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)

1. The metabolism of an intravenous pulse dose of double-isotope-labelled cholecalciferol has been studied in control subjects with widely differing states of vitamin D nutrition and in patients with primary disorders of parathyroid function. 2. The formation of labelled 1,25-dihydroxy-cholecalciferol [1,25-(OH)2D3] and labelled 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] has been related to the prevailing concentrations in serum of 25-hydroxycholecalciferol [25-(OH)D3], immunoreactive parathyroid hormonel, calcium and orthophosphate (Pi). 3. In control subjects with relative vitamin D deficiency [serum 25-(OH)2D3 was related inversely to the serum 25-(OH)D3 and serum calcium, and directly to serum immunoreactive parathyroid hormone. No formation of 1,25-(OH)2D3 was detectable to form labelled 24,25(OH)2D3 preferentially. 4. No control subject produced significant amounts of both labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously. 5. All subjects with primary hyperparathyroidism produced significant amounts of labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously; the renal turnover of 25-(OH)D3 was apparently greater than in nutritionally matched controls. Serum labelled 1,25-(OH)2D3 in this disease was not correlated with serum 25-(OH)D3, immunoreactive parathyroid hormone, calcium or Pi. Production of labelled 24,25-(OH)2D3 was inappropriately high for the prevailing nutritional state. 6. The indirectly estimated their concentration of 1,25-(OH)2D3 showed only a fourfold variation in control subjects (45-180 pmol/l), compatible with its having a regulated hormonal function. 7. The data suggest that the production of 1,25-(OH)2D3 from a pulse dose of cholecalciferol is normally regulated, directly or indirectly, by the parathyroid hormone.
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PMID:Vitamin D metabolism and parathyroid function in man. 16 31

Responsiveness of urinary cyclic AMP and phosphate to 200 units of parathyroid extract was evaluated in 5 normal subjects, 2 patients with idiopathic hypoparathyroidism, 4 patients with pseudohypoparathyroidism and 3 patients with primary hyperparathyroidism. Among them, 3 patients with pseudohypoparathyroidism were examined prior to and during therapy with vitamin D. Two patients with primary hyperparathyroidism were examined before and after removal of adenomas. In control subjects, percent increase in cyclic AMP after parathyroid extract administration was 7265 plus or minus 3312%, and in phosphate 290 plus or minus 72%. It was found that in idiopathic hypoparathyroidism the response of cyclic AMP was in the normal range, though that of phosphate was higher than normal. In pseudohypoparathyroidism, as distinguished from what Drezner et al. called pseudohypoparathyroidism type II, the response of cyclic AMP was uniformly low, while that of phosphate was variable. Similar results were obtained during treatment with vitamin D. In primary hyperparathyroidism, the responses of both cyclic AMP and phosphate were lower than normal. After removal of adenomas, the response of phosphate became norma., but the response of cyclic AMP rose to a subnormal level in one patient, and remained low in the other. For the diagnosis of pseudohypoparathyroidism, the response in cyclic AMP was considered to be a more reliable index than that in phosphate whether the patient was being treated with vitamin D or not.
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PMID:Responsiveness of urinary cyclic AMP and phosphate to parathyroid extract in patients with parathyroid disorders. 16 73

Urinary cyclic AMP (UcAMP) appropriate for the serum calcium concentration was determined in normal subjects during the base-line state and during alteration in their serum calcium concentrations by saline and calcium infusions. This was compared to the UcAMP in 76 patients with hypercalcemia and 5 patients with hypocalcemia. In 54 of 56 patients with primary hyperparathyroidism, the UcAMP was inappropriately high for their serum calcium concentration, the 2 exceptions having renal failure. In four patients with vitamin D intoxication, sarcoidosis, milkalkali syndrome, and thiazide-induced hypercalcemia and in five patients with hypocalcemia due to hypoparathyroidism, the UcAMP was appropriately low for their serum calcium concentration. In 16 patients with nonparathyroid neoplasms, 10 had UcAMP levels that were inappropriately high suggesting ectopic parathyroid hormone (PTH)-mediated hypercalcemia and 6 had UcAMP levels that were appropriately low suggesting that their hypercalcemia was due to osteolytic factors other than PTH. Correlations between UcAMP, serum calcium concentration, and carboxyl-terminal immunoreactive PTH suggest that random UcAMP is a sensitive accurate reflection of circulating biologically active PTH. If there is adequate renal function (serum creatinine concentration less than 2.0 mg/dl), a random UcAMP expressed as mumol/g creatinine and analyzed as a function of the serum calcium concentration completely separates patients with PTH and non-PTH-mediated hypercalcemia.
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PMID:Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia. 18 21

