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)

Administration of the antifungal drug ketoconazole reduces serum 1,25-dihydroxyvitamin D (1,25-D) levels in normal subjects. To determine whether a similar effect occurs in hypercalcemic patients, ketoconazole (200 mg every 8 h for 7 days) was given to nine patients with confirmed primary hyperparathyroidism, three patients with probable primary hyperparathyroidism who were awaiting surgery, and three patients with mild hypercalcemia of uncertain etiology who were being followed. Ketoconazole administration led to a significant reduction in mean serum 1,25-D levels in the hypercalcemic patients [basal, 64 +/- 7 (+/- SEM) pg/mL (154 +/- 17 pmol/L) vs. 36 +/- 5 pg/mL (86 +/- 12 pmol/L) after ketoconazole; P less than 0.001]. Serum total calcium fell slightly but significantly [basal, 11.05 +/- 0.17 mg/dL (2.76 +/- 0.04 mmol/L) vs. 10.77 +/- 0.16 (2.69 +/- 0.04 mmol/L) after ketoconazole; P less than 0.02], but the falls in total serum calcium and serum 1,25-D after ketoconazole treatment were not correlated with one another. Ketoconazole administration did not alter serum ionized calcium, 25-hydroxyvitamin D, phosphate, alkaline phosphatase, or PTH concentrations or urinary cAMP excretion. The responses to ketoconazole were similar in all three patient subgroups. We conclude that short term administration of ketoconazole to hypercalcemic patients causes a substantial fall in serum 1,25-D and a small fall in total serum calcium. These effects render ketoconazole a potentially useful agent for investigation of the importance of 1,25-D in patients with hypercalcemic disorders and for their treatment.
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PMID:Ketoconazole-induced reduction in serum 1,25-dihydroxyvitamin D and total serum calcium in hypercalcemic patients. 336 Sep 1

This study was designed to follow the evolution of serum 1,25(OH)2D after surgery for primary hyperparathyroidism. Ten patients were studied before and for up to 85 d after removal of a single parathyroid adenoma. Blood and 24 h urine were obtained at various time points, for the measurement of serum or urinary phosphate and calcium indices. Before surgery, serum calcium (2.91 +/- 0.06 mmol/l; mean +/- SEM), parathyroid hormone (354 +/- 47 pg/ml) and 1,25(OH)2D (61.2 +/- 7.8 pg/ml) were elevated while serum phosphate (1.01 +/- 0.07 mmol/l) tended to be low. Relative hypoparathyroidism was evident for up to 5 d after surgery with the lowest value for serum parathyroid hormone (41 +/- 16 pg/ml) on day 1, serum calcium (2.12 +/- 0.06 mmol/l) on day 3 and highest value for serum phosphate (1.41 +/- 0.13 mmol/l) on day 5. As expected, serum 1,25(OH)2D levels decreased to 35.9 +/- 4.2 pg/ml 24 h after surgery. Stabilization of serum and urinary parameters to normal values was seen between day 5 and day 27; the only exception was serum 1,25(OH)2D, which increased again at day 27 to 57.6 +/- 5.0 pg/ml, a value as high as that before surgery. It was still elevated at day 50 (58.3 +/- 4.3 pg/ml), but returned towards normal values in three out of four patients (44 +/- 3.9 pg/ml) by day 80. No variation in 25(OH)D or 24,25(OH)2D was seen throughout the study. 1,25(OH)2D values could be related to serum parathyroid hormone values before surgery (r = 0.659, P less than 0.05) but not after. The secondary increase in serum 1,25(OH)2D could not be related to variations in serum calcium, phosphate, parathyroid hormone or diet. Further studies will be required to explain this phenomenon.
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PMID:Late increase in serum 1,25-dihydroxyvitamin D one month after surgery for adenomatous hyperparathyroidism. 375 58

