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)

We studied the relationship between the bone mass and biochemical parameters in 175 normal premenopausal, 72 normal postmenopausal and osteoporotic postmenopausal women, between 20 and 88 years old, and in 40 patients with hyperthyroidism, and 23 patients with primary hyperparathyroidism, between 13 and 64 years old. The bone mineral density (BMD) of the spine (L2-L4) and proximal femur (femoral neck) was measured by dual-energy X-ray absorptiometry using a QDR-1000, Hologic. The bone mineral content (BMC) of the radius was measured by single photon absorptiometry (SPA) using a model 2780, Norland. Serum PTH, BGP and calcitonin (CT) were determined by radioimmunoassay. The BMD of the spine (L2-L4), and the proximal femur in postmenopausal women were negatively correlated with age. The mean BMD in patients with postmenopausal osteoporosis was significantly lower than that in normal postmenopausal women. In postmenopausal women, age was positively correlated with BGP, PTH, CT and negatively correlated with P. In patients with osteoporosis, the BMD of the spine was negatively correlated with serum BGP. The BMC of radius in patients with hyperthyroidism decreased significantly compared with that in the controls, and was negatively correlated with F-T3. The BMC of the radius in patients with primary hyperparathyroidism was significantly lower than that in the controls, and was negatively correlated with serum BGP and serum calcium. The measurements of biochemical parameters such as serum BGP, ALP and PTH may be useful in the assessment of metabolic bone diseases.
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PMID:[Bone mass and biochemical parameters in metabolic bone diseases]. 194 67

A RIA for PTH-related protein (PTHrP) is described, using a polyclonal goat antiserum against synthetic PTHrP-(1-40) and recombinant PTHrP-(1-84) as standard. The detection limit is 2 pmol/L, and intra- and interassay coefficients of variation are 4.8% and 13.6%, respectively. This assay does not detect PTH even at concentrations of up to 2000 pmol/L. Cross-reactivity studies using various synthetic PTHrP peptides localize the antibody-binding epitope between residues 20 and 29. Hypercalcemic patients with a range of solid tumors and no evidence of bone metastases on radionuclide scanning (n = 27) all had detectable PTHrP levels (range, 2.8-51.2 pmol/L). Of 17 patients with solid tumors (other than breast) and bone metastases, 11 (64%) also had detectable PTHrP levels (range, 4.9-47.5 pmol/L). Twenty samples from breast cancer patients with hypercalcemia, 19 with evidence of bone metastases, and 1 with a negative bone scan were assayed, and detectable PTHrP levels were found in 13 (65%; range, 3.8-61.6 pmol/L). Patients with squamous cell carcinomata and normal serum calcium levels (n = 11) had no detectable PTHrP or levels close to the detection limit of the assay (range, less than 2 to 3.7 pmol/L). Plasma levels in normal volunteers were below the detection limit of the assay in all but 1 of 38 normal subjects. Patients with chronic renal failure on hemodialysis (n = 18) and patients with primary hyperparathyroidism (n = 14) all had undetectable PTHrP in this assay. This assay allows positive identification of patients with PTHrP-mediated hypercalcemia and, therefore, should be useful in the clinical investigation of the hypercalcemic patient. Furthermore, it has allowed detection of circulating PTHrP in hypercalcemic breast cancer patients with bone metastases, indicating a significant role for PTHrP in this disease.
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PMID:Parathyroid hormone-related protein: elevated levels in both humoral hypercalcemia of malignancy and hypercalcemia complicating metastatic breast cancer. 195 13

Parathyrin (parathyroid hormone; PTH) was measured with three immunoassays: a two-site immunochemiluminometric (ICMA) and a two-site immunoradiometric (IRMA) method for intact PTH, and a sensitive radioimmunoassay for mid-region or "total" PTH, measuring both intact hormone and inactive fragments. Single specimens from normal subjects and from individuals with primary hyperparathyroidism, hypercalcemia associated with malignancy, and hypoparathyroidism were analyzed with all three methods. All individuals with primary hyperparathyroidism showed absolutely above-normal concentrations with the mid-region RIA, 28 of 29 did with the ICMA, and 21 of 29 did with the IRMA. PTH concentrations in primary hyperparathyroidism were most increased relative to normal subjects with the mid-region assay (10.4 times), less so with the intact assays (ICMA 5.5 times; IRMA 5.3 times). Concentrations of intact PTH were suppressed below normal in nearly all patients with hypercalcemia associated with malignancy, as measured with the ICMA (26 of 30) and the IRMA (28 of 30) assays. In marked contrast, results for mid-region PTH were normal or slightly above normal, consistent with studies suggesting that the parathyroids secrete both intact hormone and inactive fragments, the former being more sensitive to suppression by hypercalcemia. In hypoparathyroidism PTH concentrations were detectable but below normal in all patients by the intact assays and in all but one patient by the mid-region assay. These low concentrations are probably due to a nonspecific serum effect that could be resolved with selection of a more appropriate standard matrix. Although all three assays are useful in the differential diagnosis of hypercalcemia, two-site intact assays are more convenient and more specific in patients with compromised renal function.
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PMID:Immunochemiluminometric and immunoradiometric determinations of intact and total immunoreactive parathyrin: performance in the differential diagnosis of hypercalcemia and hypoparathyroidism. 199 16

