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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of renal function on the cyclic AMP (cAMP) response to exogenous parathyroid hormone (PTH) was examined in patients with chronic renal failure (n = 22) and primary hyperparathyroidism (n = 19). In the patients with chronic renal failure there was marked resistance to the effect of exogenous PTH. In primary hyperparathyroidism the cAMP responses were variable; most of the patients with an abnormally small response having impaired renal function. After parathyroidectomy, responsiveness improved to varying degrees. In three patients repeatedly tested up to several months after parathyroidectomy, the recovery of responsiveness was a gradual process which began within days but did not, however, return to normal. Thus, there was an irreversible component to the resistance to PTH in these patients. A strong negative correlation between plasma creatinine and the cAMP response to PTH (P less than 0.001) was found in a group of patients, some with treated primary hyperparathyroidism and some with chronic renal failure. Thus, renal impairment is an important, but probably not the sole, contributory factor involved in the irreversible resistance to the action of PTH in hyperparathyroidism.
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PMID:Effect of renal function on renal responsiveness to parathyroid hormone in primary hyperparathyroidism and chronic renal failure. 298

The aim of this study was to investigate whether the concentration of cAMP in saliva might reflect the biologic activity of parathyroid hormone (PTH), as nephrogenous levels of cAMP reflect parathyroid function. Patients with primary hyperparathyroidism (HPT) with elevated levels of PTH, nephrogenous cAMP, and serum calcium were found to have cAMP levels not significantly different from control subjects. When the levels of these parameters were reduced following parathyroidectomy, salivary cAMP concentrations were not affected. Similarly, an oral calcium loading test (which decreased both PTH and nephrogenous cAMP in normal subjects) failed to influence salivary cAMP levels. Basal salivary cAMP concentrations were low in secondary hyperparathyroid patients due to chronic renal failure and rose almost fivefold following dialysis despite the stable plasma cAMP levels and salivary flow rate. We conclude that salivary cAMP concentrations do not appear to be influenced by changes in circulating biologically active PTH. However, salivary cAMP concentrations do change in response to certain perturbations; this suggests that they are regulated by some other modulator(s).
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PMID:Do cyclic AMP concentrations in saliva reflect PTH biologic activity? 298 41

This study examined the hypothesis that altered binding of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) to parathyroid receptors might be involved in the pathogenesis of secondary hyperparathyroidism associated with chronic renal failure. The binding of [3H]1,25-(OH)2D3 to hyperplastic parathyroid glands obtained from seven patients with chronic renal failure was measured. These values were compared with those for binding to hyperplastic parathyroid tissue obtained from six patients who had received renal transplants and for binding to parathyroid adenomas removed from five patients who had primary hyperparathyroidism. We found that Nmax (an estimate of the concentration of 1,25-(OH)2D3 receptors) was reduced (42 +/- 15 fmol per milligram of protein) in patients with chronic renal failure as compared with patients with transplanted kidneys (78 +/- 24 fmol per milligram of protein) and patients with primary hyperparathyroidism (114 +/- 30). Nmax correlated inversely with the severity of renal dysfunction, the serum level of phosphorus, and the logarithm of the serum level of immunoreactive parathyroid hormone. These observations suggest that 1,25-(OH)2D3 binding by parathyroid tissue is reduced in chronic renal failure. This may contribute to the pathogenesis of secondary hyperparathyroidism by reducing the inhibition by 1,25-(OH)2D of parathyroid hormone secretion. The low serum levels of 1,25-(OH)2D in chronic renal failure may accentuate this effect.
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PMID:Reduced binding of [3H]1,25-dihydroxyvitamin D3 in the parathyroid glands of patients with renal failure. 303 73

