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)

Fourteen patients with medullary carcinoma of the thyroid (MCT) and hypercalcitoninemia were studied. Serum concentrations of calcium, phosphorus and iPTH (C-terminal) were normal. Serum 1,25-dihydroxyvitamin D (1,25-(OH)2D) levels were increased (p less than 0.001) in spite of reduced serum 25-hydroxyvitamin D (25-OHD) levels (p less than 0.02) indicating an enhanced activity of the renal 1 alpha-hydroxylase. Serum 24,25-dihydroxyvitamin D levels were normal and correlated positively with serum 25-OHD. Histomorphometric analyses of iliac crest bone biopsies after in vivo tetracycline double-labelling were performed in patients and controls. The patients showed a normal trabecular bone volume. The mean size of the cortical osteocytic lacunae was increased (p less than 0.001). Significant increases were found in fractional formation surfaces (p less than 0.05), fractional labelled surfaces (p less than 0.01) and fractional resorption surfaces (p less than 0.005) in trabecular bone. The appositional rate of newly mineralized bone was reduced (p less than 0.025). The mean osteoid seam width was normal due to an unchanged mineralization lag time and a normal osteoid appositional rate. The bone formation rate at tissue level was high normal. The altered vitamin D metabolism may be caused by a direct effect of hypercalcitoninemia on the renal l alpha-hydroxylase or may represent an adaptive change in calcium-phosphorus homeostasis. The dynamic bone changes are similar to those found in primary hyperparathyroidism and may be caused by an enhanced sensitivity to circulating PTH induced by the increased 1,25-(OH)2D.
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PMID:Altered vitamin D metabolism and bone remodelling in patients with medullary thyroid carcinoma and hypercalcitoninemia. 712 Dec 51

Plasma concentrations of 25-hydroxyvitamin D (25-OH-D) were determined in 40 healthy persons and in patients with primary osteoporosis (n = 43), primary hyperparathyroidism (n = 19), intestinal osteopathy (n = 13), and after small intestine bypass operations (n = 8). The control group showed physiologic seasonal variations which must be taken into account in the individual case. Whereas there were no deviations from the normal in patients with osteoporosis, significantly lower values were obtained in the other disease groups. Estimation of 25-OH-D in plasma represents a valuable contribution for the diagnosis of generalized osteopathies and for the differential diagnosis of hypercalcaemia. In addition, the effects of vitamin D treatment may be objectively assessed. Overdosage and intoxication may be recognized in time.
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PMID:[Clinical relevance of 25-hydroxyvitamin D estimation in plasma (author's transl)]. 730 6

Fifty patients with primary hyperparathyroidism were studied with an oral calcium-tolerance test, measurements of plasma levels of vitamin D metabolites, and determination of calcium excretion on both a low-normal (400 mg) and high-normal (1000 mg) calcium intake. There were strong positive correlations between plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D) and both the calciuric response to the calcium-tolerance test (r = +0.75, P less than 0.001) and calcium excretion on the 1000-mg calcium diet (r = +0.65, P less than 0.001). The patients were classified into two subpopulations: 30 patients showed hyperabsorption with the calcium-tolerance test, striking hypercalciuria, marked elevations in plasma 1,25(OH)2D, and a high incidence (19 of 30 patients) of renal stones; 20 patients had a normal response to the tolerance test, normocalciuria, normal or high-normal plasma 1,25(OH)2D, and a low incidence of stones (three of 20 patients). The findings emphasize the importance of circulating 1,25(OH)2D in the pathogenesis of hypercalciuria and stone formation in primary hyperparathyroidism.
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PMID:The importance of circulating 1,25-dihydroxyvitamin D in the pathogenesis of hypercalciuria and renal-stone formation in primary hyperparathyroidism. 735 50

