[ABC of practice management. U--taking over a dental practice (1)].
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Biomedical subjects
Publications and source records attributed to J Pietrek.
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Plasma 25-OH-D levels of normotensive and hypertensive subjects living in a highly industrial and in a nonindustrial area, were estimated. Significantly higher values were found in normotensive subjects than in hypertensive patients. Severity of arterial hypertension was not related to plasma 25-OH-D. Both groups of subjects (normotensive and hypertensive) living in the industrial area with high air pollution had lower 25-OH-D concentrations than those living in the nonindustrial region. Data presented in this paper suggest that antihypertensive treatment by pharmacologic agents exerts a depressive effect on plasma 25-OH-D level.
The present study was aimed at answering the following two questions: (1) What is the effect of high dose vitamin D treatment on the serum level of 25-hydroxyvitamin D (25-OH-D) in patients with chronic renal failure (CRF)? (2) Is there any effect of urinary protein loss on the serum 25-OH-D levels during treatment with pharmacological doses of vitamin D? 42 patients with CRF were studied. They were treated conservatively by a low protein diet and received 15 mg of vitamin D2 once a week. Long-term administration of vitamin D caused a significant (5- to 7-fold) increase of plasma 25-OH-D level irrespective of the degree of proteinuria. This increase was noted only during the first 5 months of vitamin D2 treatment. Surprisingly only in some patients moderate hypercalcemia (> 2.75 mmol/l) was found. From the results obtained it is concluded that (1) patients with CRF differ from normal subjects in handling of high doses of vitamin D and (2) high dosage treatment with vitamin D may prevent hypocalcemia in patients with CRF in spite of high proteinuria.
The concentration of 25-hydroxyvitamin D was measured in serum of 90 healthy and 123 sick infants. The mean concentration of 25-OH-D in the group of healthy infants given intermittent prophylactic doses of vitamin D3 was 44.0 microgram/l and was nearly three times higher than the average concentration in healthy adults not given any vitamin D substitution. In the 123 clinically treated infants the average 25-OH-D concentration was 86.2 microgram/l, and 59.4% of infants had values over 40 microgram/l. In the subgroup of infants admitted to the hospital because of diarrhea, lower values were found than the average ones of clinically-treated infants. Two children with clinical rickets had very low 25-OH-D concentrations. The 25-OH-D half life in serum of infants varied from 19 to 27 days and single dose--300,000 IU (7.5 mg) of vitamin D3 was found to assure a sufficient 25-OH-D concentration in serum for as many as 190 days. It is concluded that high intermittent oral doses of vitamin D3 give an effective protection against rickets but at the cost of several times higher 25-OH-D concentration in serum and at the risk of hypervitaminosis D in some healthy infants.
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In 40 renal transplant patients the serum concentration of parathyroid hormone, 25-hydroxycholecalciferol, calcium and inorganic phosphate were estimated. The results of these biochemical studies were compared to X-ray soft tissue and bone pathologic findings. The serum immunoreactive parathyroid hormone (iPTH) was normal in 37 patients and increased in 3 cases. 19 (47.5%) renal transplant recipients showed decreased serum 25-hydroxycholecalciferol levels. In 23 out of 40 patients (57.5%) serum phosphate was lower than 3.0 mg/100 ml. X-ray soft tissue changes were observed in 28 (70%) and bone changes in 18 (45%) patients; both frequencies were higher when compared to occurrence during regular dialysis treatment. Features of hyperparathyroid osteopathy were frequently observed in renal transplant recipients. Femoral head necroses were predominant in men, whereas osteomalacia with Looser's zones were found mainly in women. The pathogenesis of X-ray bone changes in patients with renal transplants seems to be multifactorial and related to the duration of secondary hyperparathyroidism before renal transplantation as well as to phosphate depletion and 25-hydroxycholecalciferol deficiency.
Skeletal radiological changes were analyzed in 22 patients treated by chronic haemodialysis. Furthermore, the serum parathormone and 25-hydroxycholecalciferol concentrations were determined. X-ray evidence of renal osteopathy was found in 13 patients (59%). Extraskeletal calcification, subperiostal erosions and cystoids were the predominant lesions. Serum iPTH concentrations were increased in 21 out of 22 haemodialyzed patients. The serum 25-hydroxycholecalciferol concentration was normal. The results of this study seem to indicate that other factors apart from secondary hyperparathyroidism have a share in the development of renal osteopathy in patients on chronic haemodialysis.
Six patients with chronic renal failure on regular dialysis treatment were given low doses (0.5--1.0 microgram/day) of 1alpha-hydroxyvitamin D3, monitoring the serum calcium, inorganic phosphate, immunoreactive parathyroid hormone concentration (IPTH) and alkaline phosphatase activity. The serum calcium rose in all patients after 7 days' treatment, in some subjects to hypercalcemic range; this effect persisted 6--14 days after withdrawal of 1alpha-hydroxyvitamin D3. The elevated serum IPTH rose in the first days of treatment, but later decreased to normal values. It is suggested that active vitamin D metabolites are necessary for normal response of parathyroid glands to variation in serum calcium. Low-dose 1alpha-hydroxyvitamin D3 treatment appears to be a promising method of correcting hypocalcemia and secondary hyperparathyroidism in chronic renal failure. Careful control of serum calcium is necessary, as hypercalcemia may occur even after minute doses of 1alpha-hydroxyvitamin D3.
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Asian families living in Glasgow were studied between December, 1973, and June, 1974. One group of families served as a control; their mean serum-25-hydroxy-vitamin-D (25-hydroxy-cholecalciferol and 25-hydroxyergocalciferol) remained low, being 5-1 +/- 0-8 (S.E.M.) ng/ml at the end of the study. A second group was given 3000 units of vitamin D2 in a capsule weekly; this raised the mean concentration of 25-hydroxy-vitamin-D to 18-1 +/- 2-9 ng/ml. The variable effectiveness of this supplement was attributable to some subjects not taking the capsules regularly. The third group of families was provided with chupatty flour fortified with vitamin D(6000 units per kg). This increased mean serum-25-hydroxy-vitamin-D very uniformly to a mean value of 19-5 +/- 1-2 ng/ml. It is concluded that vitamin-D deficiency in Asian immigrants could be substantially reduced by fortification of chupatty flour with vitamin D.