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)

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

Malignant disease and primary hyperparathyroidism are the most common causes of hypercalcemia, but there are many minor causes. Mechanical or humoral factors, or both, may underlie the increase in bone resorption. Parathyroid hormone (PTH) is a major mediator of bone resorption, but many other humoral agents have the same effect, eg, prostaglandin, osteoclast-activating factor, and thyroid hormone. Serial determination of total calcium concentration is the most important laboratory test in hypercalcemia. Other useful tests include the determination of serum and urinary phosphorus concentration, chloride/phosphate ratio, urinary cyclic adenosine 3',5'-monophosphate (cAMP) level; carboxyl-terminal PTH assay; corticosteroid challenge; and appropriate radiologic studies. Nephrogenous cAMP and urinary prostaglandin determinations are research tools that hold great promise in the future. Differentiation between PTH- and non-PTH-mediated hypercalcemia determines subsequent steps in diagnosis and treatment.
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PMID:Differential diagnosis of hypercalcemia: a mechanistic approach. 48 78

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

A new method for the localisation of abnormal parathyroid tissue is reported. This is carried out by selective venous blood sampling from the thyroid veins and the large veins of the neck. Parathyroid hormone levels are measured by radioimmunoassay. The peak hormone level indicates the site of the tumor suspected. Parathyroid venous blood was taken in 15 patients with primary hyperparathyroidism. In 12 patients localisation of the parathyroid tumor was achieved pre-operatively. The procedure is especially valuable in patients with previous unsuccessful parathyroid surgery. There are no complications or contraindications to the method.
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PMID:[Localization diagnosis of epithelial-body tumors through selective determination of parathyroid hormone. Surgical sequelae of a new method]. 114 69

The physiologic relationship between the thyroid and parathyroid glands remains poorly understood. A high incidence of coexistent thyroid disease and primary hyperparathyroidism has been well documented. Elevation of serum 1,25-dihydroxyvitamin D3 (vitamin D) has been detected in some patients with primary hyperparathyroidism. A report of specific binding sites and uptake of vitamin D by the thyrotrophs of the anterior pituitary indicates that vitamin D may modulate production or secretion of thyroid-stimulating hormone (TSH). To test this concept, we investigated the influence of elevated serum levels of vitamin D on basal and stimulated TSH. Vitamin D was administered by subcutaneously implanted sustained-release pellets at four dosages. Thyrotropin releasing hormone (TRH) stimulation tests were performed at time zero, 72 hours, 1 week, 2 weeks, and 5 weeks. Animals administered vitamin D became significantly hypercalcemic and demonstrated elevations of vitamin D, which peaked at 72 hours and remained elevated for 2 weeks after pellet implantation. TRH-stimulated TSH levels were significantly elevated at 72 hours and at 1 week and returned to normal after 5 weeks. Parathyroid hormone levels were suppressed at 72 hours and at 1 week and displayed significant elevation at 2 weeks. These results provide in vivo evidence for an interaction and a possible regulatory role of 1,25 on pituitary TSH secretion and parathyroid function.
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PMID:Altered TSH levels associated with increased serum 1,25-dihydroxyvitamin D3: a possible link between thyroid and parathyroid disease. 251 35

Parathyroid hormone radioimmunoassay (RIA), specific for mid-region of the PTH molecule, has been proven to be extremely useful for the differential diagnosis of abnormal calcium metabolism. Recently, we developed a highly sensitive RIA for PTH, consisting of PTH antiserum (CH9), 125I labelled Tyr42 hPTH (43-68) and synthetic hPTH (1-84) as standard. This RIA cross-reacted with mid-region and carboxyl terminals of PTH. The within-assay and between-assay coefficients of variation were less than 4.6% and less than 8.6%, respectively. The limit of detection was 50pg/ml. The levels of serum calcium, serum phosphate, serum creatinine, Tmpo4/GFR and creatinine clearance (Ccr) in normal healthy volunteers aged 20 to 50 years remained almost constant and showed 9.24 +/- 0.34mg/dl (mean +/- SD, n = 242), 3.34 +/- 0.38mg/dl (n = 242), 0.870 +/- 0.121mg/dl (n = 242), 3.20 +/- 0.54mg/dl GF (n = 189) and 103 +/- 17ml/min (n = 137), respectively. All healthy volunteers (n = 326) had measurements of PTH in the blood. From 20 to 50 years, normal PTH mean was 374 +/- 97pg/ml (+/- SD, n = 237) and ranged from 180-568pg/ml, and from 60 to 80 years it was 471 +/- 133pg/ml (n = 34) and ranged from 205-737pg/ml. Since we found that PTH was markedly elevated above normal when Ccr was below 40ml/min, and PTH was very significantly correlated with the reciprocal of Ccr (r = 0.8996, P less than 0.001) using a multivariate analysis, all of the patients whose Ccr was higher than 40ml/min were selected and examined in the following studies. Serum PTH values completely separated patients with surgically proven primary hyperparathyroidism (1 degree HPT) from malignant associated hypercalcemia (MAH), and patients with idiopathic hypoparathyroidism (IHP) from pseudohypoparathyroidism (PHP), both of which were diagnosed by Ellsworth-Howard test. PTH values in all of the patients with 1 degree HPT (n = 23) were above normal, but those with MAH (n = 6) were below the normal or lower normal range. PTH values in patients with PHP (n = 7) showed above normal, while those with IHP (n = 5) were below the normal range. PTH was normalized in post operative status in all patients after parathyroidectomy (n = 6). These results indicate that this PTH RIA is extremely useful for the differential diagnosis in diseases with calcium abnormalities.
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PMID:[Clinical studies using a highly sensitive radioimmunoassay for mid-region and carboxy terminus of parathyroid hormone in normal, hypo- and hypercalcemic states]. 255 7

