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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in plasma adenosine 3'5' (cAMP) and guanosine (cGMP) monophosphate, measured by specific radioimmunoassay, after 150 USP/M2 of bovine parathyroid hormone (bPTH) iv administered were studied in children with pseudohypoparathyroidism, and idiopathic hypoparathyroidism, and in normal controls. Basal concentrations of plasma cAMP (17 nmole/1 +/- 1, 6 SEM) and cGMP (8,7 nmole/1 +/- 1, 3 SEM) were the same in all studied children. Plasma cAMP in normal and idiopathic hypoparathyroid children significantly (30-fold, P less than 0.001) and constantly rose with a peak value (537 nmole/1 +/- 210 SEM) observed 5--10 min after bPTH injection. By contrast, no significant change in plasma cAMP occurred in children with pseudohypoparathyroidism. The data confirmed further the unability of pseudohypoparathyroid children to increase cAMP after exogenous PTH, while the cGMP response did not appear to be significantly modified. It is suggested that an injection of 150 USP/m2 bPTH with plasma samples for cAMP assay taken before and 10 min after hormone administration represents a simplified assessment of Ellsworth-Howard's test.
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PMID:Plasma cyclic nucleotide determination in the investigation of hypocalcemia. 22 72

Propranolol alone was used to prepare 20 thyrotoxic patients, 19 women and 1 man, for subtotal thyroidectomy. Serum thyroxine (T4) and triiodothyronine (T3) concentrations were measured immediately before, at several stages during and after the surgical procedure. As judged primarily by the cardiovascular response, an average of 80 mg (range 40 to 120 mg) of propranolol qid for 8 days (range 3 to 18 days) was required to prepare the patients. During the various stages of surgical removal there was no change from the initial mean (+/- SEM) T4 concentration of 25.0 +/- 2.5 microgram/dl (321.8 +/- 32.2 nmol/l) or T3 concentration of 4.2 +/- 0.6 microgram/l (6.45 +/- 0.92 nmol/l) (P greater than 0.2). At discharge on the fifth postoperative day values were significantly lower, 12.9 +/- 1.5 microgram/dl (166.0 +/- 19.3 nmol/l) and 1.9 +/- 0.2 microgram/l (2.9 +/- 0.31 nmol/l), respectively (P less than 0.001). There were no operative complications but four patients had transient hypoparathyroidism. After 1 year 2 of 18 patients had permanent hypoparathyroidism and 4 of the 18 followed up for 1 year had permanent hypothyroidism requiring thyroid hormone replacement. There was no instance of recurrent thyrotoxicosis. The authors conclude that during surgical manipulation of the gland no release of thyroid hormones into the circulation was detected and that, using propranolol as the sole agent, thyrotoxic patients can be rapidly and safely prepared for subtotal thyroidectomy.
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PMID:Propranolol in thyrotoxicosis: II. Serum thyroid hormone concentrations during subtotal thyroidectomy. 58 22

Here we report a highly sensitive and convenient ligand binding assay for the determination of 1,25(OH)2D3 in small volumes of human plasma. This method involves: (1) extraction of vitamin D3 and its metabolites using methanol-methylene chloride with separation of phases by centrifugation; (2) gel chromatography and high pressure liquid chromatography for the quantitative isolation of 1,25-(OH)2D3; and (3) a sensitive ligand binding assay for 1,25-(OH)2D3 employing cytosol receptor from the intestinal mucosa of rachitic chicks. Using modified rachitogenic chick diets allows early (less than 4 wks) harvesting of active receptor for 1,25-(OH)2D3 in high yield. The method includes a rapid and effective procedure for stable and long-term storage of the active cytosol receptor. A convenient dextran-charcoal means is used for the separation of receptor bound from free 1,25-(OH)2D3 resulting in the achievement of a lower (less than 5%) background (i.e., nonspecific binding) than reported for other 1,25-(OH)2D3 assays. Analysis of this receptor shows it to be a saturable, single class of binding sites with a dissociation constant (Kd) of approximately 3.7 x 10-11. The final recovery of 1,25-(OH)2D3 following extraction and chromatography is 80 +/- 3% and triplicate determinations can be made on a 3 ml plasma sample. The ligand binding assay routinely detects less than or equal to 5pg of 1,25-(OH)2D3 per assay tube and the inter- and intraassay variation, based on repeated determinations of 1,25-(OH)2D3 in pooled normal human plasma, is less than 5%. Preliminary studies indicate that our methodology will permit measurement of plasma 1,25-(OH)2D3 levels in all normal subjects and in pathophysiologic states where 1,25-(OH)2D3 levels may be below or above normal values. 1,25-(OH)2D3 values (pg/ml +/- SEM) in human plasma obtained from both normals and patients with various untreated calcium homeostatic disorders were: normals = 33.5 +/- 1.8; end-stage chronic renal failure = 5.1 +/- 1.2; primary hypoparathyroidism = 18.3 +/- 2.8; primary hyperparathyroidism = 61.4 +/- 7.1; and hyperthyroidism with associated hypercalcemia = 42.1 +/- 8.4.
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PMID:An improved method for the measurement of 1,25-(OH)2D3 in human plasma. 75 33

