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)

Plasma hCT levels were less than 50 pg/ml in 50 normal subjects. In 16 patients with medullary carcinoma of the thyroid (MCT), plasma hCT levels were distinctively elevated and they fell significantly after total thyroidectomy, but in 11 of them plasma levels were still high, indicating the presence of metastases. In 74 patients with the other types of malignancy, plasma hCT levels were found to be high in 9 cases (3 oat cell carcinoma of the lung, 4 malignant carcinoids, one malignant pheochromocytoma and one acute myelocytic leukemia). Except for the leukemic case, all these tumors were derived from neural crest. In 12 patients with primary hyperparathyroidism, plasma hCT levels were less than 20 pg/ml. In 13 hypoparathyroid patients, two with pseudohypoparathyroidism and one with pseudoidiopathic hypoparathyroidism, plasma hCT levels were slightly elevated. Some patients with uremia had elevated plasma hCT levels, but there was no relation between plasma levels of hCT and those of PTH, urea nitrogen or creatinine. In response to Ca (4.5 mg/kg/10 min) or tetragastrin (4 mug/kg/5 min) infusion, a marked increase in plasma hCT was observed in all patients with MCT, but not in normal subjects. In 5 hypoparathyroid patients, a significant increase to both stimuli was also observed in all cases. Two patients with pseudopseudohypoparathyroidism responded to the Ca load. These results indicate that the determination of plasma hCT levels especially after a short Ca or tetragastrin infusion is important to study various pathological conditions.
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PMID:Plasma human calcitonin (hCT) levels in normal and pathologic conditions, and their responses to short calcium or tetragastrin infusion. 19 Dec 50

The findings of 152 patients with proven primary hyperparathyroidism are reportedmthe purpose of the analysis was to find difference between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups, Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in an atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck; The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The sucess of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There ist still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are reposible for the different action on bone and kidney is discussed; In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting, abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in over 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcenia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparthyroidism. Analysis of 152 patients with special reference to acute life threatening complications (acute hyperparathyroidism)]. 20 39

Tthe findings of 150 patients with proven primary hyperparathyroidism are reported. The purpose of the analysis was to find differences between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups. Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck. The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The success of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There is still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are responsible for the different action on bone and kidney is discussed. In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in ov er 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcemia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparathyroidism. An analysis of 152 patients with special references to acute life threatening complications (acute hyperparathyroidism)]. 79 28

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

Two patients with primary hyperparathyroidism had hyperuricemia due to the decrease in urate clearance. In analysis by 4-component model system, the tubular secretion of urate commonly decreased without changes in either filtered urate or presecretory reabsorption of urate. Both patients had a reduction of urea clearance, and both parathyroidectomy in the former case and intravenous infusion of saline in the latter case could reduce the serum urate level associated with the increase in the ratio of urate clearance to creatinine clearance. It is of interest that the former case with a higher serum urate level had a relatively higher postsecretory reabsorption, even with the decrease in tubular secretion of urate. However, the latter patient with a lower serum urate level had a decrease in postsecretory reabsorption of urate in proportion to the decrease in tubular secretion. These results suggest that in hyperuricemia patients with primary hyperparathyroidism, the reduction of tubular urate secretion via hypoperfusion of the capillary network is typically present, however, the severity of the hyperuricemia might be dependent on the dysfunction of the postsecretory reabsorption of urate.
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PMID:Renal handling of urate in two patients with hyperuricemia and primary hyperparathyroidism. 139 85

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.
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PMID:[Physiopathology, exploration and treatment of calcium lithiasis]. 178 95

Experience in the diagnosis and treatment of the renal form of primary hyperparathyroidism in 57 patients with bilateral nephrolithiasis was summed up. The main diagnostic criterion was the detection of biochemical changes in the blood and urine (hypercalcemia, hypophosphatemia, hypercalciuria) and the use of some tests (Howard's test and parathyroidin test). Parathyroidectomy was performed after establishing diagnosis. A new stage in therapy of such patients was a study of renal function and phosphocalcium metabolism after parathyroidectomy. The improvement of some indices (an increase in glomerular filtration, urea excretion with urine and relative urine density, and a decrease in hypercalciuria and hyperphosphaturia) indicated the effectiveness of surgical intervention for primary hyperparathyroidism in patients with bilateral nephrolithiasis. It was also confirmed by a decrease in lithogenic relapse after parathyroidectomy.
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PMID:[Primary hyperparathyroidism in patients with bilateral nephrolithiasis]. 258 27