Serum vitamin D metabolites, the renal tubular maximum reabsorptive rate for phosphate (TMP/GFR) nephrogenic cyclic AMP (NcAMPI, and CaE (urinary calcium excretion per litre of glomerular filtrate) were measured in 14 adults with familial hypocalciuric hypercalcaemia (FHH). The findings were compared with analyses in 14 patients with surgically proven primary hyperparathyroidism matched for serum calcium, creatinine clearance and vitamin D status (assessed by serum concentrations of 25 hydroxyvitamin D). Vitamin D metabolites were also measured in 16 normocalcaemic relatives of patients with FHH. The serum concentration of 24,25 dihydroxycholecalciferol was appropriate for the prevailing 25 hydroxyvitamin D and no difference was found between groups. The serum concentration of 1,25 dihydroxycholecalciferol was significantly greater in primary hyperparathyroidism (P less than 0.0005) compared with patients with FHH and their normocalcaemic relatives. TMP/GFR was reduced in both primary hyperparathyroidism (0.53 +/- 0.12 mmol/l GF, mean +/- SEM) and FHH (0.86 +/- 0.14 mmol/l GF). Patients with primary hyperparathyroidism showed an increase in NcAMP output in the urine (38.5 +/- 16 mmol/l GF) which was significantly greater (P less than 0.0001) than the normal NcAMP (13.5 +/- 9.2 nmol/l GF) found in FHH. CaE was low in FHH indicating increased renal tubular reabsorption of calcium. It is concluded that there is no abnormality of vitamin D metabolism in FHH comparable with the changes observed in primary hyperparathyroidism. It is suggested that the biochemical abnormalities in FHH cannot be explained solely upon an increased sensitivity of the renal tubules to the effects of endogenous parathyroid hormone.
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PMID:Familial hypocalciuric hypercalcaemia: observations on vitamin D metabolism and parathyroid function. 631 24

An oral calcium tolerance test was administered to 22 hyperparathyroid patients and 162 normal subjects to determine its value in the diagnosis of mild primary hyperparathyroidism. Basal urinary excretion of calcium was higher in patients [0.217 mg/100 ml glomerular filtrate (GF)] than in normal subjects (0.090 mg/100 ml GF), but there was 50% overlap between the two groups. Phosphorus excretion, expressed as the ratio of the maximal tubular reabsorption of phosphorus to the glomerular filtration rate, was lower in patients (2.77) than in normal subjects (3.7), but 38% of the patients fell within the normal range. Urinary excretion of total cAMP also failed to separate hyperparathyroid patients from normal subjects [5.8 +/- 0.32 (+/- SEM) nmol/100 ml GF in patients vs. 3.41 +/- 0.11 in normal subjects]. Determination of nephrogenous cAMP failed to increase the utility of cAMP as a predictor of hyperparathyroidism. In response to oral calcium, the elevation in serum calcium concentration was the same in both groups. The rise in urinary calcium was greater in patients, but showed 77% overlap with that in normal subjects. Conversely, serum immunoreactive PTH, measured with a midregion-specific RIA, was elevated in 90% of the patients. Some normal subjects also had high levels of PTH, but none of these had hypercalcemia. We conclude that the oral calcium tolerance test and measurement of urinary cAMP do not adequately distinguish hyperparathyroid patients from normal subjects. In the absence of renal insufficiency, the combination of hypercalcemia and elevated serum PTH concentration most accurately predicts the diagnosis of primary hyperparathyroidism.
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PMID:Assessment of adenosine 3',5'-monophosphate excretion and an oral calcium tolerance test in the diagnosis of mild primary hyperparathyroidism. 631 54

Severe secondary hyperparathyroidism is still observed at present in 5-10% of haemodialysis patients. It requires surgical correction. Fifty-eight haemodialysis patients had neck surgery and their 222 parathyroid glands analysed. The individual gland weight was comprised between 22 and 3880 mg (mean +/- SEM, 689 +/- 62 mg). Mean total parathyroid gland weight per patient was comprised between 2 and 3 g. Schematically, 4 types of gland architecture could be distinguished: diffuse hyperplasia alone; diffuse hyperplasia associated with incipient nodule formation; hyperplasia with pronounced nodule formation; and nodule formations alone. Total gland weight was significantly higher for the latter two histological forms than for the former suggesting transformation with time of pure hyperplasia to nodular hyperplasia. Patients with chronic pyelonephritis had a mean gland weight higher than that of patients with chronic glomerulonephritis (3308 +/- 498 mg versus 1824 +/- 358 mg, p less than 0.01). No relation was found between total gland weight and plasma calcium, phosphate or alkaline phosphatases. However, a weak relation existed between total gland weight and plasma immunoreactive parathyroid hormone. In addition, a negative relation was observed between highest prior plasma aluminium and gland weight when considering only patients with a gland weight less than 2000 mg. Parathyroid gland aluminium content was significantly higher in haemodialysis patients than in nonuraemic patients with primary hyperparathyroidism. A direct relation was found between parathyroid gland and bone aluminium. In conclusion, in haemodialysis patients with evolving hyperparathyroidism initially diffuse gland hyperplasia appears to be associated progressively with nodule formation. Circulating immunoreactive parathyroid hormone is positively related to total gland weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hyperparathyroidism secondary to renal insufficiency: anatomo-clinical relations and the potential role of an aluminum overload]. 648 74