Forty-eight dialysis patients undergoing bone biopsy were analyzed for clinical history, blood biochemical values, bone histologic findings, bone aluminum content (BAC), bone iron content (BIC), bone iron stores, and histochemical staining of bone aluminum and bone iron. Four patients had significant trabecular bone iron staining alone; eight patients had significant bone iron and bone aluminum staining; 13 patients had significant bone aluminum staining alone; and 23 patients showed no significant bone aluminum or iron staining. Patients with significant bone iron staining were younger (37.4 +/- 5.3 years v 53.2 +/- 2.3 years, P less than 0.01, mean +/- SEM) and were more likely to be anephric (P less than 0.001) and to have a history of prior renal transplantation (P less than 0.10). The 12 patients with significant bone iron staining had received more blood transfusions than those without bone iron staining (96 +/- 22.8 U v 22 +/- 5.8 U, P less than 0.005). Patients with bone iron accumulation had higher levels of serum ferritin (3,594 +/- 1,138.4 micrograms/L [ng/mL] v 265 +/- 60.1 micrograms/L, P less than 0.01) and lower levels of immunoreactive parathyroid hormone (iPTH) (349 +/- 150 microLEq/mL v 1,801 +/- 397 microLEq/mL [386 +/- 166 pmol/L v 1,990 +/- 439 pmol/L], P less than 0.005). BIC was also higher in these patients (1,008 +/- 149 micrograms iron/g bone v 300 +/- 46.5 micrograms iron/g bone, P less than 0.001) and higher than normal BIC (256 +/- 44.2 micrograms iron/g bone, eight normals). Bone marrow iron stores were positively related to serum ferritin levels (P less than 0.01) and trabecular bone iron staining (P less than 0.10). All 13 patients with osteomalacia demonstrated significant bone aluminum staining; seven of these patients demonstrated concomitant significant iron staining. Fourteen of 15 patients with severe hyperparathyroidism showed no significant iron or aluminum staining. Our data indicate that iron will probably not accumulate within bone until all other storage sites (eg, bone marrow) are fully saturated. The presence of lower levels of iPTH in iron-overloaded patients raises the possibility that iron overload may induce a state of relative hypoparathyroidism. The most important determinant for the presence of osteomalacia seems to be the presence of significant aluminum staining. No specific bone histologic finding was related to the presence of bone iron staining, but the rarity of isolated significant bone iron staining makes it difficult to evaluate bone histologic diagnoses that might be solely attributable to iron.
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PMID:Clinical and histologic features of iron-related bone disease in dialysis patients. 202 57

Synthetic human parathyroid hormone (1-34) (hPTH(1-34] infusion test has been utilized in the differential diagnosis of hypoparathyroidism by examining the incremental response of urinary phosphate and cyclic adenosine monophosphate (AMP). The response of plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D) in parathyroid hormone (PTH) infusion test was studied as a new criterion for the differential diagnosis of idiopathic hypoparathyroidism (IHP) and pseudohypoparathyroidism (PHP). Fourteen patients with IHP, 4 patients with PHP, and five control subjects were studied. All subjects received an intravenous infusion of 30 micrograms hPTH(1-34) over 5 minutes. The basal levels of plasma 1,25(OH)2D in patients with IHP and PHP were significantly lower than those in control subjects, but there was no significant difference between the levels in patients with IHP and in patients with PHP. The plasma levels of 1,25(OH)2D increased after the infusion of hPTH(1-34) and reached a peak 6 to 24 hours afterward. The 1,25(OH)2D increase at 24 hours afterward the infusion (delta 1,25(OH)2D) in control subjects and in patients with IHP were 18.1 +/- 3.91 (mean +/- SEM) and 24.1 +/- 2.80 pg/ml, respectively. There was no significant increase in patients with PHP (delta 1,25(OH)2D = 4.9 +/- 1.97 pg/ml). From these results, the measurement of delta 1,25(OH)2D in hPTH(1-34) infusion test is useful as a criterion for the differential diagnosis of hypoparathyroidism.
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PMID:Response of plasma 1,25-dihydroxyvitamin D in the human PTH(1-34) infusion test: an improved index for the diagnosis of idiopathic hypoparathyroidism and pseudohypoparathyroidism. 215 33

