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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parathyroid carcinoma is a rare tumor responsible for 0.5-5% of primary hyperparathyroidism. It is usually small (not more than 27 g) and the precise diagnosis of malignancy is made when local or distant metastases are found. We describe a case of a 37 yr old male presenting with a substernal goiter and no specific symptoms except hypertension. This mass had cysts and calcifications and it was in the anterior upper mediastinum. The patient had severe hypercalcemia (Ca greater than 14 mg/dl), high PTH levels and mild renal failure. Bone scanning showed signs of hyperparathyroidism. The patient was subjected to total thyroidectomy and removal of the mass en block. The tumor was circumscribed lobulated and mostly cystic. It weighed 1,200 g (380 g after evacuation of cysts) and measured 12 x 9 x 4.5 cm. Histologic examination showed a highly differentiated adenocarcinoma of parathyroid with metastasis in a regional lymph node. Almost 4 years later the patient is alive and well without hypercalcemia and without evidence of distant metastases.
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PMID:Large parathyroid functioning carcinoma (1,200 g) presenting as a substernal goiter. 156 Jan 89

A 67-year-old white male presented with symptomatic hypercalcemia (15.6 mg/dl) in December 1989. He had undergone thyroidectomy for removal of a mucin-producing adenocarcinoma of the thyroid in 1967, and after eight years of follow-up during which time no other neoplasms were detected, he was reported as a unique case of this syndrome. Mild hypercalcemia (less than 11.0 mg/dl) was first noted in 1987, and this had remained stable until shortly before the acute presentation. Multiple lung nodules were observed radiographically and presumed to be granulomatous until increased size was observed shortly before presentation. Serum intact PTH was 190 pg/ml (n 10-55), but at neck exploration no parathyroid tissue was found and surgery did not resolve the hypercalcemia. Serum PTHrP was undetectable. Biopsies from all three lobes of the right lung revealed numerous nodules of metastatic adenocarcinoma with cords of tumor cells surrounded by mucin. The histology was similar to that obtained 23 years earlier. Following left upper lobe resection with removal of a 3-cm nodule, hypercalcemia resolved. The tumor stained strongly positive with a peroxidase stain for PTH using a polyclonal antibody. Northern blot hybridization of total RNA from the tumor confirmed the presence of message for PTH but not PTHrP. The original diagnosis has been revised to that of a unique case of mucin-producing parathyroid cancer with an extraordinarily long latency period before recurrence.
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PMID:Mucin-producing parathyroid carcinoma. 158 Nov 11

Spontaneous recovery of parathyroid secretion during correction of tumor-associated hypercalcemia by bisphosphonates provides a unique clinical opportunity to further unravel the complex relationship between Ca and PTH levels. We measured plasma ionised Ca (Ca2+) and serum intact PTH concentrations in 31 hypercalcemic cancer patients every 2 (range, 1-3) days over a period of 3-21 (median, 7) days after pamidronate therapy. The mean (+/- SD) initial Ca2+ concentration was 1.64 +/- 0.20 mmol/L (normal, 1.05-1.26 mmol/L), with a corresponding PTH level of 4.9 +/- 2.6 (median, 4.5; range, less than 2.0-14.7) ng/L. PTH levels were subnormal in 30 of 31 patients. During correction of hypercalcemia, the relationship between Ca2+ and PTH concentrations was best described by a polynomial regression (r = 0.89; P less than 0.001). The curve of the regression entered the normal range of PTH levels (10.5 ng/L) for a Ca2+ concentration of 1.21 mmol/L. Similarly, the mean Ca2+ level that caused a reproducible increase in PTH levels compared to baseline values was 1.21 +/- 0.12 (median, 1.17; range, 1.00-1.45) mmol/L. Comparable values were obtained when day to day variations in PTH levels were considered; the mean Ca2+ threshold level was 1.24 +/- 0.12 (median, 1.25; range, 1.00-1.43) mmol/L. This PTH secretory threshold was not significantly influenced by several factors, including the type of cancer hypercalcemia, the day to day variations in Ca2+ levels, various biochemical parameters of calcium metabolism, or the number of days to obtain a normal Ca2+ concentration. In summary, contrary to previous reports, our data show that the PTH secretory threshold during correction of tumor-associated hypercalcemia lies in the upper part of the normal range of Ca2+ concentrations and is not significantly influenced by the rate of change in Ca2+ levels.
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PMID:Recovery of parathyroid hormone secretion during correction of tumor-associated hypercalcemia. 159 85

