Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A unique case of familial hyperparathyroidism associated with carcinoma of the colon is presented. Two brothers presented initially with colonic carcinoma and years later both were found to have primary hyperparathyroidism on the basis of parathyroid hyperplasia. This raises the issue of associated malignancies in patients with hyperparathyroidism, especially if they are found to be familial. One member of the family developed severe, recurrent hypercalcemia with bone disease, and thus the need for continued follow-up is emphasized.
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PMID:Familial hyperparathyroidism in association with colonic carcinoma. 359 82

The use of magnetic resonance (MR) to preoperatively evaluate patients with primary hyperparathyroidism was assessed using a 1.5 T system and surface coil reception. Twenty-five patients with primary hyperparathyroidism were studied before surgical exploration. Axial images, 5 mm thick, were obtained from the thyroid cartilage to the sternal notch. Both T1-weighted [short repetition time (TR), short echo time (TE)] and T2-weighted (long TR, long TE) spin echo sequences were performed in most cases. Parathyroid adenomas typically demonstrated greater signal than surrounding tissues on T2-weighted sequences, yet demonstrated signal intensity that was less than or equal to normal thyroid tissue on T1-weighted sequences. Using these criteria, MR correctly identified 17 of 20 surgically proven parathyroid adenomas in the neck. Magnetic resonance appeared less sensitive in two patients with parathyroid hyperplasia, identifying only one of six hyperplastic glands. We conclude that MR with surface coils provides high contrast, anatomic delineation of the neck and is useful for preoperative localization of parathyroid tumors.
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PMID:MR imaging with surface coils in primary hyperparathyroidism. 365 50

Occasionally, patients with other causes of hypercalcemia undergo parathyroidectomy for suspected primary hyperparathyroidism. We studied the parathyroid glands from 12 persons with nonparathyroid hypercalcemia. Glands from these individuals were similar to normal glands in size and fat:parenchymal ratio, showing neither atrophy nor hyperplasia. A distinctive histologic feature, also seen in hyperparathyroid hypercalcemia, is the presence of pale, vacuolated cells arranged in a trabecular pattern. Recognition of normal parathyroid parenchymal weight and the nonspecific nature of these vacuolated cells is necessary to prevent false-positive diagnoses of parathyroid hyperplasia. For glands which have not been weighted, parenchymal cross-sectional area can only be used as a rough index of parenchymal weight.
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PMID:Parathyroid gland morphology in nonparathyroid hormone-mediated hypercalcemia. 397 Feb 97

Circulating human pancreatic polypeptide (hPP) concentrations in the plasma of 61 patients were determined by radioimmunoassay and compared with concentrations in normal age-matched subjects to assess the role of plasma hPP in diagnosis and detection of pathologic dysplasias in endocrinopathies. Basal fasting plasma hPP concentrations greater than 3.0 times normal values were found in six of six patients with multiple endocrine adenopathy syndrome, type I (MEA I) who had islet cell tumors that contained hPP and in only three of 15 nonfamilial patients with sporadic islet cell tumors. An exaggerated plasma hPP response to meal stimulation that exceeded greater than 4.5 times the basal value was found in 15 of 18 patients with MEA I, which indicated the presence of endocrine cell hyperplasia as the underlying genetic trait. The abnormal plasma hPP response to meal stimulation correlated most strongly with islet cell hyperplasia in both the genetic and sporadic endocrinopathies and to some extent with antral G cell hyperplasia. In patients with primary hyperparathyroidism, an exaggerated plasma hPP response to meal stimulation is highly indicative of genetic parathyroid hyperplasia in MEA I and not of sporadic parathyroid adenoma. Informed consent was obtained from all patients who were subjects of these investigations.
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PMID:Pancreatic polypeptide update: its roles in detection of the trait for multiple endocrine adenopathy syndrome, type I and pancreatic polypeptide-secreting tumors. 613 85

Postmortem bone and parathyroid gland histology in nine hypercalcemic cancer patients without bone metastases was compared to bone and parathyroid histology in ten normocalcemia patients. Parameters of parathyroid function, including serum immunoreactive parathyroid hormone, acid base status, serum phosphate, and nephrogenous cyclic AMP were measured in the hypercalcemic group and compared to normals and to patients with primary hyperparathyroidism. Bone histology in all nine hypercalcemic cancer patients showed increased osteoclastic bone resorption and increased fibrous connective tissue in the bone marrow. Parathyroid glands were of normal size in all nine patients but contained little or no fat, one criterion of parathyroid hyperplasia. In the normocalcemic cancer patients only 2/10 had minimally increased bone resorption while 7/10 had decreased or absent stromal fat in the parathyroid glands. Despite the hyperplastic appearance of the parathyroid glands, serum biochemical parameters in the hypercalcemic cancer patients indicate a state of suppressed parathyroid function suggesting that the osteoclastic bone resorption is related to a humoral substance elaborated by the tumors which is distinct from parathyroid hormone.
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PMID:Abnormal bone and parathyroid histology in carcinoma patients with pseudohyperparathyroidism. 627 64