The cause of hypercalcemia in familial benign hypercalcemia (FBH; also called familial hypocalciuric hypercalcemia) is unclear, although it is PTH dependent. It is also uncertain how plasma PTH levels are related to the severity of biochemical abnormalities in FBH. Because the PTH-related peptide (PTHrP) has many PTH-like actions, it might have a role in the hypercalcemia of FBH. Thus, we studied 29 patients with FBH from 11 families, 29 age- and sex-matched controls, and 42 patients with primary hyperparathyroidism (1 degree HPT), measuring PTH with a highly sensitive two-site immunochemiluminometric assay and the hypercalcemic tumor factor PTH-related peptide (PTHrP) with an extraction/concentration RIA. Plasma PTH values were elevated in 86% of 1 degree HPT patients (36 of 42), but in only 20% of FBH patients, (6 of 29). Plasma PTHrP was elevated in 1 FBH patient, and the group mean value was normal. Plasma PTH was positively correlated with calcium (Ca) in 1 degree HPT (r = 0.66; P less than 0.0001) and in FBH (r = 0.53; P less than 0.004), but the slopes of the regressions were markedly different: 1 degree HPT, 6.72; FBH, 1.61 (P less than 0.0001). There was a negative correlation between PTH and phosphorus (P) in 1 degree HPT (r = -0.39; P less than 0.01) and in FBH (r = -0.41; P less than 0.03), but, again, the slopes differed greatly: 1 degree HPT, -6.57; FBH, -1.95 (P less than 0.0001). There were no correlations between PTHrP and Ca or between PTH and PTHrP. The sums and products of PTH and PTHrP were not better correlated with Ca than PTH alone. Thus, PTH values are lower at given Ca and P levels in patients with FBH than in those with 1 degree HPT, suggesting that PTH is more effective in raising Ca and lowering P in FBH than in 1 degree HPT. The enigma of FBH remains: what molecular defect can simultaneously cause parathyroid cell insensitivity to Ca, enhanced renal tubular reabsorption of Ca, increased renal rejection of P, and enhanced or retained sensitivity to PTH?
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PMID:Plasma intact parathyroid hormone (PTH) and PTH-related peptide in familial benign hypercalcemia: greater responsiveness to endogenous PTH than in primary hyperparathyroidism. 199 10

Serum total, ultrafiltrable and protein-bound magnesium, and urinary fractional excretion of magnesium were studied in patients with primary hyperparathyroidism (before and after surgery) and in patients with hyperparathyroidism, malignant hypercalcemia and chronic renal failure with or without hemodialysis. Whereas serum total Mg was unchanged in patients with primary hyperparathyroidism, the ultrafiltrable magnesium concentration was higher than in the control group and higher before than after surgery. The total and the ultrafiltrable magnesium concentrations were highly correlated in the overall patients with Ca-related metabolic disorders, suggesting that renal function had no influence on the relation between these two parameters. Moreover, in malignant hypercalcemia, our results suggested that PTH-like peptides might be less effective than PTH in renal handling of Mg as previously described for Ca.
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PMID:Total and ultrafiltrable plasma magnesium in hyper- and hypoparathyroidism, and in calcium-related metabolic disorders. 202 73

We describe three cases of women who developed symptoms of primary hyperparathyroidism originated by a parathyroid functional tumor. Ostoporosis, arterial hypertension and nefrolitiasis were the most frequent antecedents. The PTH and calcium levels in bood and urine were elevated. The CT and ultrasound confirmed the diagnosis of parathyroid tumor, which was identified histopathology as oxifilic adenoma. All patients underwent surgical treatment. We consider these cases of clinical interest because this kind of adenoma hardly ever produces hyperparathyroidism.
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PMID:[Oxyphillic adenoma as a cause of primary hyperparathyroidism]. 210 96

Primary hyperparathyroidism can be caused by a solitary parathyroid adenoma and sometimes by hyperplastic parathyroid glands, multiple adenomas, or carcinoma. In the majority of patients, the diagnosis is made tentatively by chemistry profiles that show elevated serum calcium. It is confirmed by repeated serum calcium values and PTH determination. The parathyroid abnormality, if an adenoma, can usually be localized preoperatively by thallium-technetium scan, ultrasound, or computed tomography. In the case of persistent disease with hypercalcemia, an angiogram with selective venous sampling for PTH is helpful. At exploration, both sides of the neck may need exploration. A unilateral procedure may be sufficient, if the preoperative localization tests are confirmatory and if biopsy of another "normal" gland shows normal histologic findings. During the postoperative period, suction drains will lessen the likelihood of hematoma formation and serum calcium levels are monitored for the first 3 to 5 days. Symptomatic patients with low calcium levels receive intravenous and oral calcium supplements until values are brought to the low-normal range. Supplements are tapered as the calcium in the serum rises. The majority of patients who undergo parathyroid surgery will benefit both symptomatically and metabolically.
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PMID:Hyperparathyroidism. 211 Jun 44

