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)

A patient presented with the classic features of anticonvulsant-induced osteomalacia. Following discontinuance of diphenylhydantoin therapy and repletion with physiologic quantities of vitamin D, hypercalcemia and persistent biochemical hyperparathyroidism developed, and a parathyroid adenoma was removed. A history of nephrolithiasis and hypercalcemia preceding the institution of drug therapy allowed this patient's underlying parathyroid disease to be defined as primary hyperparathyroidism, which had been obscured by anticonvulsant therapy.
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PMID:Primary hyperparathyroidism presenting as anticonvulsant-induced osteomalacia. 19 3

Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1 degrees HPT), and 10 patients with chronic hypoparathyroidism. In the group with 1 degrees HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium </=10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 ml/min), and 10 patients with moderate renal insufficiency (mean glomerular filtration rate, 43 ml/min). Plasma iPTH was increased in 41 patients (73%). The development of a parametric expression for UcAMP was found to be critically important in the clinical interpretation of results for total cAMP excretion. Because of renal impairment in a large number of patients, the absolute excretion rate of cAMP correlated poorly with the hyperparathyroid state. Expressed as a function of creatinine excretion, UcAMP was elevated in 81% of patients with 1 degrees HPT, but the nonparametric nature of the expression led to a number of interpretive difficulties. The expression of cAMP excretion as a function of glomerular filtration rate was developed on the basis of the unique features of cAMP clearance in man, and this expression, which provided elevated values in 51 (89%) of the patients with 1 degrees HPT, avoided entirely the inadequacies of alternative expressions. Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed the validity of the measurements and the expressions employed.
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PMID:Nephrogenous cyclic adenosine monophosphate as a parathyroid function test. 19 23

The diuresis of cAMP in primary hyperparathyroidism was significantly higher at 7.3 +/- 2.5 mumol/g creatinine X 24 h (P less than 0.005) than that in healthy subjects (3.5 +/- 0.7 mumol/g creatinine X 24 h). After successful operation on the parathyroid gland, cAMP diuresis usually decreased within 24 hours to normal or subnormal values. In primary or secondary hypoparathyroidism subnormal amounts of cAMP (P less than 0.005) were excreted. The method gives false-negative results in functional disorders of the parathyroid glands accompanied or caused by renal failure.
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PMID:[The diuresis of cyclic adenosine-3'5'-monophosphate (cAMP) in primary and secondary disorders of the parathyroid glands]. 20 Apr 7

The urinary excretion of adenosine 3', 5'-monophosphate (cAMP) was investigated in 15 subjects with primary hyperparathyroidism prior to parathyroidectomy and in 13 of them also after the operation. In comparison with healthy control subjects the cAMP excretion was raised in 8 of the patients pre-operatively and after operation all values had become normal. The discriminatory value of the cAMP analyses seemed to be increased by relating the cAMP values to the urinary excretion of calcium. With the applied methods determination of urinary cAMP was superior to a radioimmunoassay of parathyroid hormone in recognizing patients with primary hyperparathyroidism. In normal subjects it appeared that the cAMP excretion expressed per gram creatinine was somewhat higher in women than in men.
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PMID:Urinary excretion of cyclic AMP in hyperparathyroidism. 20 93

It is uncertain whether normocalcemic, normocalciuric patients with calcium nephrolithiasis have a disorder of calcium metabolism. We studied the effect of a parathyroid extract (PTE) INFUSION (1.4 U/kg body weight) on the urinary cyclic AMP excretion in 16 such patients. For comparison, we investigated groups of normal individuals and patients with primary hyperparathyroidism, renal insufficiency and different gastrointestinal diseases. The increase of cyclic AMP above basal excretion in patients with nephrolithiasis was only 1.2 +/- 0.3 mumol/h (mean +/- SEM), versus 2.5 +/- 0.5 mumol/h in normal subjects (p less than 0.05) although the basal excretion was similar. Patients with renal insufficiency had low basal excretion of cyclic AMP and little stimulation of excretion by PTH (increase, 0.3 +/- 0.06 mumol). Patients with primary hyperparathyroidism had high baseline cyclic AMP excretion but sub-normal stimulation by PTE (increase, 0.46 +/- 0.13); in contrast, patients with different gastrointestinal disease had high baseline excretion and supranormal stimulation of cyclic AMP excretion (increase, 5.2 +/- 0.6). We speculate that an impaired response to PTH might be involved in the slightly increased urinary calcium excretion in normocalcemic stone formers suggested by others.
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PMID:Effect of parathyroid extract on renal cyclic AMP excretion in patients with normocalciuric nephrolithiasis. 20 1

