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K Glass

Publications and source records attributed to K Glass.

35 records · Page 2Linked to original sources
PubMed1983

Long term 25-hydroxyvitamin D3 therapy in postmenopausal osteoporosis: demonstration of responsive and nonresponsive subgroups.

Previous studies from our laboratory have demonstrated that 25-hydroxyvitamin D3 (25OHD3) therapy is effective in raising the impaired intestinal calcium absorption (alpha) associated with postmenopausal osteoporosis. In the present study we have assessed the effects of long term 25-OHD3 therapy (50 micrograms/day; mean treatment period, 1.3 yr) in 12 women with postmenopausal osteoporosis (mean age, 62.5 yr). Our results indicate that there was a significant increase in alpha for the group during therapy. However, we found that the patients could be divided into 2 groups based upon their ability to raise alpha in response to 25OHD3 therapy. In those who responded (n = 7), alpha increased from 0.36 +/- 0.05 to 0.49 +/- 0.08 (+/- SD; P less than 0.005) while no significant change was observed for the nonresponders (0.44 +/- 0.03 to 0.48 +/- 0.07). During therapy, there were significant increases in serum 25OHD and 24,25-dihydroxyvitamin D [25,25-(OH)2D] for both groups. Serum 1,25-(OH)2D significantly increased in the responders (21 +/- 8 to 39 +/- 13 pg/ml; P less than 0.01), but not in nonresponders (25 +/- 11 to 28 +/- 8 pg/ml). Between-group comparisons for responders vs. nonresponders before therapy disclosed significant reductions in 24,25-(OH)2D (0.4 +/- 0.3 vs. 2.2 +/- 0.8 ng/ml; P less than 0.005) and alpha (0.36 +/- 0.05 vs. 0.44 +/- 0.03; P less than 0.01). During therapy, there were no significant differences in any parameter between the two groups, except for serum I,25-(OH)2D which was significantly higher in the responders (39 +/- 13 vs. 28 +/- 8 pg/ml; P less than 0.05). These data would suggest that in postmenopausal osteoporosis, the ability to raise alpha in response to 25OHD3 therapy is due in part to increases in serum 1,25-(OH)2D during therapy. This suggests that in some patients with menopausal osteoporosis, renal 25OHD3-1 alpha-hydroxylase may be impaired.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

Ability of 25-hydroxyvitamin D3 therapy to augment serum 1,25- and 24,25-dihydroxyvitamin D in postmenopausal osteoporosis.

Six women (mean age, 62 yr; range, 48--77 yr) who were considered to have postmenopausal osteoporosis, as demonstrated by radiological evidence of vertebral crush fractures, low intestinal calcium (Ca) absorption, and bone biopsies consistent with this diagnosis, received a pharmacological dose of 25-hydroxyvitamin D3 (25OHD3; 20 microgram/day) for 3 months. This treatment increased the serum concentration of 25OHD from 8.7 +/- 4.6 to 30.2 +/- 9.5 (SD) ng/ml (P less than 0.0025), increased the serum concentration of 24,25-dihydroxyvitamin D from 1.2 +/- 1.2 to 7.7 +/- 2.7 ng/ml (P less than 0.025) in three patients, and increased the serum concentration of 1,25-dihydroxyvitamin D from 2.1 +/- 1.7 to 4.3 +/- 1.5 ng/dl (P less than 0.025). Moreover, there were commensurate increases in fractional intestinal Ca absorption from 0.38 +/- 0.03 to 0.49 +/- 0.06 (P less than 0.025) and in urinary Ca from 69 +/- 31 to 127 +/- 67 mg/day (P less than 0.025). There were no significant changes in serum Ca (9.6 +/- 0.5 vs. 9.5 +/- 0.4 mg/dl), serum phosphorus (3.4 +/- 0.2 vs. 3.6 +/- 0.4 mg/dl) or alkaline phosphatase (87 +/- 27 vs. 91 +/- 30 IU/liter) before or after therapy. It is concluded that orally administered 25OHD3 is not only effective in raising the low intestinal Ca absorption observed in postmenopausal osteoporosis but also in increasing the serum concentrations of 24,25-dihydroxyvitamin D and 1,25-dihydroxyvitamin D.

24,25-Dihydroxyvitamin D 3↗
PubMed1979

An unique form of osteomalacia associated with end organ refractoriness to 1,25-dihydroxyvitamin D and apparent defective synthesis of 25-hydroxyvitamin D.

A 28-yr-old woman presented with hypocalcemia, hypophosphatemia, secondary hyperparthyroidism, and biopsy-proven osteomalacia despite treatment with vitamin D2, (17.5 mg/day). Three weeks after vitamin D2 treatment was stopped, she was found to have a low normal serum 25-hydroxyvitamin D (25OHD) and high serum 1 alpha, 25-dihydroxyvitamin D [1,25(OH)2D] of 18.6 ng/ml and 21.2 ng/dl, respectively. The fractional intestinal calcium absorption was low at 0.26. Treatment with 25OHD3 (20--50 micrograms/day) corrected the hypocalcemia and secondary hyperparathyroidism, raised intestinal calcium absorption, and reversed the skeletal lesions of osteomalacia. Serum 25OHD concentration rose to 51 ng/ml, while 1,25(OH)2D remained elevated. This case illustrates the probable operation of dual abnormalities in vitamin D metabolism. An impaired end organ responsiveness to 1,25(OH)2D was suggested by a low intestinal calcium absorption in the face of high serum 1,25(OH)2D. Moreover, there may have been a defective vitamin D-25-hydroxylase, since there was a relative refractoriness to treatment with large doses of vitamin D2, an inappropriately low serum 250HD after vitamin D2 therapy, and a responsiveness to treatment with 25OHD3.

Adult↗
PubMedDate not supplied

[Detection of the clusters of negative charges on the surface of erythrocyte cytoplasmic membranes by fluorescent probes].

When charges on the membrane surface are distributed unequally and, especially, when they are in clusters, the concept of Goue-Chapman is not valid. Clusters of the negative charges on the cell surface can be detected by the combination of two fluorescent probes and a polycation which is capable of neutralizing the electrostatic field of the cluster. Clusters of the negative charges have been detected on the membranes of erythrocyte ghosts. Protamine was used as polyanion and fluorescent probes ANS and DSM were used as a fluorescent anion and cation, respectively.

Anions↗