Successful renal transplantation may be complicated by persistent hyperparathyroidism due to diffuse parathyroid hyperplasia remaining from a prolonged period of pretransplant chronic renal failure treatment. Posttransplant hyperparathyroidism is distinct from primary hyperparathyroidism, being characterized by multiple gland involvement and diffuse hyperplasia rather than a single adenoma. The gross pathologic anatomy of the parathyroid glands was assessed in 17 successful renal transplant recipients. Individual and total gland volumes were measured at the time of total parathyroidectomy and forearm reimplantation. Parathyroid hyperplasia was heterogenous in both location and gland size. Right-sided glands were enlarged more than left-sided ones. Subjects with primary tubulointerstitial disease exhibited greater hyperplasia than patients with glomerular disorders. Clinicians should be aware of the heterogeneity of the gland enlargement in patients with diffuse parathyroid hyperplasia, so that these patients are not misdiagnosed as suffering from adenomatous parathyroid disease.
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PMID:Anatomical heterogeneity of parathyroid glands in posttransplant hyperparathyroidism. 307 Nov 45

In the course of chronic renal failure, aluminium may deposit and accumulate in different tissues. The aluminium content of parathyroid glands was measured in 31 haemodialysis patients at the time of a parathyroidectomy. The values were compared with those obtained from ten control patients with primary hyperparathyroidism without renal failure, and were related to bone remodelling. Of the 31 patients, 27 had a bone biopsy after double tetracycline labelling, at the time of parathyroidectomy. Twenty-one patients had severe hyperparathyroidism, three patients had hyperparathyroidism associated with osteomalacia, three patients had mild hyperparathyroidism with reduced bone formation. Seven patients had bone aluminium deposits, associated with osteomalacia in one case. The parathyroid aluminium was 62 +/- 35.7 (mumol/g glandular dry weight) in haemodialysis patients and 14.3 +/- 6.3 in control patients (P less than 0.001). A significant positive correlation existed between parathyroid aluminium and serum aluminium (P less than 0.01). The parathyroid aluminium was not different in the patients with and without bone aluminium deposits. A weak correlation was found between parathyroid aluminium and plasma parathyroid hormone. A significant negative correlation existed between parathyroid aluminium and osteoblastic surfaces (P less than 0.05), but no correlation was found with bone formation rate at tissue and bone multicellular units levels. We conclude that aluminium accumulates in parathyroid glands of dialysed patients. Severe hyperparathyroidism may coexist with aluminium overload of parathyroid glands. A marked aluminium overload, however, may cut short the course of hyperparathyroidism and may decrease parathyroid function and cellular activity in bone.
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PMID:Aluminium overload of parathyroid glands in haemodialysed patients with hyperparathyroidism: effect on bone remodelling. 314 Jan 27

We measured the serum concentrations of 2 biochemical markers of bone formation, bone Gla-protein (BGP) and bone alkaline phosphatase (BAP), in 164 normal subjects and 164 patients with metabolic bone disorders. The data were reported as Z scores (deviation in SDs from the sex-specific age regression in normal subjects). Both serum BGP and BAP distinguished abnormalities well (mean Z scores for BGP and BAP, respectively) and gave concordant results in patients with hypoparathyroidism (-1.7, -1.4), hyperthyroidism (+1.1, +1.8), primary hyperparathyroidism (+3.6, +2.5), acromegaly (+1.2, +2.8), and postmenopausal osteoporosis (+0.4, +1.9). The 2 markers gave discordant results, however, in patients with glucocorticoid excess (-2.4, +0.9), Paget's disease (+1.8, +41.8), chronic renal failure (+16.3, +0.4), and osteolytic metastases (-1.4, +5.9). These discrepancies may have occurred because serum BGP and BAP concentrations reflect different aspects of osteoblast function or because there are differences in their clearance from the circulation. Consequently, more information is derived about the level of bone formation across the wide range of metabolic bone disorders when both biochemical markers are assayed.
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PMID:Concurrent assays of circulating bone Gla-protein and bone alkaline phosphatase: effects of sex, age, and metabolic bone disease. 325 70

