[Calcium pidolate and bone metabolism parameters].
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Biomedical subjects
Publications and source records attributed to H Rico.
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Because of the controversy about the loss of bone mass in premenopausal women, we decided to study the total mineral bone content (TMBC), measured by dual-photon absorptiometry (DPA), a technique with low variation coefficient and high level of discrimination, in a group of 96 premenopausal women with a age range between 20-49 years, who were selected by homogeneous criteria of habits and life stile and body mass lower than 25. In all women, the TMBC were quantify in supine with the densitometer type Norland XR-26 and its value correlated with age following the "Pearson's test"; there were not statistical significance. We concluded that women in a fertile period of life do not lose bone mass as a TMBC, which mean the importance of obtaining the bone mass peak during the childhood and adolescency.
Alcohol is considered to be an important risk factor for various bone diseases but recent studies have shown that moderate alcohol intake can be beneficial to bone structure. Alcohol decreases osteoblastic activity, leading to decreased bone formation and defective mineralization. The changes reported in calciotropic hormones, mainly vitamin D and parathyroid hormone, are observed due in part to a deficient intestinal absorption of vitamin D and an inadequate synthesis of its hepatic metabolite, although greater emphasis has been given to dietary deficiencies or lack of exposure to sun. The changes in parathyroid hormone are not consistent and since there is no greater incidence of hyperparathyroidism in alcoholic patients, it suggests that alcohol does not have a long-term effect on the parathyroid glands. Alcohol increases calcitonin secretion acutely; calcitonin is an inhibitor of bone resorption and may be the mechanism by which moderate alcohol intake protects bone structure. Alcohol increases urinary calcium, magnesium and zinc excretion. Zinc deficiency has been postulated as a cause of oesteoporisis because it causes hypogonadism. The decrease in the levels of the gonadal hormones and the increase of cortisol, observed in chronic alcoholics, may indirectly cause osteopenia and aseptic necrosis. To these actions must be added the acidosis due to alcohol and the greater tendency of the alcoholic to fall, all of which influence bone changes and increase the incidence of bone fractures.
Osteocalcin was evaluated by radioimmunoassay at the time of delivery in mothers and in the umbilical arteries of newborns in a group of pregnant drug users (eight heroin users and seven cocaine users) and compared with findings from a group of normal mothers and their newborns (N = 18). Drug users had lower osteocalcin values than did the normal women (1.3 +/- 0.7 versus 2.7 +/- 0.8 ng/mL, P less than .001); and infants of drug users had lower values than normal infants (14.1 +/- 3.8 versus 19.0 +/- 4.0 ng/mL, P less than .005). The birth weights of drug users' infants were smaller (3160 +/- 402 versus 3591 +/- 374 g, P less than .05) and there was a significant negative correlation (P less than .001) between osteocalcin and drug intake during pregnancy, but no changes in osteocalcin dependent on the type of drug used. These results suggest a toxic effect of these drugs on the osteoblast, which could account for the lower birth weights and skeletal alterations reported in the infants of drug users.
Radiogrametry was done on 100 hands by two observers using two methods: (1) caliper and (2) magnifying glass measurement. At the mid-point of the second metacarpal, the total width (D) and medullary width (d) were measured and cortical thickness (C) was calculated from the difference (D-d). Statistical analysis disclosed that the intra-observer CV is smaller for both observers using the magnifying glass than with the caliper (1.9 and 2.1% vs. 2.8 and 4.3%, respectively). The inter-observer CV is also less with the magnifying glass (4.2 and 5.7% vs. 6.2 and 6.9%, respectively). Although measurements made with each method correlate significantly, the values (mean +/- SD) obtained in isolated measurements using each method differ significantly, with C for both observers, as well as the intra-observer coefficient of variation (CV), being smaller. These results, which demonstrated different bone mass values as quantitated using a caliper or magnifying glass, indicate the greater reliability and precision of the latter method.
The mechanism underlying diabetic osteopenia is still unclear and may involve osteoblastic activity and/or the deficit of insulin's anabolic action. Bone gla protein (BGP) is synthesized by the osteoblast and its synthesis increases with 1,25(OH)2D3 and fluoride. Because 1,25(OH)2D3 also stimulates insulin secretion, sodium fluoride administration can be used to investigate deficient osteoblastic activity in diabetics, as reflected by BGP levels. BGP was determined before and after administering sodium fluoride at a dosage of 50 mg/day/15 days to three groups: 14 patients with insulin-dependent diabetes, 16 diabetics on oral antidiabetic treatment, and 25 controls, all of similar age, sex, and characteristics. Basal BGP values (mean +/- SD) were low in diabetics on insulin treatment (4.3 +/- 1.1 ng/ml) and in diabetics on oral antidiabetics (5.8 +/- 1.2 ng/ml) as compared with controls (6.5 +/- 0.7 ng/ml) (P less than 0.001 and less than 0.05, respectively). After giving fluoride, BGP values did not change in the two diabetic groups but did vary in controls (8.1 +/- 0.6 ng/ml, P less than 0.001). These results suggest that deficient osteoblast function could be responsible for osteopenia in diabetics.
