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

Many hormones initiate their biologic actions by augmenting the intracellular concentrations of 3',5'-adenosine monophosphate (cyclic AMP). The nucleotide has been found in body fluids; its determination in plasma and urine can be performed by a rapid, simple and specific method: the cyclic AMP assay kit of the Radiochemical Centre (Amersham, England). The assay is based on the competition between unlabelled cAMP and a fixed quantity of the tritium labelled compound for binding to a bovine muscle protein which has a high specificity and affinity for cAMP. Different factors must be considered in evaluating the 24 h urinary content of the nucleotide: the renal or extrarenal origin of cAMP and the functional status of the kidneys. In basal conditions the urinary cAMP excretion is significantly correlated with creatinine excretion (n = 67; r = 0.47; p less than 0.001) thus confirming that the most part of cAMP excreted is derived from the plasma by glomerular filtration. Parathyroid hormone (PTH) stimulates adenylate cyclase predominantly in the renal cortex, whereas vasopressin (ADH) stimulated the enzyme in the medulla; thus PTH and ADH could increase the amount of cAMP in the urine from the renal source. In a case of diabetes insipidus and infusion of ADH caused a prompt rise in cAMP urinary excretion. In 5 normals an infusion of bovine synthetic parathyroid hormone caused an increased excretion of cAMP that preceded the phosphaturic response. An infusion of salmon synthetic calcitonin caused a rise in phosphate excretion and no increase in cAMP urinary content. As it concerns the two calciotopic hormones, PTH and CT, it is reasonable to assume that renal receptors are distinct. The 24 h urinary excretion of cAMP in 55 control subjects (3613 +/- 1460 D.S. n moles) was contrasted with the lower excretion in 25 elderly subjects (70-93 years: 1804 +/- 699 n moles), with the high cAMP excretion in a patient with hyperparathyroidism (that fell to normal values following removal of the parathyroid adenoma) and with the low cAMP excretion in patients with primary or surgical hypoparathyroidism. The mean 24 h cAMP excretion in patients with renal insufficiency was significantly decreased when compared to control subjects. These findings and recent reports confirm that the 24 h urinary output of cAMP may be considered an useful index of pharathyroid function in man.
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PMID:[The diagnostic value of the determination of cyclic 3',5'-adenosine monophosphate (cAMP) in urine]. 19 Jun 33

The findings of 152 patients with proven primary hyperparathyroidism are reportedmthe purpose of the analysis was to find difference between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups, Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in an atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck; The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The sucess of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There ist still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are reposible for the different action on bone and kidney is discussed; In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting, abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in over 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcenia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparthyroidism. Analysis of 152 patients with special reference to acute life threatening complications (acute hyperparathyroidism)]. 20 39

Tthe findings of 150 patients with proven primary hyperparathyroidism are reported. The purpose of the analysis was to find differences between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups. Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck. The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The success of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There is still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are responsible for the different action on bone and kidney is discussed. In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in ov er 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcemia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparathyroidism. An analysis of 152 patients with special references to acute life threatening complications (acute hyperparathyroidism)]. 79 28

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

Findings in a case of neonatal tetany in a child whose mother had elevated blood parathyroid hormone levels because of a parathyroid adenoma are given. The child was found to have hypocalcemia, hypomagnesemia, and hyperphosphatemia. Parathyroid hormone in the infant was found to be elevated. It has been postulated that the pathophysiologic mechanism of the hypocalcemia in this syndrome is transient hypoparathyroidism. The present case suggests a different mechanism: hypomagnesemia and end-organ refractoriness to parathyroid hormone, a state analogous to pseudohypoparathyroidism.
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PMID:Transient neonatal hypocalcemia, hypomagnesemia, and high serum parathyroid hormone with maternal hyperparathyroidism. 116 99

An asymptomatic 11-year-old boy was found to have primary hyperparathyroid secondary to an isolated parathyroid adenoma. This rare disorder of childhood can have asymptomatic hypercalcemia as its only manifestation. Parathyroid hormone assays and studies of urinary calcium excretion, especially the calcium-creatinine clearance ratio, distinguish parathyroid hormone excess from hypocalciuric forms of hypercalcemia. Real-time ultrasonography and dual-isotope subtraction scanning provide accurate, noninvasive, preoperative localization of abnormal parathyroid tissue. The prognosis of untreated, asymptomatic primary hyperparathyroidism in children is not known, and the indications for surgery are unclear. Diagnostic certainty is, therefore, especially important prior to surgical exploration.
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PMID:Asymptomatic primary hyperparathyroidism in children. Newer methods of preoperative diagnosis. 352 97

Parathyroid hormone has been measured by radioimmunoassay in eight patients with hyperparathyroidism due to parathyroid adenoma. Secretion of hormone by the adenomatas was demonstrated direct by estimating the arteriovenous gradient of parathyroid hormone across the tumours. Serial estimations following surgical removal of the adenoma showed a rapid fall in the concentration of circulating parathyroid hormone. The calculated half-life of endogenously secreted parathyroid hormone in man varied from 11.4 to 28.8 min., with a mean of 19.8 min.
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PMID:Radioimmunoassay of parathyroid hormone in primary hyperparathyroidism: studies after removal of parathyroid adenoma. 578 13

