Assessment of Crohn's disease activity and alpha 1-antitrypsin in faeces.
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Adolescent↗
Biomedical subjects
H Schmidt-Gayk
Publications and source records attributed to H Schmidt-Gayk.
Subacute effects of thiazide administration on renal hemodynamics and calcium metabolism.
To elucidate the renal effects of thiazides as a function of sodium intake, 8 healthy volunteers without renal disease were studied at baseline and 1 day as well as 4 days after the administration of 100 mg hydrochlorothiazide/day. The subjects were compared on two different dietary sodium intakes (120 mmol/day and 220 mmol/day). Measurements comprised inulin clearance (Cin) and paraaminohippurate clearance (Cpah) by infusion clearance technique, total and ionised calcium, immunoreactive parathyroid hormone (1.84 iPTH), 1.25 (OH)2 vitamin D3, and indices of hemoconcentration. Acute administration of hydrochlorothiazide (HCTZ) caused no change in Cin (before 111 +/- 3 ml/min 1.73 m2; 24 h after, 107 +/- 2 ml/min 1.73 m2) or Cpah (before, 579 +/- 9 ml/min 1.73 m2; after, 584 +/- 12 ml/min 1.73 m2), while a significant (P less than 0.01) decrease was noted on the 4th day after 100 mg HCTZ/day and normal sodium intake. No significant change of creatinine clearance (Ccr) was seen with either manouever. Renal hemodynamic changes after HCTZ administration were marginal when hemoconcentration was prevented by a high salt intake. Acute administration (1 h) of HCTZ caused suppression of 1.84 iPTH (before, 2.3 +/- 0.5 pmol/l; after, 1.9 +/- 0.2 pmol/l; P less than 0.01), but after 4 days a lower ionised calcium (baseline, 1.25 +/- 0.01 mmol/l; day 5, 1.20 +/- 0.02 mmol/l; P less than 0.01) was noticed in parallel with hemoconcentration, metabolic alkalosis, and reduced 1.25 (OH)2 vitamin D3 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Disturbed calcium metabolism in subjects with elevated diastolic blood pressure.
Essential hypertension has been associated with disturbed calcium metabolism, but the available data are controversial. We measured parameters of calcium metabolism in groups of untreated male subjects (n = 78) with elevated diastolic blood pressure (101 +/- 6 mmHg, mean +/- SD) and age-matched male subjects (n = 79) with low diastolic blood pressure (62 +/- 4 mmHg). The participants of the study were drawn from a random population sample. Subjects with high diastolic blood pressure had significantly higher carboxy-terminal parathyroid hormone (PTH) plasma concentrations than controls with low diastolic blood pressure (median 114 vs. 43 pmol/l, P less than 0.01). The 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations were comparable in both groups. Individuals with high diastolic blood pressure had significantly lower total serum calcium (2.41 +/- 0.10 vs. 2.47 +/- 0.10 mmol/l, mean +/- SD; P less than 0.01). PTH concentrations were correlated with diastolic pressure (r = -0.39, P less than 0.001). The data are compatible with increased parathyroid activity despite unchanged concentrations of vitamin D metabolites in human hypertension.
Adult↗
Long-term therapy with cyclosporin A does not influence serum concentrations of vitamin D metabolites in patients with multiple sclerosis.
