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    Home > Active Ingredient News > Endocrine System > Get out of the misunderstanding: Should active vitamin D be used with calcium group "CP"?

    Get out of the misunderstanding: Should active vitamin D be used with calcium group "CP"?

    • Last Update: 2022-02-22
    • Source: Internet
    • Author: User
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    *For medical professional reading reference Osteoporosis is the most common bone disease, a systemic bone disease characterized by low bone mass and damage to the microstructure of bone tissue, leading to increased bone fragility and susceptibility to fractures [1] ]
    .

    In clinical practice, calcium is an important choice for the prevention and treatment of osteoporosis
    .

    However, whether it is a patient or a clinician, there may be such a misunderstanding: taking calcium tablets can treat osteoporosis
    .

    In fact, calcium is only a nutritional supplement for bone health, and cannot be used as a drug for osteoporosis treatment.
    Its single use in the treatment of osteoporosis is limited [2]
    .

    It is well known that vitamin D can promote intestinal calcium absorption and reduce the risk of falling [3], and is often used in combination with calcium as the basic treatment for osteoporosis
    .

    So, are calcium and vitamin D an inseparable therapeutic "CP"? Eating calcium may not necessarily supplement calcium: the “pain” of intestinal calcium absorption The bioavailability of calcium in the human body includes calcium intake, absorption and excretion, and calcium metabolism involves the regulation of multiple organs such as the intestines, kidneys, bones and thyroid
    .

    Among them, intestinal calcium absorption is an important way of calcium absorption, which is regulated by various hormones such as 1,25(OH)2D3 [3]
    .

    Calcium ions in the gut are absorbed into the blood by the intestinal epithelial monolayer through transcellular (active transport) and paracellular (passive transport) pathways [4]
    .

    Notably, dietary calcium intake determines the transport pathway of calcium ions
    .

    In the case of normal or low dietary calcium, intestinal calcium absorption is dominated by active transcellular pathways; in the case of high dietary calcium intake, intestinal calcium absorption is dominated by passive paracellular pathways [5]
    .

    In fact, eating calcium is not necessarily the same as calcium supplementation
    .

    A systematic study included 12 studies of calcium metabolism in healthy Chinese adults aged 18-60 years published before March 2015 under typical Chinese dietary conditions, including 13 aggregated data aggregated from 257 individual data from 137 subjects.
    , the study aims to explore the characteristics of calcium metabolism under the habitual dietary calcium intake level of Chinese adults [6]
    .

    A systematic review of studies showed that the average daily dietary calcium intake of various studies in China was between 288-948 mg, the aggregated average dietary calcium intake was 583 mg/day, and the average calcium retention was only 72 mg/day [6]
    .

    At the same time, intestinal calcium absorption (FCA) decreases with age, especially in women over 60 years old [7]
    .

    This increases the risk of osteoporosis and fractures, seriously affecting bone health
    .

    "Porter" of intestinal calcium: Active vitamin D and active vitamin D include common vitamin D and active vitamin D.
    Common vitamin D must be hydroxylated into active vitamin D to promote intestinal calcium absorption
    .

    Through the combination with vitamin D receptor (VDR), active vitamin D enters the nucleus, accelerates DNA transcription of mRNA, and promotes the biosynthesis of Ca2+ transport-related proteins (TRPV6, calcium binding protein, PMCA1b, etc.
    ) [8,9]
    .

    Active vitamin D also stimulates the activation of basement membrane adenylyl cyclase, and under the action of PMCA1b and Ca2+-ATPase, Ca2+ is transported to the blood through active energy consumption [8]
    .

    After the active vitamin D is combined with the VDR of intestinal mucosal epithelial cells, it also directly acts on the brush border, changing the structure and composition of membrane phospholipids (increasing the content of phosphatidylcholine and unsaturated fatty acids), thereby increasing the permeability of calcium [8] ]
    .

    For traditional active vitamin D drugs, in addition to promoting intestinal calcium absorption through the above mechanism, it also further up-regulates the expression of claudin-2/12/15, thereby promoting passive calcium transport [10]
    .

    The two pathways of intestinal calcium absorption are shown in Figure 1: Figure 1 Two pathways of intestinal calcium absorption Unlike this, a new active vitamin D analog, idecalcidol, uses microbial hydroxylation technology to introduce 3-hydroxypropane at the 2β position Acid, more stable in blood and cell level, more stable in combination with VDR, and longer half-life [11,12]; at the same time increase the duodenal mRNA expression of TRPV6 and calcium binding protein Calbindin-D9k, more effectively promote the active calcium Transportation increases FCA (Figure 2) [13]
    .

