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PubMed1988

Results of a stimulatory therapy of low bone metabolism in osteoporosis with (1-38)hPTH and diphosphonate EHDP. Protocol of study I, osteoporosis trial Hannover.

In contrast to prevention, the therapy of manifest osteoporosis remains a clinically significant problem. So far all therapeutic attempts have yielded unsatisfying results. For this reason we have tried to achieve a positive bone balance by sequential stimulation and inhibition of the osseous metabolism. The therapy consisted of six 14-day courses with 400 units (1-38)hPTH per day and, in addition, starting with the 2nd week of PTH therapy, EHDP 5 mg per kg body weight per day for a total of 2 weeks. Already the initial therapeutic course resulted in a stimulation of decreased bone metabolism which could be documented by an increase in the calcium-47 accretion rate (six patients). An increase of the alkaline phosphatase could be noted (four patients); this, however, did not correlate with the calcium accretion. A positive calcium balance could, nonetheless, only be attained in four of eight patients within this period, while neither the alkaline phosphatase nor the kinetics would allow a prediction of this effect. Changes of the balance coincided with equal changes in the net calcium absorption. The urinary calcium excretion increased temporarily during the therapeutic phase. We were not able to detect an influence on the vitamin D metabolites. Histomorphometric studies did not demonstrate an increase in bone mass in the iliac creast after six therapeutic courses. Nevertheless, progressive deformations of vertebral bodies did not occur. We conclude that already after 2 weeks this therapeutic concept can lead to a stimulation of bone metabolism.

Adult↗
PubMed1989

Unidirectional duodenal and jejunal calcium and phosphorus transport in the rat: effects of dietary phosphorus depletion, ethane-1-hydroxy-1,1-diphosphonate and 1,25 dihydroxycholecalciferol.

Unidirectional calcium (Ca) and phosphorus (Pi) transport was studied in vitro by means of a modified Using technique in the absence of electrochemical gradients between the mucosal and serosal buffer medium. Duodenum and jejunum of male albino Sprague-Dawley rats were investigated after Pi depletion alone (0.03% diet-Pi), Pi depletion and EHDP treatment (40 mg/kg per day s.c. X 4), and Pi depletion, EHDP and 1,25(OH)2D3 (500 pmol i.v. X 2) treatment. Mucosal-to-serosal Ca and Pi fluxes (Jms) changed in parallel, depending on the 1,25(OH)2D3-status of the animals. Regarding serosal-to-mucosal fluxes (Jsm), Pi depletion resulted in an increase in Jsm for Ca and Pi, associated with a rise in Gt and Isc in the duodenum but not in the jejunum. EHDP administered to block synthesis of 1,25(OH)2D3 caused further augmentation in duodenal Jsm for calcium but not phosphorus, which was paralleled by an increase in Gt and Isc. After repletion with 1,25(OH)2D3, an increase in Jsm for Ca and Pi and a rise in Gt and Isc were observed in the duodenum and in the jejunum. Serosal-to-mucosal fluxes for Ca and Pi were related to tissue conductance (Gt) in the duodenum (r = 0.89, P less than 0.001 and r = 0.84; P less than 0.001, respectively), as well as in the jejunum (r = 0.55; P less than 0.01 and r = 0.66; P less than 0.001, respectively). Changes in Jsm also paralleled changes in transmural shortcircuit current (Isc). The data are compatible with the assumption of an increase in Jsm for Ca and Pi and a rise in Gt, both reflecting an increase in water recycling across the tight junctions caused by a rise in sodium absorption. They provide further evidence that the overall effect of 1,25(OH)2D3 on intestinal Ca and Pi transport is to increase both cell-mediated active mucosal-to-serosal transport and paracellular diffusional serosal-to-mucosal ion movement.

Animals↗