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)

Various hormones have been implicated in the genesis of hypercalcemia in patients with malignancy. Ectopic secretion of PTH by tumor has been documented in only a few patients; rather, elevated levels of circulating iPTH have been presumed to reflect tumor production of hormone in most patients. Small fragments of PTH, as well as polypeptides larger than native PTH, have been described; their biological roles are unclear. The pattern of immunoreactivity, however, has been used to differentiate patients with ectopic hyperparathyroidism from patients with concomitant primary hyperparathyroidism. Vitamin D-like sterols produced by breast cancer seldom reach plasma levels necessary for physiological effects. Members of the prostaglandin family have been proposed to induce hypercalcemia through osteoclast activation or alteration of the immune system and also to affect the frequency of bone metastases. At present, no direct evidence is available to prove a direct role for these effects and prostaglandins are most useful as possible indicators of disease activity.
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PMID:Mechanisms of hypercalcemia in malignancy. 65 92

Vitamin D metabolites in serum and calcitriol receptor concentration in parathyroid tissue were examined in 52 patients operated on for primary hyperparathyroidism. The calcitriol receptor levels were not different in parathyroid adenomas (mean 224 fmol/mg of protein, range 29-509, N = 43), normal parathyroid tissue (mean 245, range 31-690, N = 20), and primary parathyroid hyperplasia (mean 172, range 46-477, N = 9). Preoperative serum levels of calcitriol concentration correlated inversely to the calcitriol receptor in normal parathyroid tissue in patients with adenoma (r = -0.57, N = 17, p = 0.017), but no such correlation was found in the corresponding adenomas (r = 0.14, p = 0.59). In 31 patients in whom both pre- and postoperative vitamin D metabolite analyses were carried out, 23 had lower calcitriol postoperative concentrations compared to preoperative values (p = 0.012, sign test). No change was found in the other vitamin D metabolites postoperatively. By multiple regression analysis calcitriol concentration in serum was inversely correlated to the serum concentration of urea and phosphate (p = 0.003). We conclude that calcitriol may influence calcitriol receptor expression in normal parathyroid tissue, but not in adenomatous parathyroid gland. Furthermore, serum calcitriol was correlated to the renal function, and phosphate level, and in most patients the calcitriol concentration was lower after the operation.
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PMID:Serum vitamin D metabolites and calcitriol receptor concentration in parathyroid tissue in primary hyperparathyroidism. 133

A seventeen-year-old youth was presented with muscle cramps and convulsions. A brain CT scan showed calcification in the region of the ganglia, and a diagnosis of brain tumor was thus made and an anticonvulsant given for two years. At age nineteen, the patient developed pseudohypoparathyroidism owing to low serum calcium and high serum PTH levels. However, serum alkaline phosphatase and serum osteocalcin levels were high, lesion was detected in the femur neck. These data indicated that the bone remodeling response to PTH had remained intact in this patient. Serum osteocalcin is known to increase in primary hyperparathyroidism. However, unlike patients with hyperparathyroidism, those with pseudohypoparathyroidism show no increase in serum 1,25(OH)2D. The present case was thus useful for examining the direct effect of PTH on serum osteocalcin. The patient was administered 1 alpha (OH)D, and his condition monitored for two years. During this period, osteocalcin and PTH levels decreased while that of 1,25(OH)2D increased. Osteocalcin and PTH levels were found to be closely correlated (r = 0.68, p less than 0.01). The present results indicate the possibility that PTH may increase serum osteocalcin independent of Vitamin D.
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PMID:[Serum osteocalcin concentration in a patient with pseudohypoparathyroidism type Ib]. 188 14

The physiologic relationship between the thyroid and parathyroid glands remains poorly understood. A high incidence of coexistent thyroid disease and primary hyperparathyroidism has been well documented. Elevation of serum 1,25-dihydroxyvitamin D3 (vitamin D) has been detected in some patients with primary hyperparathyroidism. A report of specific binding sites and uptake of vitamin D by the thyrotrophs of the anterior pituitary indicates that vitamin D may modulate production or secretion of thyroid-stimulating hormone (TSH). To test this concept, we investigated the influence of elevated serum levels of vitamin D on basal and stimulated TSH. Vitamin D was administered by subcutaneously implanted sustained-release pellets at four dosages. Thyrotropin releasing hormone (TRH) stimulation tests were performed at time zero, 72 hours, 1 week, 2 weeks, and 5 weeks. Animals administered vitamin D became significantly hypercalcemic and demonstrated elevations of vitamin D, which peaked at 72 hours and remained elevated for 2 weeks after pellet implantation. TRH-stimulated TSH levels were significantly elevated at 72 hours and at 1 week and returned to normal after 5 weeks. Parathyroid hormone levels were suppressed at 72 hours and at 1 week and displayed significant elevation at 2 weeks. These results provide in vivo evidence for an interaction and a possible regulatory role of 1,25 on pituitary TSH secretion and parathyroid function.
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PMID:Altered TSH levels associated with increased serum 1,25-dihydroxyvitamin D3: a possible link between thyroid and parathyroid disease. 251 35