Studies in animals and tissue culture have shown the importance of prolactin and growth hormone in regulating renal 1 alpha-hydroxylase activity and plasma concentrations of 1,25-dihydroxycholecalciferol (1,25(OH)2D3). Evidence for a similar role for these hormones in man was sought by using a radioreceptor assay to measure plasma 1,25(OH)2D3 concentrations in 20 normal subjects, 12 patients receiving dialysis, 11 patients with primary hyperparathyroidism, 10 pregnant women, seven women with prolactinoma, and 14 patients with acromegaly. Circulating 1,25(OH)2D3 concentrations were appreciably raised in the patients with primary hyperparathyroidism and the pregnant women (P less than 0.001), slightly but significantly increased in the patients with prolactinoma (P less than 0.05), and greatly raised in those with acromegaly (P less than 0.001). These results suggest that prolactin and growth hormone are important regulators of renal vitamin D metabolism in the physiological conditions of pregnancy, lactation, and growth in man.
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PMID:Role of pituitary hormones in regulating renal vitamin D metabolism in man. 735 40

Antibodies to 1 alpha, 25-dihydroxy vitamin D3 25-hemisuccinate linked to albumin were produced and an immunoassay for 1,25-dihydroxy vitamin D developed. Plasma 1,25-dihydroxy vitamin D concentrations were compared using an immunoassay and cytosol radioreceptor assay. Both assays gave comparable results but the immunoassay was more reproducible, slightly more sensitive and had a lower detection limit. Using the immunoassay the plasma 1,25-dihydroxy vitamin D was 110.5 pmol/l (S.D. 29.4) in normal subjects; there was no difference between males and premenopausal females. It was negatively related to plasma phosphate. In renal failure and primary hyperparathyroidism plasma 1,25(OH)2D was positively related to radiocalcium absorption. Following 1 and 2 microgram of 1,25-dihydroxy vitamin D3 given orally the peak plasma concentration occurs within 12 h.
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PMID:Plasma 1,25(OH)2 vitamin D measured by radioimmunoassay and cytosol radioreceptor assay in normal subjects and patients with primary hyperparathyroidism and renal failure. 735 41

To evaluate the efficacy of subtotal parathyroidectomy (STP) in the treatment of primary hyperparathyroidism due to multiple gland disease, 12 patients with multiple endocrine neoplasia (MEN) type I syndrome were reviewed out of 132 patients undergoing parathyroidectomy. Each patient had yearly follow-up examinations and calcium determinations for a minimum of four years except for one patient who died one year after S.T.P. Permanent hypoparathyroidism occurred in three patients. Two patients remained persistently hypercalcemic, and two patients developed recurrent hypercalcemia. One patient required oral administration of calcium and vitamin D for ten years following STP before recurrent hypercalcemia developed. Another patient was normocalcemic for three years before recurrent hypercalcemia was noted. Only five of these 12 patients remain normocalcemic without need of calcium and vitamin D therapy. In patients with MEN type I, the long-term results of STP are less than satisfactory. Not only is it difficult to gauge how viable parathyroid tissue must be left to prevent both permanent hypoparathyroidism and persistent hyperparathyroidism but there is also a long-term risk of recurrence.
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PMID:Subtotal parathyroidectomy for primary chief cell hyperplasia of the multiple endocrine neoplasia type I syndrome. 745 47

Vitamin D and parathyroid hormone (PTH) constitute the main regulators of systemic calcium homeostasis. As well as its calcaemic effects, active vitamin D3(1,25(OH)2D3) has a direct regulatory role on parathyroid cells. Active vitamin D3 acts via its receptor (VDR), and binding of the ligand-receptor complex to specific promoter regions of the PTH gene inhibits transcription. Active vitamin D3 constitutes a principal regulator of parathyroid cell growth, and polymorphism in the VDR gene has recently been related to bone mineral density and suggested as predisposing to osteoporosis. Impaired effects of active vitamin D3 may contribute to the relatively enhanced secretion and cell proliferation seen in hyperparathyroidism (HPT). Indeed, VDR dysfunction, of essentially unknown character, has been demonstrated in the pathological parathyroid tissue of primary HPT as well as HPT secondary to uraemia. Consistent with the essential role of active vitamin D3 in parathyroid regulation, the VDR gene polymorphism was studied in 90 postmenopausal women with primary hyperparathyroidism. The VDR genotype bb was found in 60.0% of HPT patients and in 33.3% of the postmenopausal female controls (P < 0.001). As the b allele has been linked to decreased transcriptional activity or messenger RNA stability, reduced VDR expression may impede regulatory actions of vitamin D and may contribute to parathyroid tumorigenesis in these patients.
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PMID:Vitamin D receptor genotypes in primary hyperparathyroidism. 870 42

