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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term "endocrine polyadenomatoses" includes two types of pathological entities in which there are an association of at least two endocrine tumors having no physiological relationships, and hereditary familial characteristics: Wermer's syndrome (Type I): pancreatic endocrine tumor, pituitary adenoma, and hyperplasia or adenoma of the parathyroids. Sipple' syndrome (Type II): medullary thyroid cancer, one of two pheochromocytomas, and parathyroid hyperplasia. The multifocal character of the pancreatic D-cell lesions in the first type, and the bilateral nature of the thyroid and adrenal lesions in the second type are particular features of each of them. Apart from some parathyroid lesions, for which the origin is still debatable, these endocrine tumors enter into the framework of the apudomes and are derived therefore from the neural crest. The association of other tumoral varieties of the APUD (carcinoid) type with nervous tissue tumors, and with dysmorphic anomalies suggests that these syndromes are the expression of a dysgenesis affecting more or less completely, structures derived from the neural crest.
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PMID:[Pathology of endocrine polyneoplasms (polyadenomatoses) (author's transl)]. 4 54

This study demonstrates that appreciable changes in serum parathyroid hormone and urinary cyclic AMP occur during experimentally induced hyper- and hypocalcemia in almost all patients with primary hyperparathyroidism regardless of histology. A single patient with tertiary hyperparathyroidism also demonstrated a significant elevation of serum parathyroid hormone and urinary cyclic AMP in response to EDTA induced reduction in ionized calcium. Thus, total autonomy of hormone secretion was not present in the great majority of the patients with a parathyroid adenoma, parathyroid hyperplasia, or the single patient with tertiary hyperparathyroidism. Therefore, preoperative evaluation of the rsponse of urinary cyclic AMP and serum parapthyroid hormone to EDTA or calcium infusion will not distinguish parathyroid adenomas from hyperplasia on the basis of total autonomy of hormone secretion. If a difference in secretory control is present between parathyroid adenomas and parathyroid hyperplasia, it is more subtle than total autonomy for adenomas and nonautonomy for hyperplasia.
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PMID:Nonautonomy of parathyroid hormone and urinary cyclic AMP in primary hyperparathyroidism. 19 97

Nine cases of primary hyperparathyroidism (PHP) in patients with urinary calculi are reported and discussed. Selective venous catheterization and parathormone (PTH) radioimmunoassay confirmed the diagnosis in all cases, preoperatively discriminated between adenoma and diffuse parathyroid hyperplasia, and permitted exact preoperative localization of 5 of 7 adenomas. The interest of the urologist in PHP and the usefulness of selective PTH radioimmunoassay are discussed and emphasized.
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PMID:Value of selective parathormone radioimmunoassay in primary hyperparathyroidism. 43 24

The analysis of 20 personal cases of parathyroid hyperplasia or adenoma suggest the following conclusions: 1. The importance of dosage of the parathormone is a decisive factor of the diagnosis and yields data: a) in relation with the volume of the adenoma; b) that return to normal 24 hours after resection; c) that constitute the proof of complete resection. 2. The little utility of the diagnosis of location bij means of elaborate paraclinical exams. The authors show false positive angiograms. Only the inspection of the four parathyroids and of the main heterotopic areas is a valid means of disclosing the lesions responsible of the hyperparathyroidism. It is essential to operate with a skilled pathologist who will read frozen sections.
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PMID:[Thoughts about 20 cases of hyperparathyroidism (author's transl)]. 43 6

The microscopical pathology of the two types of primary parathyroid hyperplasia is reviewed. The importance of the differential diagnosis between chief cell hyperplasia and adenoma is stressed. The problems of the surgical pathologist in masking this differential diagnosis of a biopsy, especially on a frozen section sample, are discussed.
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PMID:The microscopical pathology of primary parathyroid hyperplasia. 48 93

A simple, instant, and reliable test called the Density Test, based on the difference in density between the normal and the diseased parathyroid tissue, was performed intraoperatively in 73 patients with primary hyperparathyroidism. Whereas the normal parathyroid tissue floated, the diseased tissue invariably sank in a mannitol solution with a density range between 1.049 and 1.069. With the aid of this test, a diagnosis of adenoma was made in 66 patients and of primary hyperplasia in the remaining seven. In every case the diagnosis was subsequently confirmed. Forty-two of the 66 patients with an adenoma (64%) had a unilateral exploration of the neck. The Density Test saved these patients from an unnecessary contralateral exploration by the finding of an adenoma and a normal second gland in the same side of the neck. These data show that the Density Test is useful in the intraoperative diagnosis of a diseased from a normal parathyroid tissue. Tissue that sinks within the density range of 1.049 and 1.069 is without exception diseased and should therefore be either partially or completely excised even if the gland is of average size or only of slight enlargement. If it does not sink, it is virtually certain to be normal and should be spared. The Density Test provides a valuable clue in the differentiation of primary parathyroid hyperplasia from neoplasia.
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PMID:A density test for the intraoperative differentiation of parathyroid hyperplasia from neoplasia. 61 1

