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)

The long-term clinical courses of 212 "cured" (normocalcemic) patients were analyzed for 1 to 25 years (mean, 6.8 +/- 5.4 years). Preoperatively, 181 patients (85%) were classified as having typical symptoms, 22 patients (11%) as having minimal symptoms, and nine patients (4%) as having no symptoms of primary hyperparathyroidism (PHP). Although the formation of urinary calculi was stopped in 91% of patients, deteriorated renal function and hypertension were seen in patients with symptoms (14% and 8%, respectively) and patients with minimal symptoms of PHP (6% and 15%, respectively). Renal function changes and hypertension were unpredictable despite normalization of the hyperactive parathyroid metabolism and had decisive results: 7% of the patients died of uremia or of the consequences of hypertension (stroke). Large, multiple bone lesions healed functionally and were of no prognostic significance. In the majority of patients with symptoms of PHP, gastrointestinal manifestations healed postoperatively, but two patients who had no preoperative gastrointestinal complaints died of acute pancreatitis. Almost all symptoms of the hypercalcemia syndrome disappeared immediately and permanently in patients with symptoms and patients with minimal symptoms of PHP. Neither deterioration of renal function nor elevation of blood pressure were observed postoperatively in "cured" patients who showed no symptoms of PHP preoperatively. Even in these patients, immediate surgical treatment may have avoided the complications of chronic renal failure or hypertension. As soon as organic manifestations, even in mild form, have been established, it seems impossible to predict the course and to prevent an unfavorable clinical outcome.
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PMID:Successful parathyroidectomy in primary hyperparathyroidism: a clinical follow-up study of 212 consecutive patients. 368 53

Hypertension is common in primary hyperparathyroidism, but the mechanisms are not clear. Significant hypercalcemia induces elevation in blood pressure (BP), whereas excessive parathyroid hormone (PTH) lowers BP. However, in chronic renal failure (CRF) and secondary hyperparathyroidism, the hypercalcemia-induced hypertension is more severe. We examined the interaction between PTH and calcium on BP in normal rats and in those with CRF. Calcium caused a dose-related rise in serum calcium and a rise in mean arterial pressure (MAP). For a comparable rise in serum calcium, the increment in MAP in parathyroidectomized (PTX) rats (7 +/- 3 mmHg) was significantly lower (P less than 0.05) than in sham PTX rats (19 +/- 7.3 mmHg). In PTX rats receiving PTH, the MAP response to calcium infusion (17 +/- 2.4 mmHg) was similar to that in the sham PTX rats. The infusion of similar amounts of calcium in CRF rats caused a greater rise in serum calcium. In CRF-PTX rats, the changes in MAP during calcium infusion were significantly lower (P less than 0.05) than in CRF-sham PTX animals, despite similar rise in serum calcium. For a comparable rise in serum calcium, the rise in MAP in CRF rats was greater than in normal rats. These data suggest that the presence of PTH plays an important permissive role for the hypertensive action of the hypercalcemia.
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PMID:Effects of hypercalcemia and parathyroid hormone on blood pressure in normal and renal-failure rats. 370 44

Brown tumors, focal bony lesions of hyperparathyroidism, result from the direct effect of parathyroid hormone on bone. While such lesions are not uncommon in primary hyperparathyroidism, brown tumors have been associated less frequently with secondary hyperparathyroidism and have rarely been described as involving the orbital bones. We have found only four such cases previously reported in the ophthalmic literature. We report a case of orbital involvement by brown tumor in a child with chronic renal failure and secondary hyperparathyroidism. Use of long-term hemodialysis has increased the life span of individuals with chronic renal failure and produced an increased population of patients with secondary hyperparathyroidism and resultant bony changes. The ophthalmologist should consider brown tumor in the differential diagnosis of a patient with chronic renal failure and ocular symptomatology.
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PMID:Brown tumor of the orbit. Case report and review of the literature. 374 Dec 52

