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PubMed1995

Unusual cases of hyperparathyroidism.

The history, physical and radiologic findings, treatment and pathology in five unusual cases of hyperparathyroidism is presented. The hyperparathyroidism was caused by a large (113 grams) mediastinal adenoma in the first patient, who is alive 25 years after surgery. A parathyroid carcinoma with compression of the esophagus was documented in the second patient. This patient is alive and normocalcemic 23 years after surgical treatment. A third patient with hyperplasia returned with hypercalcemia 20 years postsurgery requiring reoperation. A fourth patient with advanced bone findings was found to have a parathyroid adenoma. The fifth case is a patient with tertiary hyperparathyroidism secondary to hypophosphatemic rickets.

Adenoma↗
PubMed1993

Endocrine markers in malignant tumor cells producing parathyroid hormone-related protein.

Humoral hypercalcemia of malignancy may reflect the synthesis and secretion of biologically active parathyroid hormone-related protein (PTHrP) by a given tumor. In the present study we investigated 25 human non-endocrine carcinomas which were clinically associated with hypercalcemia (Ca > 11 mg%). By applying PTHrP-specific immunocytochemistry, PTHrP could be detected in all tumors. The intra-tumorous distribution was heterogeneous with strong positivity in relatively few cells or weak positivity in the majority of cells. Surprisingly, in the PTHrP producing cells none of the marker proteins typical of endocrine cells (neuron-specific enolase, Leu-7 antigen, chromogranin, synaptophysin and endocrine granule constituent) was found. On the other hand, PTHrP producing cells of endocrine origin, such as medullary cancer, or normal and adenomatous parathyroid glands, all produce these endocrine markers. Thus for the first time, the existence of peptide hormone producing tumor cells is reported without expression of endocrine markers. This indicates a special mechanism of PTHrP secretion.

Adenoma↗
PubMed1987

[Parathyroid adenoma at an atypical site, ectopic or not].

Of 800 patients undergoing operation for primary hyperparathyroidism between 1960 and 1985, 163 presented parathyroid adenomas located in other than typical sites in normal parathyroid glands. A retrospective study of case-reports is used to demonstrate the value of complementary investigations in the localization of these lesions, and to emphasize certain operative factors indispensable for their detection.

Adenoma↗
PubMed1988

[An autopsy case of parathyroid carcinoma with primary hyperparathyroidism].

An autopsy case of a 72-year-old woman who was determined as having had a parathyroid carcinoma with primary hyperparathyroidism is reported. On autopsy, a tumor, measuring 6 X 3 X 2 cm, was found beneath the left lobe of the thyroid gland, adherent to the left recurrent nerve and the trachea, though there was no metastasis evident. The tumor was found to be lobulated on cross section inspection. Histologically, the tumor cells were arranged in trabecular and in solid patterns with fibrous bands. A few tumor cells showed mitosis. Invasions to the capsules and the blood vessels were found present. Immunohistochemically, the parathyroid hormone was found positive in the cytoplasm of the tumor cells. Otitis fibrosa generalisata, metastatic calcification, acute pancreatitis, and core pulmonale also were observed.

Aged↗
PubMed1995

Localization of an ectopic parathyroid adenoma by double-phase technetium-99m-sestamibi scintigraphy.

Double-phase planar scintigraphy using 99mTc-MIBI has been introduced as a means to detect and localize parathyroid adenomas. Focal uptake on both early and delayed imaging is typical of these entities. We report a patient with persistent hypercalcemia following subtotal parathyroidectomy, who was found scintigraphically to have an ectopic parathyroid adenoma. Following initial detection within the mediastinum using planar scintigraphy, the adenoma was more precisely localized using SPECT imaging. This case suggests that double-phase parathyroid planar scintigraphy augmented with SPECT imaging, if needed, is cost-effective, and often necessary, in the assessment of primary hyperparathyroid patients before surgical reexploration.

