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)

In a 71-year-old patient with osteomalacia, masked primary hyperparathyroidism was detected by vitamin D therapy for hypercalcemia. Surgery revealed a parathyroid tumor. Interpretation of total plasma calcium may be difficult unless the 25-hydroxyvitamin D levels are outside the normal range.
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PMID:[Hyperparathyroidism masked by osteomalacia. Is vitamin D administration in every case of osteomalacia problem-free?]. 371 42

The high incidence of renal lithiasis in hyperparathyroidism (55 p. 100) suggests that PTH plays a causal role in stone production. It also motivates a systematic search for primary hyperparathyroidism in all patients with renal stones although it is only found in about 7 p. 100 of cases. PTH acts through the stimulation of 1.25(OH)2 vitamin D production and therefore, the absorption of calcium from the intestine, which in turn increases the filtrable calcium, hence the calciuria. In renal stones, in general, hypercalciuria represents one of the major metabolic disturbances, besides the hyperoxaluria, hyperuricosuria and the reduction of the inhibitors of crystallization. However, hypercalciuria is rarely the indirect result of excess PTH. It is usually caused by increased dietary ingestion of NaCl, meat, calcium and possibly carbohydrates.
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PMID:[Renal lithiasis in idiopathic hypercalciuria and primary hyperparathyroidism]. 376 88

The sensitivity of bone to parathormone in pseudoparathyroidism is not well known. Six patients with Type I pseudohypoparathyroidism (4 with Albright's osteodystrophy) had increased alkaline phosphatase levels (5 patients) and radiological signs of periosteal resorption in the hand in one case. All patients had histological signs of increased surfaces of resorption and periosteocytic lacunae, increased osteoid surfaces and relative osteoid volume with no change of the index of osteoid thickness. These changes are identical to those observed in hyperparathyroidism which leads on to the discussion of the role of the increased parathormone secretion induced by the lack of calcium on the remodeling of bone. Our six cases show that there is no bone resistance to parathormone. The diversity of bone changes in hyperparathyroidism, similar to that of primary hyperparathyroidism, is without doubt dependent on the degree of renal insensitivity to PTH through the inactivation of vitamin D.
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PMID:[Sensitivity of bone to parathyroid hormone in type I pseudohypoparathyroidism. 6 cases]. 376 89

The synthesis of the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH)2D), is thought to be relatively insensitive to the serum concentration of its precursor, 25-hydroxyvitamin D (25-OH-D). We compared the effect of oral administration of 25-OH-D3 (50 micrograms per day for one month) on serum concentrations of calcium, phosphate, parathyroid hormone, 25-OH-D, and 1,25-(OH)2D in five healthy adults and in six patients with primary hyperparathyroidism. In normal adults the mean (+/- S.D.) serum level of 25-OH-D rose from 18 +/- 9 to 136 +/- 47 ng per milliliter; no significant changes were observed in the other serum levels. In contrast, comparable increases in the levels of circulating 25-OH-D in patients with primary hyperparathyroidism caused a consistent slight rise in serum calcium and phosphate levels, a partial suppression of parathyroid hormone, and a sharp increase in the level of 1,25-(OH)2D. During this period a significant positive correlation was found between serum concentrations of 25-OH-D and 1,25-(OH)2D (P less than 0.001). These results provide evidence that in patients with primary hyperparathyroidism, levels of circulating 1,25-(OH)2D may be more dependent on the prevailing serum concentrations of 25-OH-D than they are in normal adults.
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PMID:Substrate-product relation of 1-hydroxylase activity in primary hyperparathyroidism. 384 Feb 28

Serum 25-hydroxyvitamin D [25(OH)D], 24,25-dihydroxyvitamin D [24,25(OH)2D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] were studied in renal stone formers while on a diet containing 1,000 or 300 mg calcium per day. The patients were divided into four groups and identified as (a) normocalciuric (NSF), (b) absorptive hypercalciuric (AH), (c) renal hypercalciuric (RH) and (d) as having primary hyperparathyroidism (PHP). The results indicate that, on the 1,000-mg Ca diet, the mean 25(OH)D, 24,25(OH)2D and 1,25(OH)2D concentrations were within the normal range in all groups of patients. On the low-calcium diet, 25(OH)D concentrations decreased significantly in patients with AH and RH while 24,25(OH)2D concentrations were not affected by the low-calcium diet. 1,25(OH)2D concentrations increased significantly during dietary calcium restriction in all groups of patients. When the relationship obtained on each diet between the circulating 25(OH)D concentrations and the 25(OH)D/1,25(OH)2D concentration ratio was compared, it suggested that the increase in the 1,25(OH)2D concentrations during dietary calcium restriction may have been due to an increase in the capacity of the 25(OH)D-1 alpha-hydroxylase, or to an increase in the circulating half-life of the hormone. These results indicate that renal stone formers are able to adapt themselves to dietary calcium restriction as shown by highly significant increases in the circulating 1,25(OH)2D concentrations while on a low-calcium diet. Moreover, the increase in the circulating 1,25(OH)2D concentrations did not happen at the expense of the 24,25(OH)2D production in any of the groups of patients studied.
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PMID:Interrelationships between circulating vitamin D metabolites in normocalciuric and hypercalciuric renal stone formers. 387 4