In order to obtain a useful screening index for primary hyperparathyroidism (PHPT), seven patients with PHPT and fifty-one patients with nonparathyroid hypercalcemia (NPHC) were studied retrospectively. Serum calcium, inorganic phosphate (IP), alkaline phosphatase, albumin (Alb), chloride (Cl), total protein, urea nitrogen and creatinine (Cre) were analyzed at the same time. Discriminant analysis using a stepwise variable select method was applied to these patients. A discriminant function (F 1) was derived from three laboratory tests; F 1 = -0.660 x [IP] + 0.142 x [Cl] + 0.564 x [Alb] - 14.4 (PHPT: F 1 greater than 0.641). F 1 had sensitivity of 100% and specificity of 72.5% (14 false positives) in diagnosing PHPT. Next, another discriminant function (F 2) was derived from PHPT and the false positive patients; F 2 = -2.61 x [IP] + 0.286 x [Cl] - 4.24 x [Cre] - 19.3 (PHPT: F 2 greater than 0.412). When F 2 was applied to positive patients by F 1, final sensitivity was 100% and specificity was 98%. This screening method was tested prospectively in fifty-six consecutive samples of hypercalcemia (PHPT 4, NPHC 52), resulting in sensitivity of 100% and specificity of 98%. It was proved that our screening method using two step discriminant functions was very useful to diagnose PHPT.
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PMID:[A screening index for primary hyperparathyroidism using discriminant functions]. 260 57

We performed a series of isotopic studies in 16 normal volunteers, four patients with secondary hyperparathyroidism (SHPT), and in nine patients with primary hyperparathyroidism (PHPT). Using the primed constant infusion of stable and radioisotopes, we have determined glucose, glycerol, free fatty acids, and urea kinetics, as well as glucose oxidation. Measurements were performed both in the basal state and during glucose infusion (4 mg/kg body weight/min). Compared with normal volunteers, PHPT patients are intolerant of glucose because of a limited suppression of endogenous glucose turnover during glucose infusion (34% versus 96% suppression). In addition, the plasma cortisol level increased in the PHPT patients during glucose infusion. Glucose oxidation and fat kinetics in both PHPT patients and volunteers were similar, but the rate of net protein loss was significantly greater in the PHPT patients than in the volunteers (2.1 +/- 0.5 versus 1.4 +/- 0.2 gm/kg/day). Rates of VO2 in the PHPT patients and volunteers were similar, but the value in the SHPT patients was higher (120 +/- 9 versus 142 +/- 20 mumol/kg/min for PHPT and SHPT patients, respectively). The SHPT patients had significantly increased rates of glucose turnover, glucose clearance, and glycerol turnover, compared with the other two groups, as well as an increased reliance on glucose for energy. We conclude from these studies that (1) SHPT patients are catabolic and have increased rates of glucose and fat turnover; (2) PHPT patients have limited suppression of endogenous glucose turnover after glucose infusion compared with volunteers and higher rates of net protein loss; (3) fat metabolism and glucose utilization are unimpaired in PHPT patients; and (4) these alterations in metabolism and hormonal response to glucose infusion suggest that some of the symptoms seen in these patients may have a metabolic-hormonal basis.
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PMID:Glucose, fat, and protein kinetics in patients with primary and secondary hyperparathyroidism. 328 78

The hospital course of 218 consecutive patients with primary hyperparathyroidism admitted over a three-year period for parathyroidectomy at the Massachusetts General Hospital was reviewed to determine the incidence and identify the risk factors for the development of the hungry bone syndrome. Twenty-five patients with the hungry bone syndrome were identified (12.6 percent). Compared to patients with uncomplicated metabolic responses to parathyroid surgery, these patients were older by a mean of 10 years; they had higher preoperative serum levels of calcium, alkaline phosphatase, N-terminal parathyroid hormone, and blood urea nitrogen; and their resected parathyroid adenomata were larger. The mean duration of hospitalization averaged three days longer in the group with hungry bone disease. Stepwise multivariate analysis of preoperative variables enabled the development of a discriminant function for prediction of postoperative hypocalcemia and hypophosphatemia. Identified predictive variables were volume of resected parathyroid adenoma, blood urea nitrogen, alkaline phosphatase, and age. When validated on an independent patient population, these readily obtainable preoperative clinical and laboratory parameters will allow identification of a subgroup of patients who are at greater risk for the development of the hungry bone syndrome following parathyroid surgery.
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PMID:Hungry bone syndrome: clinical and biochemical predictors of its occurrence after parathyroid surgery. 340 Jun 60


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