A new peptide spanning residues 28-54 of human parathyroid hormone (PTH) was synthesized and used to develop a homologous immunoradiometric assay specific for the mid-region of human PTH. The peptide was coupled to cellulose and used to absorb mid-region antibodies from a goat antiserum against intact human PTH. This assay has been applied to the measurement of circulating PTH in man: in normal subjects the concentration in serum ranged from undetectable (less than 40 pg/ml) to 70 pg/ml, the reference standard being the human PTH 28-54 peptide. In patients with primary hyperparathyroidism concentrations ranged from 120 to 1800 pg/ml. Hormone was not detected in patients with hypoparathyroidism. In normal subjects and in patients with primary hyperparathyroidism the mid-region PTH concentrations were similar to those obtained in an amino-terminal specific assay. By contrast, carboxy-terminal PTH concentrations were markedly higher being 10-fold greater in both groups studied. In patients with primary hyperparathyroidism undergoing parathyroidectomy and in chronic renal failure patients who were infused with calcium, mid-region and amino-terminal PTH disappeared much more rapidly than carboxy-terminal PTH. However, although mid-region PTH was initially cleared as quickly as amino-terminal PTH, it then reached a plateau and remained at a higher level. Thus the mid-region specific assay described here is proving to be of value in the study of the secretion and metabolism of PTH.
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PMID:Development and application of a mid-region specific assay for human parathyroid hormone. 374 32

Depending on their symptomatology 152 cured (i.e., normocalcemic) patients with surgically proven primary hyperparathyroidism (pHPT) showed typical symptoms preoperatively. Besides hypercalcemia and elevated parathyroid hormone levels, 15 patients suffered only from hypertension and/or diffuse osteoporosis and/or complaints caused by the hypercalcemic syndrome (oligosymptomatic patients). Nine patients had no complaints (asymptomatic patients). The long-term clinical course of all patients was analyzed up to 22 years. Although the formation of urinary calculi was stopped in 94% of cases, a deterioration of renal function and hypertension was seen in symptomatic (12.5% and 9.2%, respectively) and oligosymptomatic patients (6.7% and 13.3%, respectively). Renal function and hypertension were unpredictable despite normalization of the hyperactive parathyroid metabolism and were of decisive prognostic significance; 6% died of acute or chronic renal failure, or of the consequences of hypertension. Multiple bone lesions, even large, healed functionally and were of no prognostic significance. In the majority of symptomatic patients gastrointestinal manifestations held postoperatively, but two patients died of acute pancreatitis without gastrointestinal complaints preoperatively. Almost all symptoms of the hypercalcemic syndrome disappeared immediately and permanently in symptomatic and oligosymptomatic patients. No deterioration of renal function and no elevation of blood pressure was observed in cured asymptomatic patients postoperatively. Immediate surgical treatment even in asymptomatic patients may have avoided complications of chronic renal failure or of hypertension. As soon as organic manifestations, even in a mild form, have been established, it seems impossible to predict the course and to prevent an unfavorable clinical outcome.
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PMID:[Clinical experiences following the surgical therapy of asymptomatic, oligosymptomatic and symptomatic parathyroid gland hyperfunction]. 378 42

A radioimmunoassay for bovine osteocalcin has been developed. Human osteocalcin reacted identically with the bovine standard, allowing the use of this assay to measure human plasma osteocalcin. Levels were determined in 212 healthy subjects (124 men, 88 women) with an age range of 20 to 66 years. The distribution of these was skewed to the right, with the mean being 14.7 ng/ml (range 4 to 40) and the geometric mean 12.2 ng/ml. There was no alteration with age and no difference between males and females. High levels were found in chronic renal failure, Paget's disease of bone, and in primary hyperparathyroidism with severe bone disease, and there was a significant positive correlation of osteocalcin with plasma alkaline phosphatase. Low levels were found in pregnancy. Evidence is presented which suggests that the high levels measured probably reflect intact osteocalcin and not immunoreactive fragments. Our data are compared with those reported by others. Areas of disagreement are noted and discussed.
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PMID:Plasma osteocalcin in man. 387 1

The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5'-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4.6 pmol human PTH(1-34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middle- and carboxyl-terminal region of the PTH molecule (r = 0.503, P less than 0.001). A positive correlation (r = 0.572, P less than 0.05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P less than 0.01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0.390, P less than 0.01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal adenylate cyclase assay for biologically active parathyroid hormone: clinical utility and physiological significance. 394 39