Animal studies have shown that cyclosporin A (CyA) stimulates renal 25-hydroxyvitamin D3 [25(OH)D3]-1 alpha-hydroxylase activity; in contrast, studies in renal transplant recipients indirectly suggest that CyA reduces 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] production. To clarify the effect of CyA on vitamin D metabolite concentrations, we measured parameters of calcium metabolism in 37 CyA-treated patients (median trough whole blood levels 171-222 ng/ml) with multiple sclerosis and initially normal kidney function. The patients participated in a randomized double-blind study to assess the efficacy of CyA in multiple sclerosis. An age- and sex-matched control group (n = 39) received azathioprine (Aza). Measurements were made at the end of a 2-year treatment period. The 1,25(OH)2D3 serum concentrations were not significantly different between the two groups, although they were numerically lower in CyA-treated patients [median (range), 28.4 pg/ml (7.8-85.9) vs 41.0 pg/ml (9.2-105.1) in Aza-treated patients]. The 25(OH)D3 levels were comparable in both groups. There was no correlation between the 25(OH)D3 and 1,25(OH)2D3 concentrations. The renal function in both groups was stable in the last 6 months of the study. At the end of the study period, the endogenous creatinine clearance was significantly lower in the CyA-treated group (85 +/- 17 ml/min versus 99 +/- 22 in the Aza-treated group, P less than 0.05). The carboxyterminal parathyroid hormone (C-PTH) was within the normal range in both groups, although CyA-treated patients had significantly higher concentrations (P less than 0.01). The urinary excretion of mineral ions, cations and protein was similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Characterization of antibodies against human N-terminal parathyroid hormone by epitope mapping.
Two polyclonal antisera from goat and mouse and two monoclonal antibodies against human parathyroid hormone (1-34) were characterised by epitope mapping. Hexapeptides were synthesized on polystyrene pins, the sequences of which overlapped and represented the entire sequence of hPTH(1-34). Binding of antibodies to these hexapeptides was determined and antigenic determinants thus characterized. At least one predominant binding sequence was detected in the region of hPTH(7-14).
Amino Acid Sequence↗
Chromogranin A as tumor marker in medullary thyroid carcinoma.
We measured plasma levels of chromogranin A (CgA) and calcitonin (CT) in 61 patients with surgically confirmed medullary thyroid carcinoma (MTC). CT was elevated in 46 patients, whereas CgA was elevated in 14 patients. Plasma levels of CgA and CT were moderately correlated (r = 0.87), but CgA became elevated in most patients only in advanced disease. Patients with high plasma CT values (greater than 10 micrograms/L) also had elevated CgA in 83% of cases. An elevated plasma CgA level despite normal CT levels was found in only 1 patient. In 8 MTC patients with moderately elevated basal CT levels, pentagastrin as a secretagogue usually was not able to release detectable amounts of CgA from MTC tissue. In 2 MTC patients, i.v. catheter sampling gave sharp gradients for CT concentrations (greater than 2.7-fold peak to peripheral ratios) and, therefore, precise MTC tissue localization, whereas no gradients were demonstrable for CgA (less than 1.2-fold). One patient with MTC and elevated CgA reached normal CgA plasma levels within 8 days after thyroidectomy. In metastatic tissue from 8 patients with MTC, CgA and CT were detectable immunohistologically in all cases, but plasma CgA was elevated only in 2 and CT in 7 of them. Plasma CgA levels in patients with MTC usually became elevated only in advanced disease and were not able to detect early disease stages, were correlated with CT levels, were not useful in stimulation tests or venous localization studies, and probably resulted from the release from MTC tissue as the major tissue source, as shown in the sporadic cases.
Biomarkers, Tumor↗
Circadian rhythm and pulsatility of parathyroid hormone secretion in man.
OBJECTIVE: We wished to investigate the circadian rhythm and pulsatility of parathyroid hormone (PTH) secretion in man, as conflicting results have been published. DESIGN AND PATIENTS: To investigate the circadian rhythm during daytime, we sampled (a) peripheral blood at hourly intervals in 12 healthy young men from 0900 h until 1700 h. For observation of pulsatility, we sampled (b) peripheral blood at 1-minute intervals for 1 hour in three healthy men and three healthy women (mean 27.7 years, range 21-56 years) and (c) at 1-minute intervals for 30 minutes in 21 patients with surgically confirmed primary hyperparathyroidism (pHPT). MEASUREMENTS: The serum levels of intact PTH were measured by two-site immunoradiometric assay and special care was taken to reduce intra-assay variability, especially at the normal PTH concentration. In series (a), ionized calcium, total calcium and phosphate were also determined. RESULTS: A circadian rhythm during daytime was found for intact PTH in healthy men and women with a nadir at 0930 h and a peak in the afternoon. Ionized calcium and total calcium (protein-adjusted) decreased and phosphate increased in the afternoon. These changes were all statistically significant (P < 0.02). Pulsatility of PTH: Statistical cluster analysis of the data showed no pulsatility either in healthy persons or in patients with primary hyperparathyroidism. In two healthy women and one healthy man slight changes of longer duration were discovered, but no complete pulses. In five patients with primary hyperparathyroidism, larger differences between the highest and lowest concentrations of intact PTH were found, but no complete pulses. CONCLUSIONS: Our data show a significant circadian rhythm during daytime of intact PTH and only minor changes from minute to minute. The alterations in PTH-levels occurred at longer time intervals in healthy persons. In some patients with primary hyperparathyroidism, decreases of PTH-levels were found. The circadian rhythm of PTH may be due to slight changes in calcium or phosphate concentration.