Adenoma↗
PubMed1995

G protein mutations in tumours of the pituitary, parathyroid and endocrine pancreas.

A subset of growth-hormone (GH) producing pituitary adenomas harbour mutations at residues Arg201 and Gln227 of the alpha subunit of the stimulatory G protein (Gs alpha). One such mutation has been reported in a GH-producing tumour from a patient with multiple endocrine neoplasia type 1 (MEN 1) although mutations have not been reported in other tumours associated with MEN 1. We used PCR-induced restriction site analysis to screen for these mutations in 80 tumours of the pituitary, parathyroid and endocrine pancreas. Arg201 mutations were detected in 1 non-functioning and 4 GH-producing pituitary tumours. No mutations were found in any of the endocrine tumours tested at Arg179 of the Gi2 alpha subunit, a homologous residue to Arg201 of Gs alpha. Our results indicate oncogenesis in the majority of pituitary and parathyroid tumours is independent of mutations of Gs and Gi2 alpha.

Base Sequence↗
PubMed2001

Thoracoscopically managed parathyroid adenoma in the upper anterior mediastinum.

We thoracoscopically managed parathyroid adenoma of the upper anterior mediastinum in a 29-year-old man. He had a backache and was found to have bilateral ureteric stones, hypercalcemia, and extremely increased parathyroid hormone levels. 99mTc-methoxyisobutyl isonitrile scintigraphy showed an accumulation area projected onto the right thyroid lobe and the upper mediastinum. A diagnosis of primary hyperparathyroidism secondary to double adenomas was made. The patient then underwent surgical intervention. With the patient under general anesthesia with one-lung ventilation, a reddish brown adenoma of an upper mediastinum was removed thoracoscopically with three trocars, whereas the right superior parathyroid adenoma was excised by a standard open cervical procedure. Conventionally, the mediastinal parathyroid adenoma was removed by an open approach and was associated with perioperative distress to the patient. If the exact location of the mediastinal lesion is established, thoracoscopic excision of these lesions is feasible and is strongly recommended.

Adenoma↗
PubMed1978

Ectopic ACTH-MSH producing carcinoid tumor with multiple endocrine hyperplasia in a child.

An autopsy case of a 9-year-old Japanese girl revealed a carcinoid tumor originating in the duodenum and hyperplasia of the multiple endocrine organs as manifested by ectopic ACTH syndrome, carcinoid syndrome and giantism. The tumor cells were positive for histochemical argyrophile reaction and two types of secretory granules were identified by electron microscopy. Biochemical assay revealed the production of ACTH and beta-MSH by the tumor cells. Other changes of multiple endocrine organs included acidophil dominant hyperplasia of the pituitary, diffuse hyperplasia of the thyroid, chief cell hyperplasia of the parathyroid, hyperplasia of the islets of Langerhans and the adrenal cortex. This case was considered to be a type of multiple endocrine adenomatosis including carcinoid tumor. The relationship between the carcinoid tumor and multiple endocrine adenomatosis was discussed.

Adenoma↗
PubMed1983

Immunoreactive human chromogranin A in diverse polypeptide hormone producing human tumors and normal endocrine tissues.

Chromogranin A, the major soluble protein costored and coreleased by exocytosis with catecholamines from the adrenal medulla, has recently been detected in several bovine polypeptide hormone producing tissues. We therefore searched for chromogranin, by immunohistology, in human polypeptide hormone producing tumors as well as normal human endocrine tissues. The chromogranin A antigen was purified from catecholamine storage vesicles of human pheochromocytoma, to which rabbit antisera were developed, allowing immunohistologic studies by the indirect rabbit anti-peroxidase technique. Specific chromogranin staining was noted in all polypeptide hormone producing human tumors studied (pheochromocytoma chromaffin cells, n = 3; medullary thyroid carcinoma parafollicular C cells, n = 2; thyroidal C cell hyperplasia cells, n = 1; parathyroid adenoma chief cells, n = 1; pancreatic islet cell tumor islet cells, n = 1; oat cell carcinoma cell line M-103) as well as in all normal polypeptide hormone producing tissues (adrenal medulla chromaffin cells, parathyroid chief cells, thyroid parafollicular C cells, pancreatic islet cells, gut enteroendocrine cells, and anterior pituitary cells). Chromogranin may have a widespread distribution in human polypeptide hormone producing tissues, and may be a useful histologic marker for peptide producing tumors.