A patient with many symptoms and signs of primary hyperparathyroidism had hypocalcaemia when first seen. Bone section histology showed osteomalacia and osteitis fibrosa, and the hyperparathyroidism at this stage was considered to be secondary to osteomalacia with postgastrectomy steatorrhoea. On treatment with vitamin D (with disappearance of her bone pains and weakness) she developed hypercalcaemia. She regained her health after removal of a 6-g. parathyroid adenoma. Normal histology was shown in another parathyroid gland.We believe that the initial hypocalcaemia was due to vitamin-D deficiency, which produced ineffective hyperparathyroidism until it was corrected. A review of the few reports of patients with autonomous hyperparathyroidism with steatorrhoea and osteomalacia does not support the argument that these patients had "tertiary" disease. It suggests that most of them, like our patient, had primary hyperparathyroidism.
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PMID:Hypocalcaemic primary hyperparathyroidism. 541 47

Between September 1975 and June 1980, 27 patients with primary hyperparathyroidism caused by multiple-gland disease underwent reoperative parathyroid surgery at the National Cancer Institute. In an effort to minimize persistence and recurrence we adopted a strategy of attempting total parathyroidectomy. Immediate autotransplantation was not performed, but rather tissue was assessed in vitro for suppressibility and was cryopreserved. Patients with prolonged postoperative hypoparathyroidism underwent autotransplantation with cryopreserved tissue. Of 26 surviving patients, 23 (88%) were cured of hypercalcemia. Although 13 had hypoparathyroidism at the time of discharge, 4 of these 13 no longer required calcium or vitamin D within 1 year. At follow-up 17 were normocalcemic without medication (14 without and 3 with autografts). Thirteen patients had four or five glands removed. Two of these remain hypercalcemic, and at follow-up nine were normocalcemic without medication (seven without and two with autografts). Patients with multiple-gland disease, even those undergoing total parathyroidectomy, remain at risk for persistent or recurrent hypercalcemia. Such patients do no inevitably acquire hypoparathyroidism, and normocalcemia in patients undergoing immediate autotransplantation need not be attributed to the autograft. Selective, deferred autotransplantation with cryopreserved tissue prevents confusion regarding the source of postoperative hypercalcemia should it occur, minimizes the risk of graft-dependent hypercalcemia by restricting autotransplantation to those truly in need of additional tissue, and can effectively manage hypoparathyroidism.
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PMID:Reoperative parathyroid surgery for primary hyperparathyroidism caused by multiple-gland disease: total parathyroidectomy and autotransplantation with cryopreserved tissue. 612 56

24-h urinary cyclic adenosine 3', 5'-monophosphate/creatinine (cAMP/Cr) ratio was assessed in 10 patients with hypoparathyroidism, 6 with primary hyperparathyroidism, 7 with normocalcemic hypercalciuria and recurrent nephrolithiasis, 14 with osteomalacia, 25 with Paget's disease and 53 with symptomatic postmenopausal osteoporosis. In hypoparathyroid subjects the mean values of 24 h cAMP/Cr ratio were significantly lower than the control values, whereas in patients with parathyroid adenoma the mean values were higher and fell after parathyroid surgery. Patients with nephrolithiasis due to absorptive hypercalciuria showed low or normal cAMP/Cr ratio, whereas in those with osteomalacia and mean values of cAMP/Cr ratio were significantly higher than the control values and decreased after vitamin D treatment. The mean value of the 24 h urine cAMP/Cr ratio was normal in patients with Paget's disease or postmenopausal osteoporosis and increased significantly after long term treatment with calcitonin or diphosphonate. This increase paralleled a significant decrease of calcium plasma level. A significant improvement of fractional calcium absorption was observed in women with postmenopausal osteoporosis at the end of treatment with calcitonin or diphosphonate.
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PMID:The 24-h urinary cyclic adenosine 3', 5' monophosphate/creatinine ratio: an useful approach to the diagnosis of parathyroid disorders and function. 627 46

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

A simple method for extraction, purification and separation of the principal vitamin D metabolites from a single serum sample is described. The method involved extraction of serum with acetonitrile followed by a first purification employing C-18 Sep-pak cartridges eluted with methanol/water and acetonitrile. Final separation before assay was carried out by high pressure liquid chromatography. 1.25-dihydroxy-vitamin D was measured with radioimmunoassay using an antiserum (S11) with high selectivity for 1 alpha-OH function of the hormone at a final dilution of 1:100,000. 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D were measured employing a competitive binding assay with normal rat serum at a final dilution of 1:10,000 as source of binding protein. The mean (+/- SD) serum 1.25-dihydroxy-vitamin D, 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D concentrations for a group of healthy subjects were 50.4 +/- 17.3 pg/ml, 2.3 +/- 2.6 ng/ml and 20.8 +/- 12.3 ng/ml, respectively. 1.25-dihydroxy-vitamin D concentrations were low or undetectable in patients on dialysis or with mild renal failure. High 1.25-dihydroxy-vitamin D levels were found in 2 out of 17 patients with primary hyperparathyroidism. In 4 normal subjects treated for two weeks with large doses of 25-hydroxy-vitamin D, serum 25-hydroxy-vitamin D rose from 12.5 ng/ml to 119 ng/ml and from 0.89 ng/ml to 15 ng/ml, respectively; no changes in the 1.25-dihydroxy-vitamin D assay were found.
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PMID:Simultaneous measurement of 1.25-dihydroxy-vitamin D, 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D from a single two milliliters serum specimen. Preliminary clinical application. 633 15


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