The histological and immunohistological features of a non-functional parathyroid carcinoma obtained from a 56-year-old woman are reported. Macroscopically, the tumor consisted of many small hemorrhagic nodules and showed adhesion to the thyroid gland and esophageal wall. Histologically, the tumor cells resembled parathyroid chief cells, and showed an island-like or sheet-like arrangement, the former showing cystic degeneration and containing hemorrhagic fluid in the extracellular space. Tumor cells resembling water-clear cells and oxyphilic cells were also observed. Most of the tumor cells had glycogen in the cytoplasm. Immunohistologically, the tumor cells showed no staining with anti-thyroglobulin, JT-95 or anti-calcitonin antibodies. However, they were stained with antibodies against chromogranin A (Ch A) and the N-terminal portion of human parathyroid hormone (PTH (N)). The positive staining with anti-PTH (N) antibody disappeared when the antibody was absorbed with excess synthesized human PTH (N). Immunostaining for PTH (N) and Ch A was useful for differentiation of nonfunctional parathyroid carcinoma from thyroid carcinoma and thymoma.
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PMID:Immunohistological study of nonfunctional parathyroid carcinoma. Report of a case. 160 15

We report a family with primary hyperparathyroidism in four patients in two generations with apparent autosomal dominant transmission. A fifth member was probably affected. Two cases had definite parathyroid carcinoma (PC), and two had parathyroid adenoma with atypical features that could represent an early stage of cancer. In each of our patients, one parathyroid gland was abnormal. Five other parathyroid glands (in two patients) were normal in histology and size. There was no evidence of neoplasia in other tissues. Constitutional karyotypes were normal in all four patients. We identified three chromosomal abnormalities (a reciprocal translocation between chromosomes 3 and 4, trisomy 7, and a pericentric inversion in chromosome 9) in cultured PC tissue from one patient. These chromosomal changes are of unclear significance. Analyses on tumor DNA from one case of PC and one of atypical adenoma showed no evidence of ras gene mutations, PTH gene rearrangement, or allelic loss from chromosome 11q13 (locus of the gene for multiple endocrine neoplasia type 1). This family shows susceptibility to cancer without antecedent hyperplasia in all parathyroids. It could help identify a novel tumor susceptibility gene.
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PMID:Studies in a kindred with parathyroid carcinoma. 163 36

The hypercalcemic Walker carcinosarcoma 256 of the rat is an animal model for humoral hypercalcemia of malignancy. Previous in vivo studies suggested the production of a parathyroid hormone-related protein (PTHrP) by the Walker tumor. Therefore, we have measured immunoreactive PTHrP in serum-free conditioned medium from cells derived from this tumor using an antibody raised against human PTHrP(1-34). Walker tumor cell conditioned medium (WCM) displaced 125I-hPTHrP(1-34) from the antibody in a dose dependent manner, whereas control medium contained no immunoreactive PTHrP. In contrast, we detected no secretion of immunoreactive rat parathyroid hormone (rat PTH) by the Walker tumor cells using a midregional radioimmunoassay for rat PTH. WCM stimulated adenylate cyclase in osteoblast like cells, the dose-response curve paralleling that of hPTHrP(1-34). This effect could be inhibited by the PTH antagonist (8Nle, 18Nle, 34Tyr)bPTH(3-34) and by the addition of anti-hPTHrP(1-34) antibody. Bone resorbing activity of WCM in organ culture (calvaria of fetal rats) was not inhibited by indomethacin and glucocorticoids, suggesting a prostaglandin independent mechanism of osteoclast activation in this model.
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PMID:Osteolytic activity of Walker carcinosarcoma 256 is due to parathyroid hormone-related protein (PTHrP). 164 50

