科研之友
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摘要
Background: The deficit of 25-hydroxyvitamin D (25OHD) associated with secondary hyperparathyroidism (SHPT) are frequent findings in patients with chronic kidney disease (CKD) on hemodialysis (HD). These events are associated with increased morbidity and mortality of cardiovascular (CV). 25OHD adequate serum levels as well as the use of selective activators of the vitamin D receptor (AsRVD) have been shown to have beneficial effects on bone metabolism and mineral and cardiovascular risk independently. Currently there is still controversy regarding the type of supplementation needed by patients with CKD on HD. Aims: The aim of our study was to evaluate whether there is benefit in combination therapy with 25OHD, calcifediol and a AsRVD, oral paricalcitol on bone-mineral metabolism and inflammatory markers, compared to single treatment with each of them in a group HD patients. Material and methods: A prospective study of 6 months, over 26 patients in our HD unit. We randomized patients into two groups: group 1 (G1) received oral paricalcitol treatment at doses of 1mcg/day. Group 2 (G2) was treated with 1 ampoule calcifediol/wk (0.266mg/wk=16.000U) orally. After 3 months of treatment, was added to the G1 and G2 calcifediol and paricalcitol respectively at the same doses, keeping these treatments together for 3 months to complete the 6 months follow up. Laboratory tests were performed at months 0, 3 and 6, measuring in all patients serum markers of 25OHD, calcium (Ca), phosphorus (P) and PTH Bone turnover markers were: alkaline phosphatase (FA), aminoterminal propeptide of procollagen type 1 (Pinp1) and carboxyl-terminal telopeptide of type I collagen (CrossLaps) and inflammatory markers : IL-8. WE also collected data on levels of insulin, glucose, hemoglobin, erythropoietic agents (ESAs) and rates of resistance to EPO and HOMA (homeostasis model assessment). Results: We detected a deficit of 25-hydroxyvitamin D in all patients studied, with a mean of 13.67 +/- 4.81ng/ml. Supplementation with oral calcifediol significantly corrects this deficit without evidence of toxicity (35.36 +/- 33.68ng/ml in G1 at 6 months and 59.21 +/- 26.50ng/ml in G2 at 3 months). Paricalcitol treatment significantly reduces PTH levels in G1 at 3 months (P%26lt;039). We also noted a decrease in bone marker Pinp1 with paricalcitol, pointing to a possible direct effect on bone cells (P%26lt;001). Both treatment with paricalcitol calcifediol produced a significant decrease in levels of IL-8 (P%26lt;001), known inflammatory marker; drawing attention to a trend towards better response to etythropoiesis-stimulating agents (ESAs), possible related to the decrease in inflammation. The NOMA index did not change significantly. Conclusion: Based on our results, we cannot conclude that the association calcifediol and paricalcitol produces advantages over the effect of each marker separately Paricalcitol also by itself appears to have a direct cellular bone action.
- 出版日期2013