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To assess the dynamics of synthesis of the wall by regenerating Candida albicans protoplasts deposition of chitin and mannoproteins were investigated ultrastructurally using wheat germ agglutinin conjugated with either horseradish peroxidase or colloidal gold, and Concanavalin A coupled to ferritin respectively. Freshly prepared protoplasts lacked wheat germ agglutinin receptor sites but after 1-2 h of regeneration, they were detected. After 4-5 h of regeneration, the cell wall showed a discrete structure which was only labelled with wheat germ agglutinin in thin sections. At this stage of regeneration the outermost layer of the wall was labelled with clusters of Concanavalin A-ferritin particles. After 8 h regeneration, the cell wall appeared compact, and homogenously marked with wheat germ agglutinin whereas only the surface layers appeared consistently labelled with Concanavalin A-ferritin. From these observations we conclude that C. albicans protoplasts are able to regenerate in liquid medium a cell wall consisting of a network of chitin fibrils and mannoproteins at least (glucan polymers were not determined in the present cytological study). The former are the fundamental component of the inner layers at early stages of regeneration, whereas the latter molecules are predominant in the outer layers of the wall.
Response to acute and chronic administration of calcitonin and calcium and of biphosphonates (EHDP) was evaluated in 14 patients with Paget's bone disease who were grouped on the basis of homogeneous disease activity, as appraised by bone involvement and alkaline phosphatase and hydroxyproline levels. At first, 100 MRC U of calcitonin followed 4 hours later by 500 mg of elemental calcium were given for 10 days; a significant (p less than 0.001; paired and unpaired Student t test) reduction in alkaline phosphatase (-25%) and hydroproline (-55%) was observed. Subsequently, 5 mg/kg/day of EHDP was given for 20 days. Both parameters increased to levels similar to basal values. These increases were significant (p less than 0.001 for the paired and unpaired Student test) compared with those obtained after calcitonin administration; alkaline phosphatase rose +27% and hydroxproline +135%. After this, patients were divided into 2 groups (A and B). Group A was treated with calcitonin and calcium, at the dosage indicated above, for 10 days a month during 6 months. Group B continued with the same protocol with the addition of EHDP for the 20 days during which calcitonin and calcium were not given. The results of 6 months of treatment showed that calcitonin was more active and suggested that EHDP diminishes hormonal effects. These results also demonstrate a short-term absence of EHDP activity.
Osteocalcin synthesis is dependent on the influence of the renal vitamin D metabolite, 1,25(OH)2D3. This metabolite is an etiological factor in some hypercalciurias, and osteocalcin may thus be a parameter for discovering them. In turn, parathormone, which stimulates 1,25(OH)2D3 synthesis, is also implicated in the hypercalciurias. Mean molecular parathormone, osteocalcin, 24-hour calciuria and the calcium/creatinine and hydroxyproline/creatinine ratios were determined in urine samples obtained after a 12-hour fast from 18 patients with absorptive hypercalciuria and 11 patients with renal hypercalciuria out of a total of 62 patients with renal lithiasis. No changes were observed in osteocalcin or parathormone, indicating that neither is valid for the diagnosis of hypercalciuria. Significant differences were only found in the Ca/Cr ratio (p less than 0.001), which was higher (0.31 +/- 0.07 vs. 0.13 +/- 0.04 mg/mg) in renal hypercalciuria than in absorptive hypercalciuria. No changes in osteocalcin have been reported in the hypercalciurias, but variations in parathormone have been reported, therefore requiring further study and thought to understand the processes involved.
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Mannoproteins from cell walls of Saccharomyces cerevisiae synthesized at successive stages of the population growth cycle have been solubilized with Zymolyase and subsequently analyzed. The major change along the population cycle concerned a large size mannoprotein material; the size of the newly-synthesized molecules varied from 120,000-500,000 (mean of about 200,000) at early exponential phase to 250,000-350,000 (mean of about 300,000) at late exponential phase. These differences are due to modifications in the amount of N-glycosidically linked mannose residues, since the size of the peptide moiety was 90,000-100,000 at all growth stages and the level of O-glycosylation changed only slightly. After incubation of the purified walls with concanavalin A-ferritin and subsequent analysis by electron microscopy, labelling was localized at the external and internal faces of the walls. The middle space of these was labelled after digestion of the glucan network with Zymolyase, which demonstrate the presence of mannoproteins in close contact with the structural glucan molecules throughout the wall.
A study was made of 26 patients diagnosed as phase I reflex sympathetic dystrophy. In all of them, a bone:soft tissue uptake index was quantified by scintigraphic scanning before treatment and 3 months later. Eighteen patients were treated with 100 MRC units salmon calcitonin, followed by 500 mg elemental calcium 4 hours after hormone administration. The treatment was administered 10 days a month separated by intervals free of therapy. The other 8 patients were treated without interruption with 500 mg naproxen every 12 hours. In the group treated with calcitonin and calcium, the uptake index declined from 13.3 +/- 8.2 to 4.1 +/- 1.8 (p less than 0.001). The uptake index rose from 2.1.3 +/- 17.7 to 31.1 +/- 23.0 (NS) in the naproxen group. Using the Student t-test for paired samples to evaluate individual changes, a highly significant difference was reached (p less than 0.005) in the calcitonin-calcium group. The difference was also significant (p less than 0.01) in the naproxen group, but it was negative (t = 3.620). These results confirm the efficacy of treating reflex sympathetic dystrophy with calcitonin and calcium and the superiority of this treatment as compared with nonsteroidal anti-inflammatory drugs.
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