This report describes the case of a 60-year-old woman with severe metabolic bone disease and fractures due to vitamin D deficiency and hyperparathyroidism. 25OHDH3 and 1,25(OH)2D3 serum levels were undetectable and increased immediately following 25OHD3 oral administration. Serum 1,25(OH)2D3 following vitamin D repletion reached values above the normal range, and remained elevated with strict dependence on the serum 25OHD3 levels. Parathyroid hormone and alkaline phosphatase decreased during treatment, without reaching normality during 1 year of observation. Bone biopsies before and after 8-month 25OHD3 treatment showed disappearance of the osteomalacic and hyperparathyroid lesions. During treatment an increase in serum and urine calcium and formation of renal stones were observed. The patient underwent neck exploration with the finding and removal of a lipoadenoma, a rare parathyroid tumor, followed by complete and permanent remission of the disease. In conclusion, this case is suggestive of the key role played by the long-term vitamin D status in the clinical expression of primary hyperparathyroidism.
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PMID:Severe vitamin D deficiency in a case of primary hyperparathyroidism caused by parathyroid lipoadenoma, effect of 25OHD3 treatment. 261 20

Two groups of patients with primary hyperparathyroidism, one early group surgically treated operated between 1970 and 1979 (n = 90), and the other late group from 1980 to 1984 were compared concerning signs, symptoms and laboratory parameters in order to find out the changing trends in the clinical spectrum of this disease during these years. The decade of manifestation decreased from the age of sixty to fifty. The most common mode of presentation in the early group were renal (30%), gastrointestinal (27%), and osseous (18%) symptoms of primary hyperparathyroidism, and 21% symptoms due to hypercalcemia. In the later series severity of the typical symptoms decreased, diagnosis was made in nearly half of the patients (47%) by the incidental finding of hypercalcemia on routine biochemical screening. Careful investigation revealed that the severity but not the occurrence of organic and functional manifestations differed between the two groups. Mean serum calcium level decreased from 3.4 mmol/l in the early group to 3.1 mmol/l in the recent series. Parathyroid hormone level was increased in 90% respectively 79% of the patients. The localization of the parathyroids was done in 58% by ultrasound in the late group. Diagnosis was clearly made in 60% of the recent group by the combination of elevated serum calcium and parathyroid hormone levels and two associated symptoms. Diagnosis was more difficult in 10% when serum calcium was elevated and only one symptom was present. There is a trend in symptoms of primary hyperparathyroidism from typical "disease of stones, bones and abdominal groans" to a mild and nearly asymptomatic presentation detected by routine calcium screening.
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PMID:[Primary hyperparathyroidism--changes in the disease picture]. 272 26

Parathyroid hormone (PTH) has been shown in vitro to enhance erythrocyte osmotic fragility (EOF) and has been incriminated as a factor in the anaemia seen in patients with primary hyperparathyroidism and in patients with renal disease and secondary hyperparathyroidism. Enhanced EOF has also been shown in patients with chronic renal failure but did not correlate with PTH levels. We studied a group of patients with primary hyperparathyroidism with and without anaemia, and patients with secondary hyperparathyroidism and anaemia. We found that EOF studies in these patients did not differ from normal control groups and that there was no relation between PTH, EOF, and haematocrit in either study group. We conclude that PTH over a range of concentrations seen in vivo does not affect erythrocyte osmotic fragility or cause anaemia.
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PMID:Parathyroid hormone and anaemia--an erythrocyte osmotic fragility study in primary and secondary hyperparathyroidism. 281 31

Parathyroid hormone (PTH) is strongly concerned with the pathogenesis of urinary stones. PTH is mainly regulated by the serum calcium concentration and not by other hormones, as is usually the case. We studied whether PTH is also regulated by adrenocorticotrophic hormone (ACTH) or not. ACTH (0.25 mg) was injected intravenously to 17 patients with primary hyperparathyroidism PHP, 7 patients with urolithiasis, 7 patients with malignant hypercalcemia, and 6 control subjects. Serum calcium was significantly increased in only PHP. The serum calcium increase rate showed a significant positive correlation with serum alkaline phosphatase, and a negative correlation with the preinjected serum calcium. PTH was slightly increased in all four groups. Serum cortisol and ACTH concentrations were not significantly different among the groups. PTH concentration in a culture medium of parathyroid tissues increased after ACTH addition. Serum calcium was significantly increased after ACTH injection in an adrenalectomized rat, and decreased in a parathyroidectomized rat. From our data and those of others, it appears that ACTH acts on the adrenal glands to decrease the serum calcium concentration, and might act directly on the parathyroid gland or bones to increase it.
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PMID:[Studies on the endocrinological metabolism of the parathyroid. II. Influence of ACTH on parathyroid function and calcium metabolism]. 300 38


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