In a retrospective study of 120 patients with surgically proved primary hyperparathyroidism, 71 patients who were normotensive and 49 patients (41 percent) who were either hypertensive at the time of parathyroidectomy or had a history of hypertension were compared. The mean serum calcium levels in the normotensive and hypertensive patients were very similar (11.6 +/- 0.1 [SEM] mg/dl, and 11.8 +/- 0.1), ruling against the hypothesis that hypercalcemia per se is the dominant cause of the hypertension of hyperparathyroidism. The mean serum creatinine levels in the two groups were also very similar (1.02 +/- 0.05 and 1.09 +/- 0.05 mg/dl), indicating that the hypertension of hyperparathyroidism is not the consequence of advanced renal parenchymal damage. The hypertensive patients did not have a significantly higher prevalence of urolithiasis. A review of the data in this and related studies leads to the conclusion that the hypertension of hyperparathyroidism is heterogeneous in origin. The mean serum phosphate level in the hypertensive patients was significantly lower than that in the normotensive patients (2.20 +/- 0.06 mg/dl versus 2.69 +/- 0.09 mg/dl, p less than 0.02), which may be due to a decrease in renal tubular phosphate reabsorption secondary to hypertension.
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PMID:Hypertension and hyperparathyroidism. Inverse relation of serum phosphate level and blood pressure. 685 80

Despite the high circulating levels of immunoreactive PTH in patients with pseudohypoparathyroidism type I (PSPI) the levels of bioactive PTH (bioPTH) have been found to be close to the normal range. To elucidate this dissociation, we have studied the recovery of the biological activity of bovine PTH added to the plasma of patients with either PSPI, or with hypoparathyroidism (PTX), primary hyperparathyroidism (HPT) or of normal subjects. In PSPI (n = 10) the recovery of biological activity was 5.6% +/- 3.6 (mean +/- SEM) whereas in PTX (n = 7), in HPT (n = 4) and in normal subjects (n = 8) it was 79% +/- 5, 75% +/- 9 and 68% +/- 4, respectively. In another PSPI patient, who had undergone total parathyroidectomy, bioPTH was undetectable but the recovery from the plasma of added PTH was 84%. Thus we have found inhibition of PTH bioactivity by plasma of PSPI patients which was absent after parathyroidectomy.
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PMID:Inhibition of cytochemical bioactivity of parathyroid hormone by plasma in pseudohypoparathyroidism type I. 707 1

In 30 normal subjects, the mean (+/- SEM) plasma concentration of PRL was 5.90 +/- 0.40 ng/ml and that of PTH was 0.51 +/- 0.03 ng/ml. There was no significant difference in plasma hormone levels according to age or sex. Ten cases of primary hyperparathyroidism showed PRL concentrations (8.90 +/- 1.80 ng/ml) significantly (P less than 0.01) higher than those of the normal subjects. After adenomectomy, the PRL concentration decreased (5.35 +/- 0.50 ng/ml). However, this decrease was only significant in the 5 of 10 patients who had preoperative plasma PRL levels of 10 ng/ml or more (P less than 0.01). The increase in PRL concentration in 10 cases of secondary hyperparathyroidism with normal glomerular function was also significant (14.25 +/- 3.9 ng/ml; P less than 0.001). Fourteen patients with prolactinoma showed PTH plasma levels (1.25 +/- 0.15 ng/ml) significantly higher than those of normal subjects (P less than 0.001). Eight of the 14 patients received 7.5 mg/24 h of bromocriptine for 3 months; their mean plasma PTH level decreased significantly from 1.60 +/- 0.35 to 0.50 +/- 0.11 ng/ml (P less than 0.01). In 9 cases of secondary hyperprolactinemia, the increase in PTH (0.80 +/- 0.16 ng/ml) was significant compared to the plasma PTH levels in the normal group (P less than 0.05). These results show that an excess of plasma PRL is associated with an excess of plasma PTH and vice versa. The mechanisms of these relationships remain unclear.
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PMID:Comparison between the plasma concentrations of prolactin and parathyroid hormone in normal subjects and in patients with hyperparathyroidism or hyperprolactinemia. 713 Mar 42