Adrenal Gland Neoplasms↗
PubMed1994

Absence of mutations in the Gs alpha and Gi2 alpha genes in sporadic parathyroid adenomas and insulinomas.

1. Activating mutations of the alpha-subunits of the Gs and Gi2 proteins give rise to the oncogenes gsp and gip2, respectively, which are found in a variety of endocrine tumours. 2. In this study the polymerase chain reaction and direct sequencing have been used to screen a small sample of parathyroid adenomas and insulinomas for these mutations. 3. No mutations were identified in nine insulinomas and 13 parathyroid adenomas screened for gsp, and 11 parathyroid adenomas and four insulinomas screened for gip2. In addition, two gastrinomas from patients with multiple endocrine neoplasia type 1 were found to be negative for both oncogenes. 4. This is the first report of screening for gip2 in parathyroid adenomas and gsp/gip2 in insulinomas, and it extends the range of tumours examined for these oncogenes.

Adenoma↗
PubMedDate not supplied

Palpable parathyroid adenomas presenting as clinical solitary thyroid nodules and cytologically as follicular thyroid neoplasms.

BACKGROUND: A palpable parathyroid mass, in a patient with primary hyperparathyroidism, is presumed to be parathyroid carcinoma until proven otherwise, with other less common causes including parathyroid cysts and adenomas. These parathyroid pathologies can be more difficult to interpret with concomitant thyroid disease. METHODS: A retrospective review was undertaken of a series of three patients with palpable parathyroid adenomas mimicking thyroid nodules. RESULTS: Two of three patients had preoperative biochemical evidence of primary hyperparathyroidism. Sestamibi scanning confirmed the presence of parathyroid pathology in one case. Fine-needle aspiration cytology revealed probable follicular neoplasms of the thyroid in all three cases. Only one of three parathyroid adenomas was diagnosed at neck exploration; the others were diagnosed at subsequent histopathology. CONCLUSION: Parathyroid and thyroid disease often occur simultaneously. Concomitant parathyroid pathology should be considered, even in the absence of biochemical and radiological evidence, at neck exploration for thyroid disease. Macroscopic identification of parathyroid disease at neck exploration can be difficult when within the thyroid gland capsule. Cytology and imaging of parathyroid adenomas may, on occasion, mimic follicular thyroid neoplasms.

Adenocarcinoma, Follicular↗
PubMed1985

[A case of primary adenocarcinoma of the urinary bladder occurring in a patient with type 1 multiple endocrine adenomatosis (MEA)].

A case of primary adenocarcinoma of the urinary bladder occurring in a patient with type 1 multiple endocrine adenomatosis (MEA) is presented. The patient was a 36-year-old female who had a past history of type 1 multiple endocrine adenomatosis, namely, adenomatosis of the parathyroid gland, insulin and gastrin-producing adenomatosis of the pancreas, and prolactin-producing pituitary adenoma. She was admitted in January 1981 with the complaints of gross hematuria, pollakisuria and micturition pain lasting for about one year and a half. Cystoscopic examination revealed four solid tumors in the posterior and left lateral walls of the bladder with diffuse mucosal hyperemia. Biopsy of the tumors disclosed that they were adenocarcinoma. Clinical examinations revealed that there was no extravesical primary malignant neoplasm in this case. Radical cystectomy with urinary diversion by ileal conduit was performed on January 22, 1981. Histological examination revealed that the tumor was adenocarcinoma originating from the vesical mucosa. Follow-up for over three years since the time of surgery has not shown any sign of tumor recurrence or occurrence of extravesical malignant neoplasm. In addition, 28 cases of primary adenocarcinoma of urinary bladder in Japan reported during the last 25 years are reviewed and analyzed.