The histological findings in 18 cases of parathyroid hyperplasia associated with chronic renal failure and haemodialysis have been compared with a series of 35 cases of primary adenomatous hyperparathyroidism. Analysis of several features suggests that there are no definite criteria for distinguishing microscopically between individual enlarged glands in primary and secondary hyperparathyroidism, although nuclear pleomorphism is more common in primary adenoma and nodules are more common in secondary hyperplasia. These findings are discussed.
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PMID:A histological comparison of adenomatous and hyperplastic parathyroid glands. 67 Apr 16

Parathyroid hormone (PTH) secretion from abnormal hyperfunctioning human parathyroid tissues was studied in vitro to determine whether abnormal tissues were responsive to changes in calcium concentration and what role their subcellular organelles played in secretion. Hyperfunctioning tissues from one patient with secondary parathyroid hyperplasia, four patients with parathyroid adenomas, and one patient with parathyroid carcinoma were incubated in media containing low calcium (0.75 mM), normal calcium (1.5 mM), high calcium (3.0 mM), or vinblastine (0.01 mM), a microtubular disrupter. Also, in order to correlate ultrastructural responses with PTH secretion, after incubation tissues of one adenoma were objectively quantitated by stereologic techniques. Low calcium consistently stimulated mean PTH secretion from hyperplastic and adenomatous tissue, but only during the 1st hour of secretion. Low calcium inconsistently stimulated carcinomatous tissue. High calcium suppressed mean PTH release from all tissues. Vinblastine did not consistently inhibit secretion from adenomatous or hyperplastic tissue. Ultrastructural analysis of adenomatous tissue showed a sparsity of granules (0.87 per cent of cellular volume) compared to previously studied bovine tissues. Low calcium significantly increased the volume fraction of pinocytotic vesicles to 300 per cent (p less than 0.01) and reduced the surface area of straight (inactive) membrane to 60 per cent (p less than 0.01) of the normal calcium control. Secretion granules, when present, were adjacent to submembrane vesicles. The number and structure of microtubules were not changed by low or high calcium or vinblastine. Our findings indicate that parathyroid adenomas and hyperplastic tissues can respond acutely to low calcium stimulation and high calcium suppression. However, the acute response to low calcium stimulation may not be sustained in some cases because of limited storage of hormone. The increase in pinocytosis in low calcium-stimulated tissue suggests a coupling of exocytosis with membrane endocytosis, possibly related to membrane recycling. Our findings with vinblastine suggest that microtubular integrity is not a prerequisite for basal PTH secretion in adenomatous tissue.
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PMID:Secretory and ultrastructural responses of hyperfunctioning human parathyroid tissues to varying calcium concentration and vinblastine. 83 34

Opinion is divided as to the necessary extent of parathyroid resection in primary hyperparathyroidism. Some surgeons urge that subtotal parathyroidectomy be performed routinely, while others reserve subtotal resections for patients with parathyroid hyperplasia. In a review of 102 patients treated by parathyroidectomy for primary hyperparathyroidism and subsequently followed up for an average of 6 years, there were 73 patients with parathyroid adenoma, 26 with hyperplasia and 3 with carcinoma. The adenoma was not found at the first operation in only 3 cases; in the other 70 after removal of the adenoma no further hypercalcaemia was observed during the follow-up period. Persistent or recurrent hypercalcaemia was a problem in 9 out of the 26 patients with primary hyperplasia who had inadequate resection at the first operation, and also in the 3 patients with carcinoma. Experience shows that peroperative biopsy with frozen section of all the parathyroids is useful in confirming their identity and can be a guide to the type of disease present and the appropriate extent of resection.
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PMID:Parathyroidectomy: extent of resection and late results. 89 Feb 55

Parathyroid hyperplasia of all four glands was found to be the cause of primary hyperparathyroidism in 85 of 557 cases seen at the Massachusetts General Hospital between 1930 and 1973. There were 66 cases of chief cell hyperplasia and 19 cases of clear cell hyperplasia that were grossly, microscopically, and ultrastructurally distinct. Although the clinical findings overlap, there are several differences in the signs and symptoms between these two forms of hyperplasia. Both types are treated by subtotal removal of all the parathyroid tissue. Removal of insufficient tissue has left residual hyperparathyroidism in 45% of those with chief cell hyperplasia and 11% of those with clear cell hyperplasia after what was thought to be definitive surgery. Postoperative hypoparathyroidism was found in 15% of the patients with chief cell hyperplasia and in none with clear cell hyperplasia. These findings further suggest that removal of three and one-half glands in the more than 86% of patients with one gland involvement (adenoma or carcinoma) as the cause of primary hyperparathyroidism is unwarranted.
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PMID:Parathyroid hyperplasia in primary hyperparathyroidism: a review of 85 cases. 99 Oct 84


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