The effects of short- and long-term calcium replacement on myocardial function in six asymptomatic patients (age 48 +/- 3, mean +/- SEM) with hypocalcemia complicating surgical hypoparathyroidism were studied. Cardiac output was determined by ascending aortic continuous wave Doppler assessment and was measured as minute distance. During intravenous calcium replacement at rest, ascending aortic minute distance increased from 6.75 +/- 1.10 to 9.17 +/- 1.29 m as the calcium level rose from 1.76 +/- 0.08 to 2.06 +/- 0.19 mmol/L without changes in heart rate and blood pressure (p less than 0.01). The peak velocity and acceleration of blood flow derived from Doppler measurement showed a similar rise during calcium infusion. Symptom-limited cycle ergometry was performed before and 3 months after normalization of calcium by long-term oral therapy. Although the resting cardiac output was unchanged, the maximum cardiac output at peak exercise also increased from a minute distance of 11.58 +/- 1.84 to 15.37 +/- 2.28 m (p less than 0.05), together with an increase of maximum heart rate from 136 to 149 beats/min (p less than 0.05). Exercise duration was also prolonged from 11.9 +/- 2.9 to 13.0 +/- 2.8 minutes. Thus hypocalcemia impairs cardiac performance, but this impairment is reversible with calcium replacement.
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PMID:Hypocalcemic myocardial dysfunction: short- and long-term improvement with calcium replacement. 238 15

Magnesium (Mg) deficiency is a possible etiologic factor contributing to neonatal hypocalcemia. In adults, parathyroid hormone (PTH) secretion is negatively feedback regulated by acute changes in serum Mg concentration, but paradoxically Mg deficiency may lead to functional hypoparathyroidism and hypocalcemia. We hypothesized that in neonates, Mg administration will cause changes in PTH secretion and serum Ca concentration that will be inversely related to serum Mg status. We also hypothesized that Mg administration will result in increased calcitonin (CT) secretion. Thirty-nine newborn infants with birth weights greater than 1500 g were studied on day 3 of life. Ten received placebo, and 29 intravenous magnesium sulfate (MgSO4), 6 mg elemental Mg/kg body weight, over 1 h. Serum Mg, Ca, PTH, and CT were measured at time 0 (baseline, preinfusion) and 1, 2, 6, 12, 24, and 48 h postinfusion. In both groups combined, baseline PTH correlated with baseline Mg (r = 0.72, p less than 0.005), and with baseline Ca (r = 0.68, p less than 0.005). In the control group there was no change in serum Mg, Ca, PTH, and CT during the study period. In magnesium sulfate-infused infants: 1) serum Mg concentration rose from 1.80 +/- 0.06 to 2.82 +/- 0.07 mg/dl (mean +/- SEM, p less than 0.001); 2) the change from baseline in serum PTH at 1, 6, and 12 h postinfusion correlated inversely with baseline Mg (p less than 0.05); 3) the change from baseline in serum Ca at 1, 2, and 24 h postinfusion correlated inversely with baseline Mg (p less than 0.005); 4) serum CT remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of magnesium in neonatal calcium homeostasis: effects of magnesium infusion on calciotropic hormones and calcium. 365 52

We studied Na transport in red blood cells (RBC) from six patients with hypoparathyroidism (HYPO; 3 postsurgical and 3 idiopathic) and 13 normal subjects. In HYPO, the effect of treatment-induced increases in serum Ca2+ on RBC Na transport also was examined. Na efflux mediated by the ouabain-sensitive Na,K pump and furosemide-sensitive Na,K cotransport (CoT) was examined by flux methodology in RBCs Na loaded to 5 levels of intracellular Na (Nai; 5-90 mM/liter cells) by the p-chloromercuribenzene method. The pump-mediated Na efflux was similar in untreated HYPO patients and normal subjects. Correction of hypocalcemia by vitamin D and oral calcium produced a mean increase in serum Ca2+ from 6.62 +/- 0.23 (+/- SEM) to 8.73 +/- 0.32 mg/dl. In HYPO patients treated with vitamin D and oral calcium, an increasing serum Ca2+ level was associated with significant (P less than 0.01) reductions in pump activity. Further, there was an inverse correlation (r = 0.813; P less than 0.001) between serum Ca2+ and pump-mediated Na efflux rate. RBC Na efflux through the CoT pathway was markedly reduced (P less than 0.05-0.01) in HYPO patients compared to normal subjects at all levels of Nai. Treatment-induced increases in serum Ca2+ had no effect on the reduced RBC CoT function in HYPO. Thus, changes in ambient serum Ca2+ can modulate the activity of the RBC Na,K pump in HYPO, with increases in Ca2+ inhibiting pump function. The markedly decreased RBC CoT activity was not related to associated hypertension or altered renal function and may represent a primary phenomenon in HYPO. These alterations in RBC Na transport may account for the higher Na, in RBCs of HYPO patients.
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PMID:Altered red cell sodium transport in hypoparathyroidism: relation to serum calcium. 373 32