In order to obtain a better resolution of circulating PTH-fragments, we developed a radioimmunoassay with an antiserum raised against the synthetic 70-84 hPTH molecule in a sheep. [125I](69 Tyr) 70-84 hPTH was used as the radioactive tracer with the antiserum at a final dilution of 1:200 000. Displacement curves showed that only the 70-84 hPTH, (69 Tyr) 70-84 hPTH and 53-84 hPTH fragments were able to compete with the tracer. Synthetic 28-48 hPTH, 44-68 hPTH, (61 Tyr)62-68 hPTH, purified 1-84 hPTH and 53-84 bPTH showed no ability to displace the tracer indicating that the idiotype of the antibody is directed against the 70-84 portion that is usually hidden within the globular structure of the intact molecule. Healthy adults revealed PTH-peptide levels of 153 +/- 86 pg/ml (mean +/- 2 SD); 2 SD range: 67-239 pg/ml. C-terminal PTH-peptide (70-84 hPTH) concentration was normal in patients with primary hyperparathyroidism and chronic renal failure, thus excluding that neither the kidney nor the parathyroid gland is involved in the generation of this C-terminal PTH-peptide sequence. Increased levels of 70-84 hPTH immunoreactivity were found in most individuals with severe cholestatic liver disease. Since the liver appears to be responsible for part of the peripheral PTH metabolism, this assay system might be used as an indicator of altered liver function.
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PMID:Selective determination of C-terminal (70-84) hPTH: elevated concentrations in cholestatic liver disease. 394 4

The in vitro secretion of PTH by dispersed human parathyroid cells was examined under conditions of low and high extracellular Ca+2 using tissue from patients with primary hyperparathyroidism and hyperparathyroidism resulting from chronic renal failure (CRF). The PTH secretion rate (nanograms of PTH per 10(5) cells/h) was lower in adenomatous tissues than in either primary hyperplastic cells or CRF cells under conditions of low (0.5 mM) or high (2.0-3.0 mM) extracellular Ca+2. Among the adenomas, a wide spectrum of degree of suppressibility of PTH secretion by high Ca+2 was found, ranging from 0% (completely nonsuppressible) to 98%. Suppression of the hyperplastic tissues in general was similar. The most suppressible adenomas demonstrated 2-fold greater PTH secretion rates in low Ca+2 conditions than the least suppressible adenomas, but in high Ca+2 conditions, the two groups had similar secretory rates. We conclude that the rate of PTH secretion by cells from adenomas was substantially lower than that of cells from tissues exhibiting either primary hyperplasia or hyperplasia resulting from CRF under these in vitro conditions. Thus, in adenomas, an increase in absolute cell number as well as alterations in the degree of calcium responsiveness may prove to be important etiological factors in the expression of hyperparathyroidism.
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PMID:Parathyroid hormone secretion from dispersed human hyperparathyroid cells: increased secretion in cells from hyperplastic glands versus adenomas. 398 Jun 67

Free hydroxyproline was measured in plasma of 67 normal subjects and in 70 patients with bone disease including primary hyperparathyroidism (n = 19), osteoporosis (n = 18), Paget's disease (n = 14), cancer involving bone (n = 8), chronic renal failure (n = 6), and osteomalacia (n = 6), and osteomalacia (n = 5). A good correlation was found between plasma and urinary values of the amino acid in normal subjects (r = 0.66; p less than 0.001). In patients with skeletal disorders a highly significant direct correlation was observed between free plasma hydroxyproline on the one hand and urinary hydroxyproline (r = 0.92; p less than 0.001) and serum alkaline phosphatase activity (r = 0.86; p less than 0.001) on the other, even though there were a few examples of dissociations among these parameters. Free plasma hydroxyproline decreased in the patients with Paget's disease following chronic administration of salmon calcitonin. Following successful parathyroidectomy, free plasma levels of hydroxyproline decreased in all the cases studied. Measurement of free plasma hydroxyproline thus appears to provide a specific index of bone metabolism that may be usefully employed as an alternative to the assay of other markers of bone turnover.
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PMID:Clinical significance of free plasma hydroxyproline measurement in metabolic bone disease. 406 20


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