Hypercalcemia occurring in a patient with an islet cell carcinoma of the pancreas suggests the diagnosis of Multiple Endocrine Neoplasia Type I and associated hyperparathyroidism. We describe a patient with an islet cell carcinoma and hypercalcemia in whom low concentrations of PTH, the absence of skeletal metastases, hypophosphatemia, and elevated nephrogenous cAMP alternatively suggested the syndrome of humoral hypercalcemia of malignancy. The peptide PTHrP was measured in the patient's serum during the course of therapy by an immunoradiometric assay directed toward the midportion of the molecule. Hypercalcemia was treated with an investigational aminobisphosphonate. The concentration of PTHrP[56-86] increased over time and fell after the patient received chemotherapy directed toward the islet cell tumor.
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PMID:Parathyroid hormone-related peptide mediates hypercalcemia in an islet cell tumor of the pancreas. 166 81

Hyperprolactinemia and prolactinoma in patients with long-term primary hypothyroidism have been recognized for decades. We report a case of 57-year-old female patient with lingual thyroid and cretinism who had a high serum prolactin level (greater than 200 ng/ml) and a pituitary tumor with suprasellar and parasellar extension. The tumor regressed to a size undetectable by CT scan after 2 years of thyroid hormone replacement therapy, but complete normalization of the hyperprolactinemia required additional bromocriptine therapy. This patient showed generalized short metacarpal and phalangeal bones, calcification of the basal ganglia and dentate nuclei bilaterally, and subcutaneous calcification at both gluteal regions, while serum calcium, phosphorus and c-PTH levels were all normal. Thus in addition to short stature, brachydactyly, a round face, and obesity, which are related to hypothyroidism, she also presented features uniquely mimicking the Albright's hereditary osteodystrophy seen in patients with pseudohypoparathyroidism and pseudopseudohypoparathyroidism. Since she had no family history of pseudohypoparathyroidism and had a normal level of Gs alpha protein on the membrane of the red blood cells, there is no evidence of pseudopseudohypoparathyroidism. The cause of the ectopic calcification remains unknown.
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PMID:Intracranial calcification and brachydactyly mimicking Albright's hereditary osteodystrophy in an adult patient with lingual thyroid and prolactinoma-like lesion. 167 15

Immobilization hypercalcemia was initially described by Albright in 1941, and has most often been noted in adolescent males, presumably because their high rates of skeletal growth increase the likelihood that alterations in the equilibrium between bone deposition and resorption will have clinically apparent effects. The etiology of immobilization hypercalcemia is controversial, but is thought to result from normal levels of PTH acting with increased activity in the abnormal environment of immobilized bone. We describe a patient, immobilized following the resection of a large, locally invasive tumor, who developed hypercalcemia in conjunction with renal insufficiency and hypertension. The pathophysiology of immobilization hypercalcemia is discussed, as are the potential contributions of renal feedback mechanisms to the patient's hypertension and renal insufficiency.
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PMID:Hypercalcemia, hypertension and acute renal insufficiency in an immobilized adolescent. 177 5

Metabolic disturbances of Na, K, Ca and glucose as paraneoplastic syndrome were reviewed on the basis of recent progress of such areas. These abnormalities usually occur due to the production of hormones or other physiologically active substances by tumor tissues. Hyponatremia is the most common abnormality of Na metabolism in patients with cancers such as lung cancer, malignant lymphoma, thymoma and so on. Usual cause of hyponatremia as paraneoplastic syndrome is inadequate secretion of Antidiuretic Hormone (SIADH), which brings dilution hyponatremia associated with water intoxication. Recently hyponatremia due to abnormal secretion of atrial natriuretic peptide has been noted. Ca metabolism disturbance associated with cancer is usually observed as hypercalcemia and it is said that such hypercalcemia is seen in about 10% of cancer patients. Main cause of hypercalcemia associated with cancer is local osteolytic hypercalcemia (LOH) due to bone metastasis or humoral hypercalcemia of malignancy (HHM). The most common etiology of HHM is the production of Parathormone (PTH) related peptide (PTH-rP) massively secreted from cancer tissues. PTH-rP has been recently well investigated and its molecular, mRNA and gene structure have been already determined. The progress of this area is very rapid and PTH-rP will be assayed in the clinical laboratory in near future. As for glucose metabolism disturbance as paraneoplastic syndrome, hypoglycemia is the most common abnormality. This type of hypoglycemia has been noted in relation with excessive production of somatomedin.
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PMID:[Metabolic disturbance as paraneoplastic syndrome]. 182 8


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