This study was designed to follow the evolution of serum 1,25(OH)2D after surgery for primary hyperparathyroidism. Ten patients were studied before and for up to 85 d after removal of a single parathyroid adenoma. Blood and 24 h urine were obtained at various time points, for the measurement of serum or urinary phosphate and calcium indices. Before surgery, serum calcium (2.91 +/- 0.06 mmol/l; mean +/- SEM), parathyroid hormone (354 +/- 47 pg/ml) and 1,25(OH)2D (61.2 +/- 7.8 pg/ml) were elevated while serum phosphate (1.01 +/- 0.07 mmol/l) tended to be low. Relative hypoparathyroidism was evident for up to 5 d after surgery with the lowest value for serum parathyroid hormone (41 +/- 16 pg/ml) on day 1, serum calcium (2.12 +/- 0.06 mmol/l) on day 3 and highest value for serum phosphate (1.41 +/- 0.13 mmol/l) on day 5. As expected, serum 1,25(OH)2D levels decreased to 35.9 +/- 4.2 pg/ml 24 h after surgery. Stabilization of serum and urinary parameters to normal values was seen between day 5 and day 27; the only exception was serum 1,25(OH)2D, which increased again at day 27 to 57.6 +/- 5.0 pg/ml, a value as high as that before surgery. It was still elevated at day 50 (58.3 +/- 4.3 pg/ml), but returned towards normal values in three out of four patients (44 +/- 3.9 pg/ml) by day 80. No variation in 25(OH)D or 24,25(OH)2D was seen throughout the study. 1,25(OH)2D values could be related to serum parathyroid hormone values before surgery (r = 0.659, P less than 0.05) but not after. The secondary increase in serum 1,25(OH)2D could not be related to variations in serum calcium, phosphate, parathyroid hormone or diet. Further studies will be required to explain this phenomenon.
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PMID:Late increase in serum 1,25-dihydroxyvitamin D one month after surgery for adenomatous hyperparathyroidism. 375 58

The response to exogenous parathyroid hormone (PTH) with urinary excretion of phosphate and cyclic adenosine monophosphate (cAMP) was tested by the use of synthetic human parathyroid hormone (1-34) [hPTH-(1-34)] on 59 patients with hypocalcemia and normal or high serum inorganic phosphorus and normal renal function without a history of parathyroidectomy for differentiation between idiopathic hypoparathyroidism (IHP), pseudohypoparathyroidism (PHP) and related diseases along with 18 normal subjects. A positive phosphaturic response to exogenous PTH was defined as the increment of 2 hours phosphate excretion (delta P) of more than 35 mg. A positive urinary cAMP response to exogenous PTH was defined as the increment by more than 1 mumole per one hour (delta cAMP) and the increase of 1 hour excretion by more than 10 times. Increments of 2 hours urinary phosphate excretion in response to hPTH-(1-34) 100 units were 60.5 +/- 7.7 mg (mean +/- SEM) in 27 patients with IHP, 23.5 +/- 5.9 mg in 21 patients with PHP type I and 24.9 +/- 4.0 mg in 17 normal subjects. Increments of 1 hour urinary cAMP excretion in response to hPTH-(1-34) 100 units were 12.0 +/- 1.5 mumole in 27 patients with IHP, 0.33 +/- 0.10 mumole in patients with PHP type I and 23.6 +/- 5.8 mumole in 15 normal subjects. Ratios of 1 hour urinary cAMP excretion were 97 +/- 10 in 27 patients with IHP, 3.6 +/- 0.5 in 21 patients with PHP type I and 54 +/- 14 in 15 normal subjects. Positive phosphaturic and negative urinary cAMP response was encountered in 3 out of 21 patients with PHP type I in response to hPTH-(1-34). This exaggerated phosphaturic response should be considered as due to the influence of treatment with Ca or vitamin D derivatives.
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PMID:[Urinary phosphate and cyclic adenosine monophosphate response to intravenous administration of synthetic human parathyroid hormone-(1-34) in idiopathic hypoparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism and normal subjects]. 609 Feb 36


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