Parathyroid hormone is mainly regulated by the serum calcium concentration and not by another hormone which is usually the case for other hormones. We examined whether the parathyroid hormone could also be regulated by a hormone such as adrenocorticotropic hormone (ACTH). Experiment I: A two-hour urine sample was collected from 6 AM to 8 AM. At 8 AM one mg of synthetic ACTH was injected intramuscularly. Blood and urine was collected two hours after the injection for determination of the concentration of serum calcium, phosphate, parathyroid hormone and cortisol. Experiment II: Adenoma tissue was obtained during operation from patients with primary hyperparathyroidism. The adenoma was digested with trypsin. Eagle MEM containing 100 ml fetal calf serum per 500 ml medium was used as the culture medium. The specimens were incubated in an atmosphere of 95% air and 5% CO2. Several days later, 25 micrograms of ACTH was added to the medium which was then incubated for 2 hours. The parathyroid hormone in the medium was measured by radioimmunoassay. Experiment III:ACTH was injected intraperitoneally into control male rats and parathyroidectomized rats. Two hours later, serum calcium and parathyroid hormone levels were measured. After ACTH injection, a remarkable increase in serum calcium level was seen in the patients with primary hyperparathyroidism, but in the other groups, no increase in the serum calcium was observed. Parathyroid hormone was increased after ACTH injection in most subjects in all groups. Serum cortisol levels increased markedly after ACTH injection in all groups. The parathyroid concentration in the culture medium was slightly increased after ACTH addition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Endocrinological characteristic of primary hyperparathyroidism]. 609 27

Thirty-nine patients with primary hyperparathyroidism were studied four to eight years after their initial operation. In six patients, both the pathologist and surgeon agreed on the diagnosis of solitary adenoma; in 16 patients, the surgeon diagnosed solitary adenoma and the pathologist parathyroid hyperplasia (microscopic hyperplasia). In 16 patients, primary chief cell hyperplasia was agreed upon by the pathologist and surgeon. In the 16 patients with microscopic hyperplasia, there have been no long-term recurrences of hypercalcemia, but, in two patients, plasma parathyroid hormone levels are high. Parathyroid hormone--total calcium regression curves demonstrate significant preoperative correlation in solitary adenoma, p less than 0.01, and primary chief cell hyperplasia, p less than 0.05. After operation, significant correlations were not found between parathyroid hormone and total calcium. T-testing slope differences of pre- and postoperative parathyroid hormone--total calcium regression curves demonstrates a significant (p less than 0.01) shift to the right of the microscopic hyperplasia patients after operation, moving them to a broader range of total calcium per picogram parathyroid hormone. We conclude that 1) in primary hyperparathyroidism, positive regulation of total calcium by autonomously released parathyroid hormone exists in patients with solitary adenoma and chief cell hyperplasia; 2) autonomously functioning parathyroid tissue has been removed by operation for solitary adenoma with coexistent microscopic parathyroid hyperplasia. In this four- to eight-year follow-up period, it is clear that microscopic parathyroid hyperplasia is not associated with recurrent hypercalcemia. Two functionally distinct forms of parathyroid suppression are suggested; positively regulated microscopic hyperplasia and negatively regulated pathologically suppressed glands.
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PMID:Primary hyperparathyroidism: four- to eight-year postoperative follow-up demonstrating persistent functional insignificance of microscopic parathyroid hyperplasia and decreased autonomy of parathyroid hormone release. 728 4

Ultrasound-guided (US) fine-needle aspiration (FNA) can successfully localize abnormal parathyroid tissue (PT) preoperatively in hyperparathyroid patients. Samples from 12 patients with primary hyperparathyroidism evaluated using this technique since 1990 at the National Institutes of Health form the basis of this report. Eleven patients had undergone previous parathyroid surgery that failed to correct their hyperparathyroidism. Cytological evaluation and C-terminal (midmolecule) parathyroid hormone radioimmunoassay (PTH RIA) were performed on all samples. When sufficient material was available, immunocytochemical stains for chromogranin and thyroglobulin were performed. All cytological diagnoses were made with-out knowledge of the PTH RIA results. Using a combined approach of cytology and immunocytochemistry, six of 12 of the samples (50%) were diagnosed as PT. Follow-up on these six patients was confirmatory. Four of 12 samples (33%) were identified as thyroid; one of these patients had a PT adenoma identified in another location (the remaining three patients await further localization studies). Two of 12 samples (17%) could not be diagnosed because of insufficient cellularity; in both patients PT lesions were found in other locations. Morphological features of PT in FNA include the presence of cellular tissue fragments with epithelial cells arranged perivascularly around capillary cores, an overall organoid or trabecular architecture, and frequent microacini. Parathyroid tissue cells have round, fairly uniform nuclei measuring 6 to 8 microns. Clusters of larger oxyphil cells may show considerable anisonucleosis. The absence of features of thyroid tissue such as hemosiderin-laden macrophages, abundant colloid, and paravacuolar granules is significant. However, in cases of intrathyroidal PT, admixed thyroid material included in the aspiration tract may be present immunocytochemical stains for chromogranin, which is present in parathyroid tissue but not thyroid follicular cells, were positive in six of six samples interpreted as PT by cytology. No thyroglobulin staining was observed in any of the four of six PT samples for which material was available. C-terminal (midmolecule) PTH RIA correlated with cytological diagnoses in 100% of samples. Parathyroid hormone levels ranged from 1,300 to 262,000 pg/mL (normal blood level, 50 to 340 pg/mL) in the six samples diagnosed as PT by cytology. Parathyroid hormone RIA levels in the six non-PT samples were below normal blood values. The combined approach of cytology and immunocytochemistry provides high diagnostic accuracy in the interpretation of US-guided FNA for preoperative localization of parathyroid tissue.
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PMID:Ultrasound-guided fine-needle aspiration of parathyroid lesions: a morphological and immunocytochemical approach. 789 Feb 88


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