This study has been carried out in order to investigate parathyroid hormone secretion in patients with primary hyperparathyroidism in basal conditions, during stimulation and suppression tests and following successful surgery. Parathyroid gland secretory activity has been evaluated by a highly sensitive immunoradiometric assay (IRMA) which detects only the biologically intact active hormone and with a well established midmolecule (MM) PTH RIA. There was a good correlation between the two assays in basal state (r = 0.779); however the correlation found between serum PTH levels and total calcium values was better for the intact hormone (P less than 0.001) than for the radioimmunoassay (P less than 0.05). Twenty-four hours following surgery, serum intact PTH levels were in all patients less than 10 pg/ml while midmolecule PTH was still detectable, thereafter remaining at a higher level during the next six days. Serum IRMA PTH levels fell rapidly in response to the increase in serum calcium, then there was a trend to reach a plateau; serum midregion PTH levels fell, although slower than those of intact hormone. The percent increase obtained for serum intact hormone levels was higher than that observed for MM RIA, following EDTA stimulation. The results obtained indicate that the assays of intact and midmolecule parathyroid hormone clearly reflect different aspects of hormone metabolism 'in vivo' and may prove therefore to be useful for its investigation in various calcium disorders.
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PMID:Two-site assay of intact parathyroid hormone in primary hyperparathyroidism: studies in basal conditions, following adenoma removal and during calcium and EDTA infusion. 212 54

We performed 6-h human PTH-(1-34) infusions in 8 control subjects, 10 subjects with primary hyperparathyroidism, and 7 men with idiopathic hypercalciuria. We measured serum calcium, serum 1,25-dihydroxyvitamin D, urinary calcium, and fractional phosphate excretion. The PTH-induced rise in serum 1,25-dihydroxyvitamin-D was significantly smaller in the hyperparathyroid patients than in either the controls or the hypercalciuric patients. The rise in serum calcium was similar in all 3 groups. The hyperparathyroid subjects had higher basal fractional phosphate excretion than the other two groups. PTH failed to increase fractional phosphate excretion in the hyperparathyroid individuals, whereas there was a statistically significant increase in the other two groups. PTH was without significant effect on urinary calcium excretion in any of the three groups. There were no discernible differences between the responses of the hypercalciuric patients and those of the normal subjects. These findings suggest that while responses to PTH are normal in hypercalciuria, some hyperparathyroid patients are resistant to exogenous PTH. This resistance is limited to specific arms of the PTH response pathway and may not involve PTH receptors.
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PMID:Parathyroid hormone sensitivity in primary hyperparathyroidism and idiopathic hypercalciuria: effects on postadenylate cyclase parameters. 215 86

An oral calcium load test (CLT) (1 gm Ca/50 kg) was administered to 11 control subjects and 35 patients with overt hyperparathyroidism to assess its efficacy in diagnosis of hyperparathyroidism. All participants were placed on a low-calcium diet 3 days before the CLT. Intact parathormone and ionized calcium (Cai) levels were measured 0, 1, 2, and 3 hours after CLT. Initial Cai and parathormone (mean +/- SE) were 1.22 +/- 0.01 mmol/L and 2.94 +/- 0.03 pmol/L in the control group compared with 1.43 +/- 0.02 mmol/L and 10.6 +/- 2.2 pmol/L in the group with hyperparathyroidism. Both groups had a similar percent increase in Cai values (control, 5.9% +/- 0.8%; hyperparathyroidism, 6.3% +/- 0.6% (p greater than 0.1). A decline in parathormone levels of 47.6% +/- 2.8% in patients with hyperparathyroidism was significantly less than the 75.3% +/- 5.3% decline observed in control subjects (p less than 0.025). Three hours after CLT, parathormone was suppressed in control subjects, whereas a rebound occurred in patients with hyperparathyroidism. Postoperative CLT demonstrated a higher mean percent Cai increase and percent parathormone decline (Cai, 8.9% +/- 1.1%; parathormone, 67.9% +/- 1.8%) compared with preoperative values (Cai, 6.0% +/- 1.0%; PTH, 49.6% +/- 4.3%) (p less than 0.025), and 3 hours after calcium intake, parathormone remained suppressed, similar to control subjects. After surgery, three patients had elevated parathormone and low normal Cai levels and parathormone response to a CLT confirmed the diagnosis of secondary hyperparathyroidism. In conclusion, a CLT (1) can confirm the diagnosis of hyperparathyroidism and successful parathyroidectomy, (2) distinguished postoperative secondary from persistent primary hyperparathyroidism, (3) demonstrated nonautonomy of abnormal parathyroid glands with a parathormone response to a calcium load characterized by an earlier nadir, decreased suppressibility, and more rapid recovery, and (4) produced dynamic changes that did not distinguish patients with hyperparathyroidism from control subjects or hyperplasia from adenoma.
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PMID:Oral calcium load test: diagnostic and physiologic implications in hyperparathyroidism. 217 92


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