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

A sensitive radioreceptor assay for 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) is utilized to quantitate the circulating concentration of this sterol in experimental animals and humans. When weanling rats are grown for 2 weeks on low calcium or low phosphate diets, limited availability of either ion elicits a five-fold increase in the plasma level of 1alpha,25-(OH)2D3. The enhancement of 1alpha,25-(OH)2D3 in calcium deficiency is dependent upon the presence of the parathyroid and/or thyroid glands, which is consistent with parathyroid hormone (PTH) mediation of this effect. In contrast, the response to phosphate deficiency is independent of these glands and may result from a direct action of low phosphate on the renal synthesis of 1alpha,25-(OH)2D3. Studies in humans indicate that the normal level of 1alpha,25-(OH)2D is 2.1--4.5 ng/100 ml plasma. Patients with chronic renal failure have markedly lower circulating 1alpha,25-(OH)2D and this kidney hormone is undetectable in anephric subjects, but returns to normal within 1 day after successful renal transplantation. Hypoparathyroidism and pseudohypoparathyroidism are associated with reduced plasma 1alpha,25-(OH)2D while patients with primary hyperparathyroidism have significantly elevated sterol hormone levels. Thus, from measurements in rats and humans, it appears that circulating 1alpha,25-(OH)2D3 is regulated by PTH and/or phosphate and that abnormal plasma 1alpha,25-(OH)2D3 is a part of the pathophysiology of renal osteodystrophy and parathyroid disorders.
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PMID:The assay of 1alpha,25-dihydroxyvitamin D3: physiologic and pathologic modulation of circulating hormone levels. 21 27

A prospective, controlled study of patients with primary hyperparathyroidism has been carried out to establish the relation of this endocrinopathy to calcium pyrophosphate dihydrate crystal deposition disease. Eight of 26 patients with documented hyperparathyroidism were found to have chondrocalcinosis compared to four of 104 individuals in the control group (p less than 0.01). Two of these eight patients had confirmed pseudogout attacks shortly after parathyroidectomy. Four other patients, including two without chondrocalcinosis, gave a history of typical pseudogout. Patients with hyperparathyroidism and chondrocalcinosis were significantly older than those without the articular lesion (p = 0.006). We could not delineate specific metabolic abnormalities of hyperparathyroidism which contributed to the development of chondrocalcinosis.
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PMID:Calcium pyrophosphate crystal deposition disease and hyperparathyroidism: a controlled, prospective study. 21 3

On the basis of a dramatic hypercalcemia revealed by digestive and neuropsychic symptoms and related to a primary hyperparathyroidism, the authors recall all the clinical circumstances which should lead to determination of plasma calcium as well as the clinical and biological particularities which, in front of a hypercalcemia, suggest a primary hyperparathyroidism. The stress the usefulness and the limits of the dosage of plasma immunoreactive parathyroid hormone as well as the difficulties to differentiale primary from paraneoplasic hyperparathyroidism. The recent pathophysiological concepts of malignant hypercalcemia reviewed.
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PMID:[Primary hyperparathyroidism. Current aspects of its diagnosis apropos of a case with digestive and neuropsychiatric manifestations]. 21 10

In man, the total amount of cyclic AMP (cAMP) excreted in urine is derived from (a) the filtered load of the nucleotide and (b) cAMP formed de novo in the kidney (nephrogenous cAMP, NcAMP). NcAMP is the only pool of the nucleotide easily quantified in vivo and appears to provide a specific index of the effects of circulating, active parathyroid hormone. Elevated values for NcAMP (4.64 +/- 1.95 nmol/100 ml GF, mean +/- SD) were found in 90% or more of 115 patients with primary hyperparathyroidism, and low values (0.31 +/- 0.16 nmol/100 ml GF, mean +/- SD) were noted in 41 individuals with absent or suppressed parathyroid function. When properly expressed (as a function of glomerular filtration rate), results for the total cAMP excretion provided similar findings. The measurement of NcAMP provides a sensitive index of parathyroid function over the entire range of parathyroid activity and has proven to be an optimal method for assessing parathyroid suppressibility in response to intravenous or oral calcium administration. These techniques, the 'calcium injection test' and the 'oral calcium tolerance test', are useful in evaluation a number of subtle disorders of calcium metabolism.
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PMID:Nephrogenous cyclic AMP as a parathyroid function test. 22 May 48


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