Aging has myriad effects on calcium homeostasis and metabolism. Levels of parathyroid hormone rise, making the diagnosis of primary hyperparathyroidism more difficult. Vitamin D levels decline, affecting the rate of calcium absorption from the intestine. As more and more physicians attempt to combat osteoporosis with calcium supplements, an increasing number of cases of hyperparathyroidism will likely be diagnosed. The use of supplemental calcium is probably appropriate for most elderly patients, particularly white women, but experimental evidence supporting this recommendation is surprisingly scanty. The patient's age is a major consideration when assessing laboratory results, disease risk, and optimal therapeutic strategies.
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PMID:Age-related changes in calcium metabolism. Why they occur and what can be done. 264 67

Vitamin D metabolism was studied in 65 patients with surgically proven primary hyperparathyroidism. The mean concentration of 1,25-dihydroxyvitamin D3 was 51.7 +/- 34 pg/ml (mean +/- SD) and was not significantly different from normal. Renal function was normal in 60 of these patients and in this group circulating 1,25-dihydroxyvitamin D3 was below the lower limit of normal in three and elevated in 17; it was related to the serum concentrations of amino-terminal parathyroid hormone, but was independent of serum calcium and the urinary excretion of calcium. The incidence of nephrolithiasis or hyperparathyroid bone disease or combined nephrolithiasis and bone disease in these patients was not related to the circulating concentration of 1,25-dihydroxyvitamin D3. In the remaining five patients, in whom renal impairment was present, circulating 1,25-dihydroxyvitamin D3 was below the lower limit of normal in four. Thus, in primary hyperparathyroidism the circulating concentration of 1,25-dihydroxyvitamin D3 is elevated in only a minority of patients and appears to be unrelated to the occurrence of nephrolithiasis or bone disease.
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PMID:Circulating concentrations of 1,25-dihydroxyvitamin D3 in patients with primary hyperparathyroidism. 350 21

A comparison of the interrelations between serum and urinary calcium values and the urinary excretion of cAMP in acromegaly (No. of subjects: 26), patients with primary hyperparathyroidism (n = 18) and control subjects (n = 42) is presented. The cAMP excretion was greatest in primary hyperparathyroidism, but acromegalics also exhibited higher values for this parameter than controls. A positive correlation was found between serum calcium values and cAMP in primary hyperparathyroidism, while acromegalics showed no correlation between these parameters. In controls there was a negative correlation between serum calcium and cAMP. Serum calcium levels corrected for variations in total protein concentrations were elevated both in acromegaly and primary hyperparathyroidism, mostly in the latter. Acromegalics and patients with primary hyperparathyroidism exhibited an increase in 24 h calcium excretion. While there was a negative relationship between urinary calcium excretion and cAMP in acromegaly, a positive correlation between these parameters as found in primary hyperparathyroidism. Controls showed a negative correlation between urinary calcium values and cAMP. It is concluded that the role of the parathyroids in the regulation of calcium metabolism in acromegaly is different from that of both normal controls and primary hyperparathyroidism. It is postulated that an active form of Vitamin D plays a major role in the regulation of calcium metabolism in acromegaly.
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PMID:Urinary 3',5'-cyclic adenosine monophosphate in relation to serum and urinary calcium in acromegaly and primary hyperparathyroidism. 625 99

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

Vitamin D appears to influence parathyroid function indirectly through its effects on calcium metabolism rather than by a direct action of its metabolites on the parathyroid glands. In states of both secondary and primary hyperparathyroidism, the quantitative production of 1,25-(OH)2D may be determined by the prevailing concentration of serum 25-(OH)D but there appears to be some constraint that limits the formation of 1,25-0(OH)2D when the provision of its precursor exceeds the physiological. From the absence of this constraint in 'type 2 vitamin D dependency' it is inferred that it may operate through 'self-inhibition' of the renal production of 1,25-(OH)2D. It is shown that the level of serum 25-(OH)D may always exert some influence on the production of 1,25-(OH)2D and that this effect is facilitated by hyperparathyroidism. In developing vitamin D deficiency the reactive secondary hyperparathyroidism may thus function as an adaptive mechanism that sustains the level of serum 1,25-(OH)2D in the face of a diminishing serum 25-(OH)D. Failure of this adaptation and the development of a critical deficiency of 1,25-(OH)2D is regarded as the direct cause of defective mineralisation of bone. This concept would explain the absence of osteomalacia in some patients with very low levels of serum 25-(OH)D and the occurrence of defective osseous mineralisation in hypoparathyroidism.
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PMID:Vitamin D and hyperparathyroidism: the Lumleian Lecture 1981. 697 36

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


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