PubMed Health⌕ Search

Biomedical subjects

A Bergans

Publications and source records attributed to A Bergans.

17 recordsLinked to original sources
PubMed1989

Correction of low circulating levels of 1,25-dihydroxyvitamin D by 25-hydroxyvitamin D during reversal of hypomagnesaemia.

The effect of 25-hydroxyvitamin D (25OHD), given orally during the reversal of hypomagnesaemia, was studied in five patients with hypomagnesaemic hypocalcaemia and low serum levels of 25OHD and 1,25-dihydroxyvitamin D (1,25(OH)2D). The results were compared to those obtained in five other patients with similar initial levels of magnesium, calcium, 25OHD and 1,25(OH)2D who did not receive 25OHD. Serum levels of 1,25(OH)2D in the ten hypomagnesaemic patients were lower than in ten control subjects with low serum levels of 25OHD. The reversal of hypomagnesaemia was similar in the two groups of patients and elicited a similar increase of circulating iPTH levels. The expected increase of circulating 25OHD was observed in patients supplemented with 25OHD; their circulating 1,25(OH)2D rose within 48 h to normal levels, contrasting with the delayed and poor increase of 1,25(OH)2D in patients receiving no 25OHD. The evolution of serum calcium was however identical in the two groups. Our results suggest that vitamin D deficiency was a significant factor leading to low circulating levels of 1,25(OH)2D in hypomagnesaemic hypocalcaemic patients. The biological consequences of low serum 1,25(OH)2D in these patients remain unclear, but clearly, normal levels of 1,25(OH)2D are not essential for the correction of hypomagnesaemic hypocalcaemia.

Adult↗
PubMed1988

Are tuberculous patients at a great risk from hypercalcemia?

The risk of tuberculous patients to develop hypercalcemia was investigated in 33 patients aged 19 to 80. Twenty-two of the 33 received no vitamin D supplements. Before antituberculous chemotherapy serum calcium corrected for albumin and urinary calcium levels were normal, serum 25-hydroxyvitamin D (25(OH)D) levels were low, but serum 1,25(OH)2D levels, oral calcium load test and intestinal 47Ca absorption were normal. After 17 to 34 days of chemotherapy serum calcium corrected for albumin and 1,25(OH)2D levels were lower without change in serum D-binding protein. In 11 patients 25(OH)D, 50 micrograms/day, was given orally for two months. 25(OH)D given three days before chemotherapy in five patients induced an increase of levels of 1,25(OH)2D which was greater than in 10 control patients with similar serum levels of 25(OH)D. When chemotherapy was added to 25(OH)D, the five patients showed high normal 1,25(OH)2D levels. The last six patients received 25(OH)D together with or after starting chemotherapy. None of the 33 patients developed hypercalcemia, even when supplemented with 25(OH)D for two months. It appears that hypercalcemia is uncommon in tuberculosis.

Adult↗
PubMed1985

Magnesium administration reverses the hypocalcaemia secondary to hypomagnesaemia despite low circulating levels of 25-hydroxyvitamin D and 1,25-dihydroxy vitamin D.

The effect of parenteral administration of magnesium was studied in five patients with hypomagnesaemic hypocalcaemia. The initial metabolic state was characterized by a normal level of serum immunoreactive parathyroid hormone (iPTH), and by low or undetectable serum 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D (1,25 (OH)2D). A parathyroid response was elicited by the acute intravenous injection of magnesium chloride. In contrast, 1,25(OH)2D did not change up to 24 h after the injection. Intramuscular magnesium sulphate restored serum magnesium and calcium to normal, whereas iPTH was transiently increased. 25OHD remained low and unchanged. 1,25(OH)2D rose very slowly, but the correction of hypocalcemia began before any change in 1,25(OH)2D levels could be demonstrated. Thus, the early correction of hypocalcemia mainly depended on the restoration of an adequate parathyroid function independently of the secretion of 1,25(OH)2D.

25-Hydroxyvitamin D 2↗
PubMed1979

Effect of rapid variation of renal function on plasma calcitonin and parathyroid hormone in man.

Plasma levels of immunoreactive calcitonin (iCT) and parathyroid hormone (iPTH) have been measured sequentially in 6 patients following successful renal transplantation (RT) and in 3 patients during the recovery phase of acute renal failure (ARF). iCT and iPTH returned to normal values within a few days when glomerular filtration improved; both hormones rose in cases of acute graft rejection. Unlike iPTH iCT did not follow closely the variations of creatinine, iCT even rising before creatinine in one graft rejection. These observations could possibly be explained by a dissociation between the renal metabolism of iCT and the glomerular filtration.

Acute Kidney Injury↗
PubMed1978

The use of a test for the differential diagnosis of hypercalciuria.

28 renal stone formers (18 men and 10 women) with idiopathic hypercalciuria (IH) and 27 controls have been subjected to a test proposed for the diagnosis of absorptive, resorptive and renal hypercalciurias. Fasting serum calcium concentration, urinary calcium and cyclic AMP excretion were measured after overnight fasting and an oral load of calcium. Absorptive hypercalciuria was demonstrated in 14 patients. High fasting urinary calcium first suggested resorptive or renal hypercalciurias in 5 other patients, but since fasting urinary calcium was normalized following cellulose phosphate therapy, absorptive hypercalciuria was more likely. Renal hypercalciuria was a possibility in 1 single case. Both fasting and post-load urinary calcium were normal in 7 men and 1 woman. The test did not appear as useful as expected since it was of no diagnostic value in about 30% of the cases and erroneously suggested resorptive or renal hypercalciuria in about 15% of the cases. On the other hand it indicated that absorptive IH is common and renal IH exceptional.

Adult↗
PubMed1977

Metabolism of human PTH by the kidney and the liver.

Immunoreactive PTH was measured by amino terminal and carboxyl terminal specific assays in the femoral artery, the right renal vein and the suprahepatic vein of ten hyperparathyroid patients. A marked arterio venous difference for amino terminal immunoreactivity was observed in the kidney and the liver. In contrast, the arterio venous difference for carboxyl terminal immunoreactivity was small in the kidney and not significantly in the liver. It is concluded that intact PTH and possibly amino terminal fragments of the hormone are metabolized by the kidney and the liver. Considering the fact that a carboxyl terminal specific antiserum is also capable of recognizing intact hormone, the finding of a small positive arterio venous difference for carboxyl terminal immunoreactivity does not permit us to exclude the possibility that the kidney and/or the liver are capable of generating carboxyl terminal fragments.

Adenoma↗