Adult↗
Circulating levels of midregional parathyroid hormone-related protein in hypercalcaemia of malignancy.
OBJECTIVE: We have developed and evaluated a sensitive radioimmunoassay directed against the midregional part of parathyroid hormone-related protein (PTHrP), which is involved in the syndrome of humoral hypercalcaemia of malignancy. PATIENTS: Midregional PTHrP levels were studied in 41 consecutive inpatients with malignancy and hypercalcaemia, 32 normocalcaemic patients with malignancy, 21 patients with primary hyperparathyroidism, 34 patients with renal failure, and 87 normals. MEASUREMENTS: The assay used an antiserum against the midregional amino acid residues 53-84 of PTHrP and PTHrP(1-86) as label and standard. Midregional PTHrP was stable in serum and plasma and could be measured directly without sample extraction. RESULTS: Normal plasma concentrations ranged from undetectable (< 5 pmol/l) to 21 pmol/l. In renal failure, PTHrP was positively correlated with serum creatinine, but PTHrP elevations of up to 30 pmol/l were found only in severe renal dysfunction with creatinine > 850 mumol/l. In hypercalcaemia caused by solid tumours, midregional PTHrP was elevated in 81% (22 of 27) of patients, ranging from undetectable to 203 pmol/l (median: 40 pmol/l). In these patients serum calcium correlated positively with PTHrP (P < 0.01). Mean PTHrP levels were indistinguishable in subgroups with and without metastatic skeletal disease. The mechanism of hypercalcaemia in 14 patients with haematological malignancy was apparently different, since all but one had normal or only marginally elevated PTHrP levels. In 21 patients with primary hyperparathyroidism midregional PTHrP was normal in 20. The assay was therefore especially useful in distinguishing the latter condition from humoral hypercalcaemia of malignancy as the second major cause of hypercalcaemia. PTHrP was normal in all 32 patients with normocalcaemic malignancy. CONCLUSION: This radioimmunoassay of midregional PTHrP provides high diagnostic sensitivity in the identification of humoral hypercalcaemia of malignancy caused by solid tumours. The assay should therefore be useful in the differential diagnosis of hypercalcaemia.
Diagnosis, Differential↗
Calcium regulating hormones after oral and intravenous calcium administration.
The aim of this study was to determine the changes in serum calcium concentration and in the concentrations of calcium regulating hormones after a single oral or intravenous calcium administration. Standard dosages of calcium, as used in routine patient care, were employed. Intact parathyrin, calcitonin, calcitriol, calcidiol, total calcium, ionized calcium, total protein and phosphate were determined in 12 healthy young men before and up to 8 h after oral and intravenous administration of calcium. During a fortnight there were four study days with 1000 mg calcium orally (p.o.), 2000 mg orally, 180 mg calcium intravenous (i.v.) and a control day without calcium. During the study the men were on a low calcium diet. We observed a sharp increase in the calcium concentration after i.v. administration (15 min: total Ca: + 0.48 +/- 0.32 mmol/l; ionized Ca: + 0.25 +/- 0.15 mmol/l; p < 0.01). The concentration increase after the two oral loads was nearly identical. The maximal concentration of total calcium was reached after 120 min (1000 mg: + 0.1 +/- 0.04 mmol/l; p < 0.001; 2000 mg: + 0.12 +/- 0.04 mmol/l; p < 0.001). There was a significant increase in urinary calcium after all modes of calcium administration. Calcitonin increased significantly only after i.v. injection of calcium (+ 9.2 +/- 3.4 pmol/l; p < 0.001) while parathyrin decreased significantly after all modes of calcium administration (i.v.: 15 min: -1.9 +/- 0.88 pmol/l; p < 0.01; 1000 mg: 90 min: -0.78 +/- 0.75 pmol/l; p < 0.001; 2000 mg: 90 min: -1.02 +/- 0.57 pmol/l; p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
Frusemide therapy and intact parathyroid hormone plasma concentrations in chronic renal insufficiency.