Hypercalcemic crisis or severe hypercalcemia represents a life-threatening emergency. The most common cause is hypercalcemia of malignancy, although granulomatous diseases, previously undetected primary hyperparathyroidism, medication-induced hypercalcemia, and a few rarer causes may result in this endocrine emergency as well. The clinical presentation and prognosis depend on the acuity of the development of hypercalcemia, the degree of hypercalcemia, and the underlying cause. Certainly, patients with malignancy who develop hypercalcemia superimposed on their already debilitated state are more likely to have a poor outcome than a previously relatively healthy patient with thiazide-induced hypercalcemia, for example. The clinical presentation of patients with hypercalcemic crisis varies depending once again on the underlying cause and degree and rapidity of the hypercalcemia. Most patients experience some constitutional symptoms, neurologic symptoms, gastrointestinal symptoms, and renal manifestations of hypercalcemia. Immediate and effective therapy directed toward the pathophysiology of hypercalcemia is essential. General measures must be implemented to reverse the dehydration, to promote urinary calcium excretion, to avoid prolonged immobilization, and to identify the underlying cause of hypercalcemia. Specific measures directed at inhibiting bone resorption, increasing renal sodium and calcium excretion, and occasionally at decreasing intestinal absorption of calcium (or more specifically blocking vitamin D metabolism) should also be implemented. Obviously the more reversible the underlying cause of hypercalcemia, the more aggressive one should be with the therapy. The literature was reviewed to compile comparative data that practitioners may use in choosing among the various pharmacologic therapies available for the treatment of acute hypercalcemia. Despite all the advances in the field, hypercalcemic crisis still carries a significant mortality risk, although with appropriate therapy with the aforementioned general and specific measures, the calcium level can effectively be lowered in most patients.
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PMID:Hypercalcemic crisis. 780 96

A large number of patients with primary hyperparathyroidism today do not undergo parathyroidectomy. In this prospective study, we evaluated the effect of untreated disease on biochemical and bone densitometric indices. In 66 patients, seven annual measurements showed no change in serum calcium, phosphorus, PTH, vitamin D, or alkaline phosphatase; in urinary calcium, hydroxyproline or hydroxypyridinium cross-link excretion; or lumbar spine, femoral neck, and radial bone mineral density. The subset of postmenopausal women also showed no change in biochemical indices or bone density at any of the three sites. Twenty-four patients met guidelines for surgery as established by the NIH Consensus Conference, 1990. They differed from those who did not meet these guidelines only by being younger (50 +/- 3 vs. 62 +/- 2 yr; P = 0.0005) and by having higher urinary calcium excretion [7.7 +/- 0.9 vs. 5.4 +/- 0.3 mmol/L (310 +/- 37 vs. 215 +/- 14 mg/g creatinine); P < 0.01]. No longitudinal changes in biochemical profile or bone mineral density at any site were noted in this subgroup. Conservative management of patients with mild primary hyperparathyroidism does not lead to progression of disease, as reflected by biochemical indices. Bone density is maintained over 6 yr of observation at sites reflecting both cortical (radius) and cancellous (lumbar spine) bone.
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PMID:Longitudinal measurements of bone density and biochemical indices in untreated primary hyperparathyroidism. 788 23

Twenty eight patients of sporadic primary hyperparathyroidism seen over a period of 10 years were studied. There were 18 females and 10 males with a mean age of 35.9 years. Bone involvement was the commonest clinical presentation (90%) followed by renal involvement (65%) and more than half the patients (54%) had involvement of both the skeletal and renal systems. The tumor was clinically palapable in six patients. Thalliumtechnetium subtraction scan had a sensitivity of 87% followed by computerised tomography (70%), and ultrasound (65%) in diagnosing parathyroid pathology. All the patients underwent surgical excision of the abnormal gland (S). Adenomas constituted the single largest group (90%). Histologically, only 32% of the patients had chief cell morphology. Clear cell (32%) mixed cell, and oxyphil cell (7.2%) types accounted for the remaining adenomas. Majority of the patients (82%) had symptomatic postoperative hypocalcemia requiring intravenous calcium with or without vitamin D supplementation. In contrast to western reports most of our patients were young, presented late with florid bone and renal disease and had large palpable tumors.
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PMID:Primary hyperparathyroidism--an Indian study. 792 52


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