We compared the utility of measurements of serum intact human PTH-(1-84) and midregion human PTH-(44-68) in patients with disorders of extracellular calcium metabolism. Serum midregion PTH was determined by RIA, and serum intact PTH was measured by a sensitive and specific immunoradiometric two-site assay. The serum intact PTH concentrations in 70 patients with primary hyperparathyroidism were above the normal range in 69, and thus widely separated from the levels in 40 patients with hypercalcemia of malignancy, in whom serum intact PTH values were usually below normal. In contrast, both groups had overlapping serum midregion PTH values. In patients after renal transplantation and those with chronic renal failure, serum intact PTH levels were in the normal range twice as often as were serum midregion PTH values. The intact PTH assay was also superior in detecting venous gradients of the hormone and changes in PTH secretion caused by altered serum calcium concentrations, and serum intact PTH was remarkably low in hepatic venous effluent. We conclude that this new assay for serum intact PTH is superior to the midregion RIA in investigating parathyroid function in several different clinical conditions.
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PMID:Two-site assay of intact parathyroid hormone in the investigation of primary hyperparathyroidism and other disorders of calcium metabolism compared with a midregion assay. 329 61

Metastatic pulmonary calcification occurs in a chronic form in patients with malignancy, chronic renal failure, and primary hyperparathyroidism. A rapidly progressive form is associated with renal transplant failure. This case report describes chronic progressive pulmonary calcification after successful transplant with no obvious underlying cause.
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PMID:Progressive pulmonary calcification complicating successful renal transplantation. 331 1

Our previous secretin provocation studies in normal volunteers and unoperated duodenal ulcer patients suggested that the gastrin rise in gastrinoma may be an exaggeration of the normal response rather than paradoxical. We report further studies in various clinical settings having normogastrinemia (normal, n = 17; unoperated duodenal ulcer, n = 13; primary hyperparathyroidism, n = 7) and hypergastrinemia (postvagotomy, n = 5; hypochlorhydria, n = 7; achlorhydria, n = 10; chronic renal failure, n = 10; gastrinoma, n = 5). Under all nongastrinoma conditions, there were similar gastrin rises of 9-19% between 2 and 5 min after bolus intravenous GIH secretin (2 CU/kg), which fell to baseline by 8 min, except for chronic renal failure. In chronic renal failure, gastrin remained elevated from 7 to 30 min and was significantly different (p less than 0.05) at 10-30 min compared to all other nongastrinoma conditions except hyperparathyroidism. Peak rises occurred within 5 min in all entities, but only three gastrinoma patients had positive secretin provocation tests by the predefined criterion of a gastrin rise greater than 200 pg/ml. The results of secretin provocation in various clinical entities with and without hypergastrinemia further support the hypothesis that the gastrin rise in gastrinoma is an exaggeration of the normal response. The prolonged gastrin rise seen in chronic renal failure may be due to altered renal clearance, inasmuch as other hypergastrinemic states had responses similar to normal and duodenal ulcer.
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PMID:Secretin provocation: gastrin results in various clinical situations. 334 35

The long-term clinical results of parathyroidectomy for primary hyperparathyroidism were analyzed in 176 patients. Preoperatively 152 patients (86%) showed classic symptoms, 15 (9%) were classified as minimally symptomatic (only hypertension, diffuse osteopenia or manifestations of the hypercalcemic syndrome), and nine (5%) were asymptomatic. All patients were normocalcemic at follow-up, but renal, skeletal or gastrointestinal symptoms were eliminated in only 88-91%. Preoperatively impaired renal function and hypertension were seldom improved by parathyroidectomy. Deterioration of renal function and hypertension occurred only in the symptomatic and minimally symptomatic patients, in whom the course was varied and unpredictable. During observation periods up to 22 years, 7% of the patients died of acute/chronic renal failure or consequences of hypertension. Death from uremia was more common when there was also skeletal involvement. Acute pancreatitis could occur without preoperative symptoms, but other gastrointestinal disorders responded to normalization of parathyroid metabolism. Multiple bone lesions responded functionally and lacked prognostic significance. Hypercalcemic syndrome was rapidly and lastingly relieved by parathyroidectomy.
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PMID:Clinical long-term results after parathyroidectomy for primary hyperparathyroidism. 342 99


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