It has been suggested that frusemide affects plasma parathyroid hormone (PTH) concentrations. To further investigate this issue we analysed plasma intact PTH in 77 patients with chronic renal failure (CCr 8.0-89.8 ml/min per 1.73 m2) as a function of frusemide therapy. The rate of increase of plasma PTH observed with progression of renal failure was faster in patients who received frusemide as compared to patients who did not receive the drug. The slope of the regression line of PTH on CCr was steeper (P less than 0.02) for patients with frusemide (n = 40, slope -0.34) than without frusemide (n = 37, slope -0.20). This effect was specific for frusemide therapy since therapy with other antihypertensive drugs (including thiazides and beta-blockers) was not correlated with PTH plasma concentrations. Frusemide therapy was also associated with a significantly greater urinary calcium excretion in uraemic patients but did not influence other parameters of calcium metabolism. To clarify mechanisms involved in the effect of frusemide on plasma PTH values, seven normal subjects were studied for 24 h before and for 24 h after oral administration of 80 mg frusemide. The main findings were: (1) Median PTH values were higher than on a control day (P less than 0.05) 3 h after frusemide (3.9 pmol/l vs 1.8) and 6 h after frusemide (4.0 vs 2.6); (2) ionised plasma calcium did not change significantly, whereas mean calcium/creatinine ratio increased from 0.20 to 0.46 after frusemide treatment through an increase in absolute calcium excretion; (3) plasma 1 alpha,25-dihydroxyvitamin D3, catecholamines, and magnesium concentrations did not change significantly after frusemide.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Immunoluminometric assay of chromogranin A in serum with commercially available reagents.
Chromogranin A (Cg A) is a useful marker of neuroendocrine neoplasia in humans. Here we describe an immunoluminometric assay (ILMA) for measuring Cg A in serum, with use of a new tube as a solid phase. The new tube has a large surface area and is coated with a polyclonal antibody. Optimized coating conditions provide a high IgG adsorption to the polystyrene wall. Serum is added to the coated tube and incubated for 2 h or overnight. After washing the tubes, acridinium ester-labeled monoclonal antibody against Cg A is added and incubation is continued for 2 h. The tubes are washed again and the bound luminescence is measured. The assay is very sensitive (detection limit 1 microgram/L, if 25 microL of serum is used), is specific for human Cg A, and offers a wide dynamic range (1-1000 micrograms/L). The range in healthy humans is 10-53 micrograms/L (median 30 micrograms/L). The correlation of serum Cg A to creatinine and parathyroid hormone is described. We also report the influence of intravenous calcium injection on Cg A concentrations in serum.
Antibodies, Monoclonal↗
Validity of intact plasma parathyrin measurements in chronic renal failure as determined by two-site immunoradiometric assays with N- or C-terminal capture antibodies.
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Humans↗
Influence of long-term erythropoietin therapy on endocrine abnormalities in haemodialyzed patients.
Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in haemodialyzed patients. Two groups of haemodialyzed patients, each of which comprised 17 subjects, were examined. The first one treated by EPO (EPO group) while the second one did not receive this hormone (NO-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9 and 12 months of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex and age-matched healthy subjects. After EPO therapy an increase of the haematocrit value from 21.8 +/- 0.9% to 32.6 +/- 0.9% was observed which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the NO-EPO group a significant although less marked rise of the haematocrit value (21.4 +/- 0.4% to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose and alkaline phosphatase plasma levels as well as plasma concentrations of calcium related hormones (PTH, calcitonin, 1.25(OH)2D3) and vasopressin (AVP). EPO treatment induced a significant decline of somatotropin (HGH), prolactin (PRO), follitropin (FSH), lutropin (LH), ACTH, cortisol, plasma renin activity, aldosterone, insulin (IRI), glucagon (IR-G), pancreatic polypeptide (PP) and gastrin plasma levels and an increase of plasma estradiol, testosterone and atrial natriuretic peptide (ANP). These EPO induced endocrine alterations were restricted mostly to the first 6 months of EPO administration.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Cortex Hormones↗
Hypomagnesaemia-induced hypocalcaemia: concentrations of parathyroid hormone, prolactin and 1,25-dihydroxyvitamin D during magnesium replenishment.
Three patients with hypomagnesaemia-induced hypocalcaemia were investigated during the phase of magnesium replenishment. Before treatment, serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were at the lower limit of normal. In spite of a rapid rise of parathyroid hormone (PTH) after intravenous administration of magnesium, a reactive increase in 1,25-dihydroxyvitamin D in serum was absent or delayed. The increase of serum calcium into the normal range occurred before any consistent change in the concentrations of this vitamin D metabolite. The rise of serum prolactin in response to the increase in PTH was blunted or absent, and is a further example of a transient PTH resistance during the phase of magnesium replenishment.
Alcoholism↗
Calcium metabolism in early chronic renal failure: implications for the pathogenesis of hyperparathyroidism.
Studies in the past showed elevated immunoreactive parathyroid hormone (PTH) serum values in early renal failure, but the assays used in these studies could not discriminate between bioinactive fragments of the PTH peptide and biologically active hormone. The availability of a sensitive PTH assay, which quantitates intact hormone, now allows the analysis of biologically active PTH in renal failure. To characterise more precisely the point of onset of hyperparathyroidism in the course of chronic renal failure and its relation to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], we measured plasma intact PTH and vitamin D metabolite serum values in 63 non-nephrotic uraemic patients (male n = 35, female n = 28, age 31-78 years) with incipient (GFR 60-90 ml/min per 1.73 m3, n = 19) mild (GFR 40-60, n = 22) and moderate (GFR 20-40, n = 22) renal failure, and in 22 age-matched healthy control subjects. Intact PTH concentrations were negatively correlated with GFR (r = -0.57, P less than 0.001). Median plasma intact PTH values (normal range 1.2-6 pmol/l) were 5.6 (range 2.2-13.0) in incipient, 8.1 (2.9-24.0) in mild, and 13.0 (5.4-59.0) in moderate renal failure. Intact PTH values in incipient renal failure were significantly greater than in 22 age-matched control subjects (P less than 0.01). The decline of GFR was paralleled by a progressive decrease in 1,25(OH)2D3 serum values (r = 0.44, P = 0.001). Median values of the hormone (normal range 35-90 pg/ml) were 32 (range 20-66) in incipient (P less than 0.01 vs. age-matched control subjects), 34 (22-74) in mild, and 26 (17-39) in moderate renal failure. In all three groups, mean serum phosphate and total calcium concentrations (corrected for serum protein) were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effect of vitamin C on endogenous formation of N-nitrosamines in ureterosigmoidostomy patients.