In our experience with operations for primary hyperparathyroidism, a recurring problem centers on patients whose solitary adenomas are too small to be appreciated at the initial exploration. We have seen four patients with parathyroid microadenomas, which we define as lesions less than 6 mm in diameter in externally undeformed parathyroid glands. Two such patients were fortuitously cured at the initial exploration even though the operative findings were inconclusive. One, a 25-year-old man, underwent excision of an externally normal gland that contained a 3 by 2 by 2 mm microadenoma. He is eucalcemic since the operation. The other patient, a 70-year-old woman with hypercalcemia, responded to prednisone. She then underwent a neck exploration at which the diagnosis of sarcoidosis was confirmed by lymph node biopsy examination. A 4 by 2 by 2 mm parathyroid microadenoma was incidentally removed. The patient is normocalcemic receiving low-dose steroid treatment since the operation. In a third patient, a 34-year-old practical nurse, three explorations were needed to find a parathyroid gland, which was negative for adenoma on frozen-section microscopy. The solitary adenoma, 6 by 3 by 3 mm, was appreciated only on permanent sections. The majority of oxyphil microadenomas should be suspected to be nonfunctioning, as in a 59-year-old woman in whom the lesion coexisted with primary chief cell parathyroid hyperplasia. The hyperparathyroidism responded well to three and a half-gland resection. The 2 by 2 by 2 mm oxyphil adenoma was also removed. Solitary parathyroid adenomas can be subtle and small. Appraisal of parathyroid disease at the operating table is not always straightforward. As more patients with early hyperparathyroidism appear on routine calcium screening, we may expect to see increasing numbers of challenging solitary parathyroid microadenomas.
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PMID:Solitary parathyroid microadenoma. 650 61

The effects of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) on parathyroid hormone (PTH) release from human parathyroid cells were investigated using an in vitro system of dispersed cells. The cells were obtained from 7 patients with primary hyperparathyroidism (HPT) and adenoma, 4 patients with primary HPT due to hyperplasia and 2 patients with parathyroid hyperplasia secondary to chronic renal failure. The dispersed cells were incubated in tissue culture medium at low, normal and high external calcium concentrations for 2-16 h. There was a gradual suppression of PTH release (5-55%) when the calcium concentration in the medium was increased from 0.5 to 3.0 mM, thus indicating retained regulation of hormone release. The addition of 1,25-(OH)2D3 in concentrations of 0.1 and 1 ng/ml and of 24,25-(OH)2D3 in concentrations of 1.0 and 10 ng/ml during the incubations did not further affect the amount of PTH released by the cells. The concentrations of the different vitamin D metabolites tested closely correspond to levels observed under normal physiological conditions and during treatment with high doses of vitamin D in vivo. Thus, the findings contradict the idea of any direct short-term regulatory effect of either 1,25-(OH)2D3 or 24,25-(OH)2D3 on the secretion of PTH from hyperfunctioning human parathyroid tissue.
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PMID:Effects of 1,25- and 24,25-dihydroxycholecalciferol on parathyroid hormone release from human parathyroid cells in vitro. 660 1

We noted the association of parathyroid carcinoma and primary parathyroid hyperplasia in a 53-year-old woman who had a clinical and laboratory profile of primary hyperparathyroidism. At surgery, three hyperplastic parathyroid glands were excised, one of which also demonstrated parathyroid carcinoma. Postoperatively, she was treated for persistent hypercalcemia and died of congestive cardiac failure. At autopsy, there was evidence of metastatic parathyroid carcinoma, and a further hyperplastic parathyroid gland was identified. The association of parathyroid hyperplasia and carcinoma is rare.
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PMID:Concurrent primary parathyroid hyperplasia and parathyroid carcinoma. 668 92

The histologic characteristics of the parathyroid glands in familial benign hypercalcemia (familial hypocalciuric hypercalcemia) are disputed, some finding parathyroid hyperplasia and others finding no abnormalities. To further investigate this issue, the histologic appearance of 82 parathyroid glands from 47 control patients (surgical and autopsy) were compared with those of 28 glands from 23 patients with familial hypocalciuric hypercalcemia who had undergone surgery for suspected primary hyperparathyroidism. Median and mean weights of 23 parathyroid glands from 12 patients with familial hypocalciuric hypercalcemia were 50 mg and 60 mg, respectively, with a range from 5 to 181 mg. Eighty-three percent of individual glands were within extreme normal limits for weight (less than 75 mg). Percent parenchymal area in familial hypocalciuric hypercalcemia was slightly but significantly less than control values (62 +/- 2 versus 71 +/- 2 percent, respectively; (p = 0.009). Conversely, percent fat was higher in familial hypocalciuric hypercalcemia than control values (30 +/- 3 versus 21 +/- 2 percent, respectively; p = 0.015). Stromal area was 8 +/- 1 percent in each group. Although 15 to 20 percent of parathyroid glands in familial hypocalciuric hypercalcemia exceeded normal size, most were indistinguishable from normal by size, weight, and microscopic appearance. The significantly reduced percent parenchyma in glands from patients with familial hypocalciuric hypercalcemia further suggests that the condition is not uniformly accompanied by typical parathyroid hyperplasia and should not be thought of as merely a variant of the latter.
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PMID:Parathyroid glands in familial benign hypercalcemia (familial hypocalciuric hypercalcemia). 673 60

The nuclear diameter of chief cells was measured in 17 cases of parathyroid adenomas, four cases of secondary hyperplasia, five cases of primary hyperplasia and six cases of tertiary hyperparathyroidism. All the cases with secondary hyperplasia and tertiary hyperparathyroidism were associated with chronic renal failure. The nuclear diameter in both the adenomatous and hyperplastic areas of tertiary hyperparathyroidism were measured. The adenomatous areas of tertiary hyperparathyroidism contained nuclei of a larger diameter than those in the hyperplastic foci of the same gland. The nuclear diameter in adenomatous foci of tertiary hyperparathyroidism was similar to that in adenomas from primary hyperparathyroidism. These findings lend support to the concept of formation of autonomous adenomas against a background of reactive parathyroid hyperplasia in cases of tertiary hyperparathyroidism. Using statistical methods there were differences between the nuclear diameter in cases of primary adenomata, and cases of primary and secondary hyperplasia. Primary parathyroid hyperplasia stood out as a distinct group. The significance of these findings is discussed.
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PMID:Nuclear diameter in parathyroid disease. 682 69


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