The cuase for the intestinal hyperabsorptionof calcium (Ca) in various forms of hypercalciurias was explored by a careful measurement of plasma 1 alpha, 25-dihydroxycholecalciferol [1 alpha, 25-(OH)I D] and by an assessment of intestinal Ca absorption and of parathyroid function. In 18 cases of primary hyperparathyroidism (PHPT), the mean plasma concentration of 1 alpha, 25-(OH)2D was significantly increased (4.9 +/- 2.2 SD ng/dl vs. 3.4 +/- 0.9 ng/dl for the control group), and was significantly correlated with fractional Ca absorption (alpha) (r = 0.80, P less than 0.001). Plasma 1 alpha, 25-(OH)2D was also correlated with urinary Ca (P less than 0.05), but not with serum Ca or phosphorus (P), P clearance, urinary cyclic AMP, or serum immunoreactive parathyroid hormone. In 21 cases of absorptive hypercalciuria (AH), plasma 1 alpha, 25-(OH)2D was elevated in one-third of cases, and the mean value of 4.5 +/- 1.1 ng/dl was significantly higher than that of the control group (P less than 0.01). Since relative hypoparathyroidism may be present, the normal absolute value of plasma 1 alpha, 25-(OH)2D, found in two-thirds of cases of AH, may be considered to be inappropriately high. Moreover, in the majority of cases of AH, the data points relating plasma 1 alpha, 25-(OH)2D and alpha fell within 95% confidence limits of values found in non-AH groups (including PHPT). The results suggest that the intestinal hyperabsorption of Ca in PHPT aw AH may be vitamin D dependent. However, the disturbance in vitamin D metabolism may not be the sole cause for the high Ca absorption in AH, since in some patients with AH, the intestinal Ca absorption appears to be inapp
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PMID:The role of 1 alpha, 25-dihydroxyvitamin D in the mediation of intestinal hyperabsorption of calcium in primary hyperparathyroidism and absorptive hypercalciuria. 19 63

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

Radiological sacroiliac (SI) changes were found in 3 patients, 2 with primary hyperparathyroidism (1 also with associated chondrocalcinosis) and 1 with osteomalacia. Osteomalacia was due to celiac disease. None of the 3 patients, all females, had a history of psoriasis, urethritis, iritis or chronic colitis. There was no renal function impairment. Peripheral joints were affected in the patient with associated condrocalcinosis. HLA B 27 was negative in all cases. Low back pain and vertebral stiffness were present in the patient with osteomalacia. A dramatic improvement in pain and stiffness ensued after vitamin D injections. These SI lesions, which may simulate ankylosing spondylitis, were attributable to subchondral bone changes related to the metabolic bone diseases. In the case of osteomalacia the SI lesions were predominantly on the right side, where there was a Looser's zone on the ischial ramus suggesting that pseudofractures could be a cause of SI changes. Metabolic osseous diseases such as osteomalacia or primary hyperparathyroidism should be investigated in cases of HLA B 27 negative radiological "sacroiliitis".
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PMID:[Sacroiliac changes, HLA-B27 negative, in primary hyperparathyroidism and osteomalacia]. 46 71

Seventy-seven patients with nephrocalcinosis as revealed by X-ray studies over a 10-year period are reviewed. A programmed clinical and metabolic study was performed on each case; the author's criteria included the different pathogenic factors considered in the etiologic definition of the disease. There were 22 cases with primary hyperparathyroidism, 19 with spongy kidney, nine with tubulointerstitial nephropathy, five with hyperoxaluria, five with distal renal tubular acidosis, four with esential hypomagnesemia, and three cases of miscellaneous etiology (vitamin D intoxication, Fanconi's syndrome, Bartter's disease). Ten other cases were classified as idiopathic nephrocalcinosis since no definite cause could be found. The clinical characteristics (symptoms, associated diseases, diet and medication intake, family history) and the biochemical findings are analysed for each group. The physiopathologic mechanisms, comparisons between each etiologic group, treatment, clinical course, and prognosis are commented on. The conclusion drawn is that nephrocalcinosis is a clinical syndrome of various etiologies which in most cases arises from an underlying metabolic disease.
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PMID:[Nephrocalcinosis as a clinical syndrome. Study of 77 cases (author's transl)]. 52 25

Twenty-five patients with end-stage renal disease, nine of whom were receiving pharmacologic doses of vitamin D, and seventeen patients with primary hyperparathyroidism underwent bone biopsy following a three-day course of tetracycline administration. The mean width of the fluorescent tetracycline bands were significantly greater in the bones of patients with uremia than in those with primary hyperparathyroidism. This difference was due to wide labels present in the patients with uremia who had not been treated with vitamin D, as no differences existed in mean label widths of patients with uremia who had received this compound and the patients with primary hyperparathyroidism. Comparison of the maximum label widths distinguished not only primary hyperparathyroid patients from those with uremia, but uremic patients who had recieved vitamin D from those who had not been so treated. Quantitative microscopy of standard, nonfluorescent histologic features failed to make this latter distinction. These data are consistent with the presence of a wide zone of instantaneously fluorescing material in uremic bone following tetracycline administration, which does not relate to bone apposition occurring during antibiotic administration. This phenomenon probably represents a delay in mineral maturation which is normalized by vitamin D. Furthermore, it is apparent that the use of a continuously administered (single) tetracycline label will result in an overestimation of bone formation rates, particularly in osteomalacic states.
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PMID:Tetracycline fluorescence in uremic and primary hyperparathyroid bone. 60 25

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44

Hypercalcemia occurred in 4 dogs with renal failure. Primary causes of hypercalcemia previously described in the dog (primary hyperparathyroidism, pseudohyperparathyroidism, vitamin D toxicosis) were not identified. Increased concentrations of circulating immunoreactive parathormone were found in 2 dogs, and thyroparathyroidectomy of 1 dog resulted in decreased serum concentrations of that hormone as well as of calcium. The latter observations indicated that hypercalcemia was related to increased parathormone activity, but the possibility of other homeostatic imbalances was not excluded. It was concluded that renal failure should be considered as a primary cause of hypercalcemia, along with other causes previously identified.
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PMID:Hypercalcemia secondary to chronic renal failure in the dog: a report of four cases. 72 83


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