Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nephrogenous cyclic AMP (NcAMP), total cyclic AMP excretion (UcAMP), and plasma immunoreactive parathyroid hormone (iPTH), determined with a multivalent antiserum, were prospectively measured in 55 control subjects, 57 patients with primary hyperparathyroidism (1 degrees HPT), and 10 patients with chronic hypoparathyroidism. In the group with 1 degrees HPT, NcAMP was elevated in 52 patients (91%), and similar elevations were noted in subgroups of 26 patients with mild (serum calcium </=10.7 mg/dl) or intermittent hypercalcemia, 19 patients with mild renal insufficiency (mean glomerular filtration rate, 64 ml/min), and 10 patients with moderate renal insufficiency (mean glomerular filtration rate, 43 ml/min). Plasma iPTH was increased in 41 patients (73%). The development of a parametric expression for UcAMP was found to be critically important in the clinical interpretation of results for total cAMP excretion. Because of renal impairment in a large number of patients, the absolute excretion rate of cAMP correlated poorly with the hyperparathyroid state. Expressed as a function of creatinine excretion, UcAMP was elevated in 81% of patients with 1 degrees HPT, but the nonparametric nature of the expression led to a number of interpretive difficulties. The expression of cAMP excretion as a function of glomerular filtration rate was developed on the basis of the unique features of cAMP clearance in man, and this expression, which provided elevated values in 51 (89%) of the patients with 1 degrees HPT, avoided entirely the inadequacies of alternative expressions. Results for NcAMP and UcAMP in nonazotemic and azotemic patients with hypoparathyroidism confirmed the validity of the measurements and the expressions employed.
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PMID:Nephrogenous cyclic adenosine monophosphate as a parathyroid function test. 19 23

On the basis of 100 cases of hypercalcemia, the authors attempt to elucidate the criteria of the etiologic diagnosis. Kidney lithiasis or nephrocalcinosis suggested a primary hyperparathyroidism (HPT I) or an intoxication due to vitamin D. X rays of the skeleton and quantitative histological exams of the bone were not useful in the diagnosis of HPT I. The level of parathormone in the plasma is the best parameter to be used in distinguishing HPT I from other diseases. In the absence of renal insufficiency or severe intestinal disorders, a phospharemia below 2.6 mg/100 ml, a chloremia above 103 m EG/l and bicarbonates below 25 m Eg/l indicate an HPT I or a paraneoplasic. A phosphoremia above 3.2 mg/100 ml runs counter to this diagnosis. The chloremia/phosphoremia ratio is not more helpful than the phosphoremia alone.
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PMID:[Etiologic diagnosis of hypercalcemia. A study of 100 cases]. 72 66

The indications for surgical treatment of renal HPT in patients with chronic endstage renal failure are symptomatic disease or failed medical management. The indications for patients who have had a kidney transplant are symptomatic disease and persistent hypercalcemia. It should be noted, however, that the current approach favored in the literature in asymptomatic, mild post-transplant hyperparathyroidism is conservative. Total parathyroidectomy with autotransplantation is the most popular surgical method reported. I have done subtotal parathyroidectomy and reserved total parathyroidectomy for selected patients. My recurrence rate is comparable to that reported. The actual survival rate in our two groups of patients was 58 percent for the dialysis patients and 79 percent for the transplant patients. The actuarial survival rates at 1, 5, and 10 years in the two groups were 95 and 92 percent; 59 and 67 percent; and 32 and 67 percent. The use of diphosphonates and medical rather than surgical control needs further study, as do the long-term effects of conservative treatment of asymptomatic post-transplant hyperparathyroidism.
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PMID:Renal hyperparathyroidism. 144 Jan 49

In order to investigate the relationships between serum calcium, urate and kidney function, serum calcium, urate, creatinine and urea were measured at 100 occasions in hypercalcemic cancer patients together with 113 preoperative measurements in HPT subjects and 106 measurements in normocalcemic control persons. When compared to normocalcemic control subjects (serum urate 336 +/- 110 mumol/l) both HPT subjects (356 +/- 98 mmol/1, p less than 0.006) and the cancer patients (407 +/- 179 mmol/l, p less than 0.001) showed raised levels of serum urate. While serum urate was correlated to serum creatinine in all groups (r = 0.40-0.59, p less than 0.0001) a significant correlation to serum calcium was only seen in the HPT group (r = 0.28, p less than 0.004). This relation persisted also after correction for age, sex and serum creatinine in the multiple regression analysis. Serum creatinine was similar in all groups but significantly correlated to serum calcium only in the HPT subjects (r = 0.29, p less than 0.003). Serum urea was not significantly correlated to serum calcium in any of the groups but was elevated in the cancer group (8.3 +/- 4.4 vs 6.2 +/- 2.9 mumol/l in the control group, p less than 0.0001). This elevation in serum urea seen in the cancer patients might rather be explained by dehydration or catabolism than an impaired kidney function. In conclusion, while serum urate is related to the kidney function both in normo- and hypercalcemia, it also seems to be related to the hypercalcemia in HPT subjects but not in cancer patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum urate and renal function in different forms of hypercalcemia. 163 24

