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Biomedical subjects

M S Christensen

Publications and source records attributed to M S Christensen.

At least 19 recordsLinked to original sources
PubMed1979

Bone loss in diabetes: effects of metabolic state.

The significance of different risk factors for the development of bone loss in diabetes mellitus was evaluated in a cross sectional study of 215 insulin treated diabetic outpatients. Bone mineral content in the forearms was measured by photon absorptiometry and the metabolic status was evaluated by three indices: residual B-cell function, insulin dosage and fasting blood glucose. The mean bone mineral content was reduced to 90.2% of sex- and age-matched normal mean values (P less than 0.001). Stratification of the patients showed that bone mineral content was 99.3% of that found in sex- and age matched normal subjects in the group with residual B-cell function, low insulin dosage and low fasting blood glucose; it was only 79.3% of normal in the group with no detectable insulin secretion, high insulin dosage and more severe hyperglycaemia. Thus, residual insulin secretion and the quality of metabolic control are major factors in determining bone mineral content in insulin treated diabetic patients.

Blood Glucose↗
PubMed1979

Impairment of vitamin D and bone metabolism in patients with bypass operation for obesity.

Thirty-four patients were studied 2--6 years after jejunoileal bypass for morbid obesity. The serum concentration of 25-hydroxyvitamin D (25-OHD) were reduced and related to the frequency fo stools and to the weight reduction. Fifteen patients were not able to normalize serum 25-OHD following a long-term regular vitamin D intake. The serum immunoreactive parathyroid hormone concentration (iPTH) and the alkaline phosphatase levels were elevated in this group, indicating a secondary hyperparathyroidism. The mean bone mineral content of the forearm was reduced 3--6 years after the operation, most severely in those with elevated serum iPTH. The desired weight reduction by jejunoileal shunt was obtained at the expense of a severely disturbed vitamin D metabolism. We suggest, that all patients with an intestinal bypass for obesity should receive regular vitamin D supplement, and serum 25-OHD should be measured in order to monitor the effect of therapy.

Adult↗
PubMed1979

Fractional intestinal calcium absorption in epileptics on anticonvulsant therapy. Short-term effect of 1,25-dihydroxycholecalciferol and 25-hydroxycholecalciferol.

Fractional intestinal 47Ca calcium absorption (alpha) in 12 epileptic outpatients receiving chronic high-dose anticonvulsant therapy was reduced (p less than 0.05) compared to 12 matched normal controls. Six of the epileptics were treated orally with 0.5 microgram of 1,25-dihydroxycholecalciferol (1,25-DHCC) per day and six with 10 microgram of 25-hydroxycholecalciferol (25-HCC) per day for 10 days. The alpha was determined before and after treatment and compared with the effect of 0.5 microgram of 1,25-DHCC per day given for 10 days to 6 controls. An increase of the same order in alpha was found in all groups (p less than 0.05). No changes were observed in the serum levels of calcium, phosphorus, alkaline phosphatase or iPTH during treatment. Urinary calcium excretion was low in the epileptic patients and rose during treatment. The investigation demonstrates that the sensitivity of the intestine to 1,25-DHCC is normal in epileptic patients on anticonvulsant therapy and that 1,25-DHCC and 25-HCC in the given doses had an equal effect on the reduced intestinal calcium absorption.

Administration, Oral↗
PubMed1979

Bone mineral loss in insulin-treated diabetes mellitus: studies on pathogenesis.

To elucidate pathogenetic factors of bone mineral loss in diabetes mellitus, bone mineral content (BMC), glucose and calcium homeostasis were evaluated in a cross-sectionsl study of 215 insulin-treated diabetics. BMC declined 10% during the first 5 years of diabetes. This coincided with cessation of insulin secretion, deterioration of metabolic control and raising urinary calcium excretion rates of calcium and phosphorus. BMC was inversely correlated to fasting blood glucose (P less than 0.02), to glycosuria (P less than 0.02) and to insulin requirement (P less than 0.002), and positively to the glucagon-stimulated serum C-peptide levels (P less than 0.005). Urinary excretion rates of calcium and phosphorus correlated positively with the degree of hyperglycaemia (P less than 0.001) and glycosuria (P less than 0.001). The skeletal calcium loss corresponded to the excess of urinary excretion during the phase of BMC reduction. There was no evidence of secondary hyperparathyroidism. The relationship between bone loss and disturbed glucose homeostasis indicates that diabetic bone loss is secondary to the metabolic abnormalities, possibly acting directly on bone.

Adolescent↗
PubMed1978

Effects of a single dose of fluoride on calcium metabolism.

Fluoride 27 mg was given perorally to 14 subjects. It was found that the serum fluoride concentration increased followed by a decrease to normal levels during 24 h. Serum concentrations of calcium and phosphate decreased initially whereas those of serum immunoreactive parathyroid hormone increased. After 24 h the measured quantities were within normal limits. The results are discussed with reference to mineralization of hard tissues and to fluoride treatment of osteoporotic patients.

Adult↗
PubMed1978

Deterioration of renal function during treatment of chronic renal failure with 1,25-dihydroxycholecalciferol.