Adenocarcinoma↗
PubMed2000

Identification of somatic mutations of the MEN1 gene in sporadic endocrine tumours.

Endocrine tumours of the pancreas, anterior pituitary or parathyroids arise either sporadically in the general population, or as a part of inherited syndromes such as multiple endocrine neoplasia type 1 (MEN 1). The mechanisms responsible for the development of sporadic endocrine lesions are not well understood, although loss of heterozygosity (LOH) of the MEN1 locus on chromosome 11q13 and somatic mutation of the MEN1 gene have been frequently associated with the development of MEN 1-type sporadic endocrine lesions. To further investigate the role of the MEN1 gene in sporadic endocrine tumorigenesis, we analysed DNA from 14 primary parathyroid lesions, 8 anterior pituitary tumours and 3 pancreatic tumours for the presence of somatic MEN1 gene mutations and LOH of seven microsatellite markers flanking the MEN1 locus. In addition, we similarly analysed 8 secondary parathyroid lesions which arose in patients with chronic renal failure. None of the patients studied had a family history of MEN 1. Three primary parathyroid lesions and one pancreatic tumour (glucagonoma) were found to have lost one allele at the MEN1 locus. Somatic mutations were identified by SSCP and sequence analysis in one of these parathyroid lesions (P320L) and in the glucagonoma (E179V). These results support previous findings that inactivation of the MEN1 tumour suppressor gene contributes to the development of sporadic MEN 1-type endocrine lesions but is not associated with the development of parathyroid hyperplasia seen in some renal failure patients.

Adenoma↗
PubMed2001

[Primary hyperparathyroidism presenting as a brown tumor of the maxilla and hard palate. Apropos of a case].

Significant controversy persists in the classification of giant cell lesions of the maxillofacial skeleton. Multifocal giant cell lesions are strongly suggestive of hyperparathyroidism brown tumors. Maxillary localization is extremely rare. We report a case of primary hyperparathyroidism manifesting in the form of giant cell tumors of the maxilla, the hard palate and long bones. Biochemistry confirmed the diagnosis. Computed tomography localized the parathyroid tumor at the cervicothoracic junction in the retrosternal area. We discuss the clinical features of skeletal involvement in primary hyperparathyroidism and stress the need for ionized serum calcium assay in case of giant cell tumors of the cranial bones.

Adult↗
PubMedDate not supplied

[The Wermer syndrome].

The difficult diagnostic and therapeutic management of patients having gastrinoma with multiple endocrine neoplasia type I (MEN I) has been discussed by reference to the literature and a personal experience of 2 patients with Wermer syndrome. The syndrome is often familial and might be inherited as an autosomal dominant trait with a high but variable degree of penetrance. Pancreatic islets, parathyroid glands and adenohypophyseal [correction of antehypophyseal] cells are the three localization main for endocrine involvement in MEN I syndrome.

Adult↗
PubMed2000

[Surgical approach in mediastinal adenomas and parathyroid carcinomas].

The authors performed retrospective analysis of medical records in a group of 176 patients, who underwent surgical treatment of primary hyperparathyroidism. Surgical strategy was the major issue of interest. Cervical collar incision represented a first-choice approach to cervical exploration in most of cases except those, in whom ectopic mediastinal localization have been diagnosed before the operation. Partial sternotomy was the most common option in surgical re-explorations as a second step following failed parathyroid surgery. We conclude that partial sternotomy is necessary further step in patients with primary hyperparathyroidism complicated by malignant hypercalcaemia on condition that the surgeon is not able to reveal adenomas from neck exploration and sternotomy is than performed immediately during the same operation.

Adenoma↗