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

Ten patients with subtle primary hyperparathyroidism and intermittent hypercalcaemia were followed serially for periods of 2--18 months (mean 10 months). Fasting serum calcium was elevated (greater than 10.6 mg/dl) in only 20% of determinations and fluctuated widely (9.1--11.2 mg/dl), yet the patients displayed a continuous, rather than episodic, basic disease process as defined by increases in nephrogenous cyclic AMP and serum iPTH. Identical findings were noted in short-term (2--3 successive days) studies in twelve patients. In response to a 1000 mg oral calcium tolerance test, twelve patients with primary hyperparathyroidism and intermittent hypercalcaemia (basal serum calcium 10.2 +/- 0.2 mg/dl, mean +/- SD) displayed: (1) hyperabsorption of calcium (mean calciuric response twice normal); (2) induced-hypercalcaemia (mean serum calcium 11.4 mg/dl, with a mean increase of 1.2 mg/dl versus 0.2 mg/cl in normal subjects); and (3) abnormal parathyroid suppressibility (nephrogenous cyclic AMP 2.66 +/- 0.57 nmol/100 ml GF versus 0.95 +/- 0.40 nmol/100 ml GF in normal subjects, mean +/- SD). The patients demonstrated striking hypercalciuria (452 +/- 123 mg/24 h) on a 1000 mg metabolic calcium diet. Serum levels of 1,25(OH)2D3, measured in ten patients, were markedly elevated at 90 +/- 20 pg/ml (mean +/- SD), and there was a strong positive correlation between the values for 1,25(OH)2D3 and the calciuric response to the calcium tolerance test (r = 0.75, P less than 0.001). These results (1) indicate that the calcium tolerance test is a simple and reliable technique for diagnosis of patients with primary hyperparathyroidism and intermittent hypercalcaemia, and (2) emphasize the important pathophysiologic features of this subtle clinical variant of primary hyperparathyroidism.
 ...
PMID:Primary hyperparathyroidism with intermittent hypercalcaemia: serial observations and simple diagnosis by means of an oral calcium tolerance test. 624 72

In 38 patients with hypoparathyroidism, electrolytes, amino-terminal PTH(1--34) and carboxyl-terminal PTH in serum and urinary cyclic AMP were measured. Serum PTH(1--34) levels were low and C-PTH levels measured simultaneously in the same sera were low except one having a high level. In pseudohypoparathyroidism, serum C-PTH was elevated and in 1 of 2 patients serum PTH(1--34) was elevated. Urinary cyclic AMP was decreased in hypoparathyroidism and there was a positive correlation between urinary cyclic AMP and serum PTH in normal subjects and parathyroid dysfunctions. Responses of urinary cyclic AMP to PTH were better in hypoparathyroidism and less in primary hyperparathyroidism than normal subjects. These data suggest that measurements of serum PTH(1-34), C-PTH and urinary cyclic AMP are important in the diagnosis and pathophysiological classification of hypoparathyroidism.
 ...
PMID:Urinary adenosine 3',5'-monophosphate, circulating amino-terminal PTH (1--34) and carboxyl-terminal PTH in hypoparathyroidism. 624 42

In 50 consecutive patients with cancer-associated hypercalcemia, we measured nephrogenous cyclic AMP, tubular phosphorus threshold, fasting calcium excretion, plasma 1,25-dihydroxyvitamin D, and immunoreactive parathyroid hormone as determined by four region-specific antiserums. Nephrogenous cyclic AMP excretion was elevated in 41 patients and suppressed in nine (means, 5.85 vs. 0.51 nmol per 100 ml of glomerular filtrate). There was no overlap between these groups. When compared with 15 patients with primary hyperparathyroidism, the group with increased cyclic AMP excretion had similar reductions in tubular phosphorus threshold; higher fasting calcium excretion (means, 0.66 vs. 0.25 mg per 100 ml of glomerular filtrate, P < 0.01); marked reductions in 1,25-dihydroxyvitamin D (means, 20 vs. 83 pg per milliliter, P < 0.001); and lower levels of immunoreactive parathyroid hormone in all four assays. The data suggest that elevated excretion of nephrogenous cyclic AMP may be a useful marker of humorally mediated cancer-associated hypercalcemia, that this type of hypercalcemia is common, that the humoral factor responsible for this syndrome is not native 1-84 parathyroid hormone, and that the various subtypes of cancer-associated hypercalcemia are biochemically distinguishable from primary hyperparathyroidism.
 ...
PMID:Biochemical evaluation of patients with cancer-associated hypercalcemia: evidence for humoral and nonhumoral groups. 625 85