The bacterially catalyzed formation of nitrosamines in the rectosigmoid is a favorite theroy for the increased risk of colon carcinomas following ureterosigmoidostomy. The urine/feces mixtures of 20 ureterosigmoidostomy patients were analyzed for nitrate, nitrite, volatile and nonvolatile nitrosamines prior to, and after, oral administration of vitamin C, a known nitrosation inhibitor. Following a 4-week period of daily ingestion of 2 g vitamin C (1 g in children) there was a slight, but not significant, decrease of volatile and nonvolatile nitrosamines and nitrite, as well as a nonsignificant increase in nitrate in the urine/feces of these patients. No correlation between the vitamin C concentration in serum or urine/feces mixture and the nitrosamine excretion was observed. These results suggest that the administration of vitamin C is not a suitable method for prophylaxis of endogenous nitrosation in ureterosigmoidostomy patients. Clinical and experimental findings implicate that factors other than nitrosamines play an important role in colon carcinogenesis of patients with ureterosigmoidostomies or other forms of urinary diversions using the small or large bowel.
Ascorbic Acid↗
Changes of vitamin D3 serum concentrations at the onset of immune-mediated type 1 (insulin-dependent) diabetes mellitus.
Several hormones such as 1,25-dihydroxy-vitamin D3 (1,25-(OH)2D3), alpha-MSH, or ACTH have been found to interact extensively with the immune system. In view of the immune-mediated nature of Type 1 (insulin-dependent) diabetes mellitus, 49 recently diagnosed diabetic patients were investigated in terms of serum 1,25-(OH)2D3-levels, 25-hydroxyvitamin D3(25-(OH)D3), alpha-MSH and ACTH, and compared with 42 healthy controls. A marked decrease of 1,25-(OH)2D3-levels was found at onset of Type 1 (insulin-dependent) diabetes compared to normal controls (39 +/- 2 vs 55 +/- 4 pg/ml, p less than 0.01). Grouping patients according to season (winter or summer) of diabetes onset and blood sampling, it was demonstrated that the decrease of 1,25-(OH)2D3 was primarily present during summer and due to a loss of the seasonal rhythm of this hormone observed in healthy controls (summer: patients vs controls 41 +/- 2 vs 63 +/- 4 pg/ml, p less than 0.001; winter: 37 +/- 3 vs 33 +/- 3 pg/ml, n.s.). Serum concentrations of 25-(OH)D3 were closely correlated with those of 1,25-(OH)2D3, both in controls (r = 0.55, p less than 0.002) and diabetic patients (r = 0.41, p less than 0.05), yielding a similar loss of seasonal variation also of this vitamin D3 metabolite in Type 1 (insulin-dependent) diabetic patients. No difference was found in the mean and median values of alpha-MSH and ACTH between IDDM patients and controls, although patients exhibited much higher variation of alpha-MSH levels than did controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenocorticotropic Hormone↗
Do limited changes in phosphate intake modulate 1,25(OH)2D3 levels in early renal failure?
A high dietary phosphate load relative to GFR is thought to explain, at least in part, diminished renal 1-alpha hydroxylase activity in early renal failure (RF). To assess the role of dietary phosphate/GFR ratio in more detail, we examined the response of 1,25(OH)2D3 concentration to a controlled isolated reduction of dietary phosphate intake for up to 10 days with no change of Ca, Na and energy intake. We studied 7 healthy controls (2 male, 5 female, median age 45 years) and 6 non-nephrotic patients with early renal failure (RF) (3 males, 3 females, median age 55 years; median Cin 60.5ml/min/1.73 m2; 41-69). During an initial 3-day period of controlled diet with usual phosphate intake no difference of UVPi (median 27.6 mmol/day, 18.9-43.8) was found between controls and RF. A diet with 15 mmol Pi/day (confirmed by duplicate meal analysis) significantly reduced median UVPi (controls: 27.7 to 11.9 mmol/d; RF 27.4 to 14.1 mmol/d) with no change of median UVCa. Median day to day variation of 1,25(OH)2D3 levels (by RIA) in controls was 15.4%. Lowering dietary phosphate intake did not significantly change median 1,25(OH)2D3 levels in controls (45.7 vs. 38.3 pg/ml) and patients with RF, respectively (23.5 vs. 19.1 pg/ml). No changes of intact iPTH values were found. The experiment had a 68% power to detect a 15% change and a 99% power to detect a 30% change at a significance level of p less than 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)
Calcitriol↗