuroendocrine system (3 pancreatic islet-cell tumours, 1 medullary carcinoma of the thyroid, 1 large bowel and 1 small bowel carcinoid tumours, 2 carcinoid tumours of the lung, 1 adenoma of the parathyroid gland, 2 pheochromocytomas of the adrenal gland). On account of the great influence of the technical treatment of the samples on the immunolocalization of Chr A, the effect of the following variables was studied in a case of pheochromocytoma: fixation in glutaraldehyde versus paraformaldehyde, postfixation in osmium tetroxide versus omission, embedding in epoxy resin versus acrylic resin. The method of choice for the better preservation of the antigenic character of the tissue was found to be fixation in 4% paraformaldehyde, omission of osmium postfixation and embedding in LRWhite acrylic resin; by this procedure we were able to find Chr A in the neurosecretory granules of all the studied cases, using three commercially available antibodies directed against Chr A. These findings further confirm that Chr A is a reliable marker for the study of neuroendocrine neoplasias by electron microscopy.

Adrenal Gland Neoplasms↗