Urinary cyclic AMP (cAMP) and phosphate were measured before and after calcium infusion in 12 patients with operatively verified primary hyperparathyroidism (PHP) and in 12 healthy persons. In normal subjects infusion of calcium caused a reduction in urinary cAMP directly correlated to the preinfusion values and inversely correlated to the serum calcium concentration determined as albumin-corrected serum calcium. In normal subjects with high normal albumin-corrected serum calcium the infusion of calcium caused no or only a small depression in the urinary excretion of cAMP. Changes in phosphate excretion were not correlated to the calcium concentration. Four of the 12 hyperparathyroid patients showed normal relative suppression in urinary cAMP after the infusion of calcium, and 5 had normal suppression of phosphate excretion. It is concluded that some patients with PHP retain calcium-sensitive secretion of PTH, and that the classical calcium infusion test is of doubtful value in the diagnosis of PHP.
 ...
PMID:Influence of calcium infusion on urinary cyclic AMP and phosphate in hyperparathyroidism. 627 Sep 86

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.
 ...
PMID:Abnormal bone and parathyroid histology in carcinoma patients with pseudohyperparathyroidism. 627 64

The effects of calcium injection (3 mg/Kg/10 min) or oral calcium administration (calcium lactate 7.7 g) on plasma iPTH and Nephrogenous cyclic AMP (NcAMP) were studied in 6 normal controls and 13 patients with primary hyperparathyroidism. In the control subjects, plasma iPTH determined by a predominantly carboxyl-terminal antiserum was less than 0.3 ng/ml before and after both calcium loads, whereas 41 approximately 98% (mean 67%) of NcAMP was rapidly and uniformly suppressed to a level lower than the normal value. In 2 patients with primary hyperparathyroidism, iPTH was clearly reduced from 8.0 to 4.6 ng/ml and 1.6 to 0.96 ng/ml, respectively, by the calcium load. However, in the other 7 patients with primary hyperparathyroidism who showed only a slight elevation of iPTH: less than 0.3 approximately 0.9 ng/ml, the reductions in iPTH were not detected after the calcium load: less than 0.3 approximately 0.7 ng/ml. In contrast, 30 approximately 54% (1.02 approximately 3.85 nmol/dl GF) of NcAMP, which was greater than the diurnal variation, was suppressed after calcium injection in 5 patients with primary hyperparathyroidism (2 of 4 patients with urological, and 3 of 5 patients with chemical hyperparathyroidism). But NcAMP was not suppressed in all 4 patients with skeletal hyperparathyroidism including one with proximal renal tubular dysfunction whose basal iPTH was elevated markedly but reduced clearly by the calcium load. In general, suppression of NcAMP was followed by a decrease of phosphate excretion. On the other hand, even in a patient with primary hyperparathyroidism whose NcAMP was not suppressed at all after the calcium injection, calcium infusion (15 mg/Kg/3h) resulted in some (23%) decrease in NcAMP. Oral calcium administration resulted in responses which were almost the same as those produced by calcium injection. These results suggest that NcAMP provides a useful index in the parathyroid suppression test in patients with primary hyperparathyroidism, especially those who display a rather mild elevation of iPTH. This is not the case, however, in a few patients who show a marked elevation of iPTH and/or proximal renal tubular dysfunction.
 ...
PMID:[Suppressibility of parathyroid function in primary hyperparathyroidism as estimated by nephrogenous cyclic AMP (author's transl)]. 628 61

To evaluate the usefulness of urinary cyclic AMP (U-cAMP) expressed as nmol/100 ml glomerulus filtrate (GF) when discriminating various hypercalcemic states, we studied 99 patients. Patients with primary hyperparathyroidism (PHPT) showed a positive correlation between individual S-calcium levels and U-cAMP, nmol/100 ml GF (females r=0.49, n=40, p less than 0.01 and males r=0.91, n=7 p less than 0.001). There was also a correlation between U-cAMP, nmol/100 ml GF, and the weight of the adenomas (females r=0.36, n=32, p less than 0.05) and males r=0.79, n=6, p less than 0.05). Patients with PHPT and normal renal function excreted more U-cAMP than controls, 6.0 +/- 1.6 versus 4.3 +/- 1.0 nmol/100 ml GF (mean +/- SD). Of 47 patients with PHPT and normal renal function, 29 showed values below the upper normal limit, 6.3 nmol/100 ml GF (mean +/-2 SD), of the control group; the overlap was 62%. When U-cAMP was expressed as mumol/24 hours, the overlap was 40/47 (85%) and, when expressed as mumol/g creatinine, 31/47 (66%). Three patients with sarcoidosis and two with malignancies and hypercalcemia showed excretory values of U-cAMP, nmol/100 ml GF, above the upper normal limit. Patients with acromegaly or prolactinoma showed normal values of U-cAMP, nmol/100 ml GF. The present data indicate that all three types of determinations of urinary cAMP based on 24 hour urine collections are of little value in the differential diagnosis of hypercalcemic states.
 ...
PMID:Urinary cyclic AMP corrected for glomerular filtration rate in the differential diagnosis of hypercalcemia. 628 11