Circulating immunoreactive parathyroid hormone (PTH) was measured by a homologous, amino-terminal, specific, immunoradiometric assay in man. In forty-two healthy subjects the concentrations ranged between < 40 pg/ml and 120 pg/ml. No hormone could be detected in the sera of eleven patients with hypoparathyroidism, but the concentrations were clearly elevated in six patients with pseudohypoparathyroidism (range 190-1120 pg/ml). In thirty-five patients with primary hyperparathyroidism the mean (+/- SEM) concentration was 283.4 +/- 42.4 pg/ml (range 100-1350 pg/ml). A significant positive correlation was demonstrated between immunoassayable hormone and serum calcium concentrations in these patients. In nine patients PTH concentrations were measured before and after parathyroidectomy. In all of them they were elevated pre-operatively but fell to the normal range after parathyroidectomy. The disappearance of exogenously administered synthetic human PTH (1-34) from the circulation of two normal subjects was rapid with an apparent plasma half-disappearance time (t1/2) between 2 and 3 min; the metabolic clearance rate was 12.9 and 9.0 ml. kg-1 . min-1 respectively. Similarly, the disappearance of endogenous, amino-terminal, immunoreactive PTH from the circulation of two patients with primary hyperparathyroidism after parathyroidectomy was rapid; the apparent t1/2 was approximately 3 min. Homologous amino-terminal specific immunoassays for PTH can thus be useful for the study of both the acute, and chronic, changes of circulating hormone in man and represent an improvement over heterologous unselected assay systems.
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PMID:Studies of circulating parathyroid hormone in man using a homologous amino-terminal specific immunoradiometric assay. 743 64

The acute effects of a single intravenous injection of 2 micrograms of 1 alpha-hydroxycholecalciferol (alfacalcidol) were studied for a 24-h period in six normal males (mean age 33 years), six women with primary hyperparathyroidism (mean age 72 years) and six women with established osteoporosis (mean age 63 years). In all three groups, serum calcitriol levels rose to a peak 2-3 h after administration of alfacalcidol. Basal levels were highest in the primary hyperparathyroidism group at (mean +/- SEM) 81 +/- 2 vs 62 +/- 12 (normal males) (p < 0.05) and 56 +/- 5 pmol/l (osteoporosis) (p < 0.01). Highest peak levels were found also in the primary hyperparathyroidism group at 150 +/- 15 vs 114 +/- 15 (normal males) (p < 0.05) and 127 +/- 15 pmol/l (osteoporosis) (p < 0.01). The rise in calcitriol was higher in the primary hyperparathyroidism group than either the normal males or osteoporotic patients (p < 0.05). No significant differences were evident in basal serum calcidiol concentrations among the three treatment groups. As might be expected, highest basal concentrations of parathyroid hormone (PTH), serum calcium and serum osteocalcin were noted in the primary hyperparathyroid group (PTH: 17.1 +/- 7.7 vs 1.9 +/- 0.5 (normal males) (p < 0.01) and 2.1 +/- 0.3 pmol/l (osteoporosis) (p < 0.01); calcium: 3.06 +/- 0.08 vs 2.50 +/- 0.02 (normal males) (p < 0.01) and 2.43 +/- 0.02 mmol/l (osteoporosis) (p < 0.01); osteocalcin: 1.10 +/- 0.08 vs 0.56 +/- 0.16 (normal males) (p < 0.05) and 0.53 +/- 0.21 nmol/l (osteoporosis) (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute effects of intravenous 1 alpha-hydroxycholecalciferol on parathyroid hormone, osteocalcin and calcitriol in man. 813 Aug 88


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