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

Renal function was investigated immediately before and 1 year following parathyroidectomy in 19 patients with moderate hypercalcaemia. On both occasions, all patients underwent five different tests of glomerular and tubular function: plasma creatinine, creatinine clearance, 51Cr-EDTA-clearance, beta 2-microglobulin excretion and the desmopressin test. Glomerular filtration rate, as assessed by plasma creatinine and clearance of both creatinine and 51Cr-EDTA, was normal in most patients, and was little affected by restoration of normocalcaemia. Renal concentrating capacity, as determined by the desmopressin test, was abnormally low in 14 of 19 patients, but increased significantly after surgery. It is concluded that serious renal damage is seldom encountered in present-day HPT patients, but that a treatable decrease in renal concentrating capacity often exists.
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PMID:Pre- and postoperative evaluation of renal function with five different tests in patients with primary hyperparathyroidism. 211 71

Although considerable effort has gone into the development and modernization of indirect parathyroid function tests, recent experience indicates that they do not possess adequate diagnostic specificity or sensitivity to provide a definitive diagnosis of HPT when they are most needed, that is, in mild or intermittent hypercalcemia. Conversely, in most research and some commercial laboratories, the combination of hypercalcemia and an elevated mid-molecule or intact PTH level will be diagnostic in more than 90% of patients.
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PMID:Laboratory diagnosis of primary hyperparathyroidism. 255 Feb 19

Parathyroid hormone radioimmunoassay (RIA), specific for mid-region of the PTH molecule, has been proven to be extremely useful for the differential diagnosis of abnormal calcium metabolism. Recently, we developed a highly sensitive RIA for PTH, consisting of PTH antiserum (CH9), 125I labelled Tyr42 hPTH (43-68) and synthetic hPTH (1-84) as standard. This RIA cross-reacted with mid-region and carboxyl terminals of PTH. The within-assay and between-assay coefficients of variation were less than 4.6% and less than 8.6%, respectively. The limit of detection was 50pg/ml. The levels of serum calcium, serum phosphate, serum creatinine, Tmpo4/GFR and creatinine clearance (Ccr) in normal healthy volunteers aged 20 to 50 years remained almost constant and showed 9.24 +/- 0.34mg/dl (mean +/- SD, n = 242), 3.34 +/- 0.38mg/dl (n = 242), 0.870 +/- 0.121mg/dl (n = 242), 3.20 +/- 0.54mg/dl GF (n = 189) and 103 +/- 17ml/min (n = 137), respectively. All healthy volunteers (n = 326) had measurements of PTH in the blood. From 20 to 50 years, normal PTH mean was 374 +/- 97pg/ml (+/- SD, n = 237) and ranged from 180-568pg/ml, and from 60 to 80 years it was 471 +/- 133pg/ml (n = 34) and ranged from 205-737pg/ml. Since we found that PTH was markedly elevated above normal when Ccr was below 40ml/min, and PTH was very significantly correlated with the reciprocal of Ccr (r = 0.8996, P less than 0.001) using a multivariate analysis, all of the patients whose Ccr was higher than 40ml/min were selected and examined in the following studies. Serum PTH values completely separated patients with surgically proven primary hyperparathyroidism (1 degree HPT) from malignant associated hypercalcemia (MAH), and patients with idiopathic hypoparathyroidism (IHP) from pseudohypoparathyroidism (PHP), both of which were diagnosed by Ellsworth-Howard test. PTH values in all of the patients with 1 degree HPT (n = 23) were above normal, but those with MAH (n = 6) were below the normal or lower normal range. PTH values in patients with PHP (n = 7) showed above normal, while those with IHP (n = 5) were below the normal range. PTH was normalized in post operative status in all patients after parathyroidectomy (n = 6). These results indicate that this PTH RIA is extremely useful for the differential diagnosis in diseases with calcium abnormalities.
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PMID:[Clinical studies using a highly sensitive radioimmunoassay for mid-region and carboxy terminus of parathyroid hormone in normal, hypo- and hypercalcemic states]. 255 7

Assays for N-terminus, C-terminus and mid-molecule parathyroid hormone have been assessed with respect to their sensitivity and specificity in the diagnosis of primary hyperparathyroidism (1 degree HPT). The mid-molecule assay was the most sensitive method studied and only failed to identify one out of 30 patients with histologically proven 1 degree HPT. In all three assays there was some degree of overlap between results observed in 1 degree HPT and in patients with non-parathyroid hypercalcaemia, with results in the latter group sometimes falling well within the hyperparathyroid range. This study highlights the limitations of currently available methods and emphasises the need for caution in the interpretation of parathyroid hormone (PTH) measurements.
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PMID:Diagnostic limitations of region-specific parathyroid hormone assays in the investigation of hypercalcaemia. 340 Sep 85

Thirty-five women with breast cancer and primary hyperparathyroidism (1 degree HPT) were admitted to Memorial Hospital during a 25-year period. The incidence of primary hyperparathyroidism in the breast cancer patients was similar to the incidence in the total patient population at Memorial Sloan-Kettering Cancer Center (0.15% and 0.14%, respectively). The patients with 1 degree HPT disease had clinical findings which distinguished them from those patients with cancer-related hypercalcemia. Eighty percent of the breast cancer patients with primary hyperparathyroidism had earlier stage disease (Stage 0, Stage 1, Stage 2); whereas 97% of the patients with breast cancer and hypercalcemia (not due to 1 degree HPT) had advanced disease. There appeared to be a trend towards improved survival in the breast cancer patients with primary hyperparathyroidism when compared to patients of similar stage of disease who did not have parathyroid disease.
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PMID:Distinguishing features of primary hyperparathyroidism in patients with breast cancer. 362 Nov 32


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