In order to evaluate the possible causal relationship between raised serum gastrin levels and the development of primary hyperparathyroidism (HPT) which is suggested from experimental studies we evaluated parathyroid function in a group of 32 patients with hypergastrinaemia and pernicious anaemia. The values for serum calcium and parathyroid hormone were determined as well as the fasting urinary excretions of cyclic AMP and calcium. There was no relationship between the serum gastrin levels and any of the other studied parameters and there was no consistent pattern suggesting parathyroid hyperfunction. A retrospective analysis of hospital records from 441 patients operated for primary HPT showed a prevalence of pernicious anaemia of 1.8%. This figure is higher than that found in the unselected age-matched population (0.31%). However, taken together this study does not support the hypothesis that hypergastrinaemia is of particular importance for the pathogenesis of primary HPT.
 ...
PMID:Evaluation of parathyroid function in patients with hypergastrinaemia and pernicious anaemia. 629 36

The analysis of nephrogenous cyclic AMP (NcAMP) has been reported to be a means of estimating parathyroid function with the advantage of being rapidly and easily performed. More specific than the analysis of urinary cyclic AMP (UcAMP), it measures biological activity of the parathyroid hormone. This study tests its use in the diagnosis of primary hyperparathyroidism (HPP) and compares the results of UcAMP with those of NcAMP. Analyses of NcAMP and parathyroid hormone were performed in a group of 21 healthy controls and two groups of hypercalcemic patients, one consisting of 12 patients with HPP and the other of 14 patients with hypercalcemia of non-parathyroid origin (HCa). It was confirmed that NcAMP is a parameter of parathyroid function, analysis of which allows the diagnosis of HPP with the same precision as analysis of the carboxyterminal plasma PTH. It has the added advantage over PTH measurements of detecting low values, thus permitting documentation of parathyroid inhibition in HCa patients.
 ...
PMID:[Usefulness of the determination of nephrogenous cyclic AMP in the diagnosis of primary hyperparathyroidism]. 630 35

Because prominent skeletal muscle dysfunction and muscle wasting are seen in both chronic uremia and in primary hyperparathyroidism, and because markedly elevated parathyroid hormone levels occur in both disorders, potential effects of parathyroid hormone on skeletal muscle protein, amino acid, and cyclic nucleotide metabolism were studied in vitro using isolated intact rat epitrochlearis skeletal muscle preparations. Intact bovine parathyroid hormone and the synthetic 1-34 fragment of this hormone stimulated the release of alanine and glutamine from muscle of control but not from chronically uremic animals. This stimulation was dependent upon the concentration of parathyroid hormone added: At 10(5) ng/ml parathyroid hormone increased alanine release 84% and glutamine release 75%. Intracellular levels of alanine and glutamine were not altered by parathyroid hormone. Increasing concentrations of the 1-34 polypeptide decreased [(3)H]leucine incorporation into protein of muscles from both control and uremic animals. Using muscles from animals given a pulse-chase label of [guanido-(14)C]arginine in vivo, parathyroid hormone increased the rate of loss of (14)C label from acid-precipitable protein during incubation and correspondingly increased the rate of appearance of this label in the incubation media. Parathyroid hormone increased muscle cAMP levels by 140% and cGMP levels by 185%, but had no effect on skeletal muscle cyclic nucleotide phosphodiesterase activities as assayed in vitro. Adenylyl cyclase activity in membrane preparations from control but not uremic rats was stimulated by parathyroid hormone in a concentration-dependent fashion. However, no stimulation of guanylyl cyclase activity was noted by parathyroid hormone, although stimulation by sodium azide was present. Incubation of muscles with added parathyroid hormone produced a diminished responsiveness towards epinephrine or serotonin regulation of amino acid release and cAMP formation in the presence compared to the absence of parathyroid hormone. In the absence of parathyroid hormone, detectable inhibition of alanine and glutamine release was produced by 10(-9) M epinephrine, whereas in the presence of parathyroid hormone (1,000 ng/ml) inhibition of alanine and glutamine release required 10(-6) M or greater epinephrine. Resistance to cyclic AMP action as well as inhibition of cyclic AMP formation by parathyroid hormone was found. Preincubation of rat sarcolemma with 1-34 parathyroid hormone produced a decreased activity of the isoproterenol-stimulable adenylyl cyclase activity but there was no apparent change in the concentration of isoproterenol required for one-half maximal and maximal stimulation of the enzyme. These findings suggest that high levels of parathyroid hormone have direct effects on skeletal muscle protein, amino acid, and cyclic nucleotide metabolism in muscle of normal but not uremic animals. Treatment with these high levels of parathyroid hormone in vitro appears to reproduce in normal muscle, the metabolic deficits and loss of hormone responsiveness observed in muscle of chronically uremic animals. It is therefore possible that direct effects of parathyroid hormone on skeletal muscle may account in part for the muscle dysfunction and wasting of primary hyperparathyroidism and chronic uremia.
 ...
PMID:Effects of parathyroid hormone on skeletal muscle protein and amino acid metabolism in the rat. 630 55


<< Previous 1 2 3 4 5 6 7 8 Next >>