A controlled study of the effects of the potent vitamin-D metabolite, 1, 25-dihydroxycholecalciferol (1,25[OH]2D3), and vitamin D3 was done in 18 non-dialysed patients with chronic renal failure (C.R.F.). Patients with a creatinine clearance below 35 ml/min and mild renal osteodystrophy were selected. After 6 months' observation of the spontaneous course the patients were randomly allocated to 6 months' oral treatment with either 1, 25 (OH)2D3 or vitamin D3 in initial daily doses of 1microgram and 4000 I.U., respectively, combined with 0.5 g calcium. 1,25(OH)2D3 quickly corrected hypocalcaemia, reduced serum-alkaline-phosphatases and serum-immunoreactive-parathyroid-hormone, and more than doubled the urinary excretion rate of calcium. D3 had similar, but less pronounced effects. 7 out of 8 patients on 1,25(OH)2D3, developed hypercalcaemia which necessitated a reduction in dosage. None of the patients on D3 treatment developed hypercalcaemia. The percentage fall in creatinine clearance was greater during treatment than before treatment in all patients on 1, 25 (OH)2D3 (P less than 0.01) and in 7 of 9 patients on vitamin D3 treatment (though the group change here was not significant). Deterioration of renal function is a major limitation of the clinical use of 1, 25(OH)2D3 and D3 in non-dialysed patients with C.R.F. In fact, the decrased formation of 1, 25(OH)2D3 seen in C.R.F. might protect renal function at the expense of abnormalities in mineral metabolism.

Administration, Oral↗
PubMed1978

A method for measuring desquamation and its use for assessing the effects of some common exfoliants.

Desquamation has been measured in the past by a counting chamber technique after corneocytes are removed from the skin surface and disaggregated in a dilute surfactant solution. However, we have found that complete corneocyte disaggregation is not always possible when these aggregates are recovered from sites where patent peeling is induced. Corneocyte counting in such instances is difficult or impossible. We have devised a method of measuring desquamation wherein the desquamating cells are determined as the total alkali-soluble protein after they are removed from the skin surface with an inert, self-hardening gel. Highly reproducible desquamation rates are obtained, characteristic of the individual subject. Using some common exfoliants, we show that pharmacologic response, observed as an increase in desquamation rate, is also an individual characteristic.

Adult↗
PubMed1978

Effect of antithyroid treatment on calcium-phosphorus metabolism in hyperthyroidism. I: Chemical quantities in serum and urine.

The effect of antithyroid treatment on the disturbed calcium-phosphorus metabolism in hyperthyroidism was studied in 16 patients. Elevated serum concentrations and urinary excretions of calcium and phosphorus were almost normalized 4 weeks after the start of medical treatment. Serum immunoreactive parathyroid hormone was decreased in the hyperthyroid state and became normal after medical treatment. Serum alkaline phosphatase levels were elevated throughout the study with an increase to a maximum peak after 8 weeks of antithyroid treatment. Urinary hydroxyproline excretion was initially markedly increased and fell rapidly during therapy. The observed changes suggest decreased bone resorption and increased bone formation with deposition of bone mineral after antithyroid treatment. Alterations in the serum albumin concentration during the investigation period influenced the total serum calcium concentration. Using albumin adjusted serum calcium values no hypocalcaemia was found during medical treatment or after a subsequent subtotal thyroidectomy.

Adult↗
PubMed1977

Minor influence of parathyroid hormone on fractional tubular reabsorption of phosphate in chronic renal failure.

In untreated patients with chronic renal failure and glomerular filtration rates (GFR) between 10 and 25 ml/min the decrease in fractional tubular reabsorption of phosphate was correlated to the degree of secondary hyperparathyroidism. This correlation was not found in patients with GFR below 10 ml/min. During treatment with 1alpha-hydroxycholecalciferol for 11 weeks: a) serum parathyroid hormone concentration decreased in all patients on average 60%, and was normal in 5 patients after treatment b) fractional tubular reabsorption of phosphate decreased significantly (on average 0.21) c) glomerular filtration rate decreased significantly (on average 27.5%). Since the reduction (or normalization) of serum parathyroid hormone concentration did not increase the fractional tubular reabsorption of phosphate, other (GFR-related) factors than parathyroid hormone play the major role for renal handling of phosphate in chronic renal failure when GFR is below 25 ml/min.

Biological Transport↗
PubMed1977

Inhibition of parathyroid hormone secretion by isoproterenol.

Intravenous infusion of the beta-adrenergic agonist isoproterenol produced a fall in the serum concentration of parathyroid hormone. It also produced a pronounced fall in the serum phosphate concentration, and significant increases in blood glucose and serum insulin concentration and in pulse rate. The fall in serum parathyroid hormone was abolished by beta-adrenergic blockage with propranolol. Oral glucose loads produced a pronounced fall in serum phosphate concentration, comparable to the fall after isoproterenol infusion, but no significant changes in serum parathyroid hormone. It is concluded that the fall in serum parathyroid hormone after isoproterenol is due to a beta-adrenergic effect. It is unknown, if isoproterenol acts directly on the parathyroid hormone secreting cell, or the fall in serum parathyroid hormone is secondary to the effect of isoproterenol on other endocrine glands or the cardiovascular system.

Adult↗
PubMed1977

Bone disease, hypophosphatemia and hyperparathyroidism after renal transplantation.

UNLABELLED: Long-term survivors after renal transplantation (RT) show: 1) decreased s-phosphorus 2) increased s-PTH 3) no correlation between s-PTH and s-phosphorus 4) increased amount of non-mineralized bone (osteomalacia), inversely correlated to s-phosphorus 5) decreased amount of trabecular bone (osteopenia) in RT patients with aseptic necorsis of bone. CONCLUSION: aseptic necrosis of bone after RT is mainly due to osteoid-induced osteopenia, perhaps aggravated by hypophosphatemic osteomalacia.

Adolescent↗