    Figure 2 Idecalcidol promotes the expression of Ca2+ transport-related proteins.
    Low calcium diet is a common feature of Chinese residents.
    Active transport is the mainstay of calcium absorption.
    Idecalcitol can promote active transport, thereby increasing FCA[13]
    .

    A randomized controlled study included 40 patients with postmenopausal osteoporosis and randomly divided them into four groups, receiving idecalcidol 0.
    75 μg/d, alfacalcidol 1 μg/d, ordinary vitamin D3 800IU/day, No drug control, continuous treatment for 4 weeks, to assess FCA [14]
    .

    The results showed that compared with the control group, after 4 weeks of treatment, the FCA value of the idecalcidol group increased by 59.
    5% and the alfacalcidol group increased by 45.
    9%, while the FCA of the ordinary vitamin D3 group had no significant increase (Figure 3 ) [14]
    .

    Figure 3 Idecalcitol treatment significantly improved FCA in patients with osteoporosis: Active vitamin D's anti-osteoporosis journey Calcium and vitamin D are common "CPs" for clinical prevention and treatment of osteoporosis
    .

    Among them, active vitamin D is an anti-osteoporosis drug.
    So, can it play a role in anti-osteoporosis treatment and reduce the risk of fractures? The answer is yes
    .

    Phase III clinical studies in China and Japan have shown that for patients with osteoporosis, without calcium supplementation, idecalcidol monotherapy significantly increases bone mineral density (BMD) and reduces the risk of vertebral and wrist fractures
    .

    ▌ China Phase III clinical study[15] included 265 Chinese osteoporosis patients aged 48-83 years, who were randomized to receive idecalcidol 0.
    75μg/d + alfacalcidol placebo or alfacalcidol 1μg/day d + idecalcidol placebo, continuous treatment for 12 months, to explore the effect of idecalcidol on bone mineral density in Chinese osteoporosis patients with low vitamin D and low calcium intake
    .

    Patients received no vitamin D3 or calcium supplementation throughout the study
    .

    The study showed that after 12 months of continuous treatment, compared with the alfacalcidol group, the lumbar spine, total hip and femoral neck BMD increased by 2.
    05%, 1.
    33% and 1.
    78% in the alfacalcidol group, respectively; alfa ossification The BMD of the lumbar spine, total hip, and femoral neck remained almost unchanged for alcohol (Fig.
    4)
    .

    There was no difference in the incidence of adverse events between the two groups
    .

    Figure 4 Compared with the alfacalcidol group, the BMD of the lumbar spine, total hip and femoral neck in the idecalcidol group increased significantly Patients were randomized to receive idecalcidol 0.
    75 μg/d (n=543) or alfacalcidol 1 μg/d (n=544) for 36 months.
    The primary endpoint was the incidence of vertebral fractures, and secondary endpoints included Non-vertebral fractures,
    etc.

    Studies have shown that idecalcidol reduces the risk of new vertebral fractures by 26% compared to alfacalcidol (Figure 5); idecalcidol has early wrist fracture inhibition effects, and fractures at 36 months The risk of occurrence was reduced by 71% (Figure 6)
    .

    Fig.
    5 Compared with alfacalcidol, the risk of new vertebral fractures in the idecalcidol treatment group was significantly reducedFig.
    6 Compared with alfacalcidol, the risk of wrist fractures in the idecalcidol-treated group was significantly reducedSummary : Intestinal calcium absorption is an important way of calcium absorption, including active transport and passive transport, and is regulated by various hormones such as 1,25(OH)2D3
    .

    FCA declines with age, increasing the risk of osteoporosis and fractures, seriously affecting bone health
    .

    A new active vitamin D analog, idecalcidol, can effectively promote the active transport of calcium by increasing the duodenal mRNA expression of TRPV6 and calcium-binding protein Calbindin-D9k, improve FCA, and can effectively increase BMD without the need for combined calcium.
    Reduce the risk of vertebral and non-vertebral fractures and become an ideal choice for anti-osteoporosis therapy
    .

    References [1] Chinese Medical Association Osteoporosis and Bone Mineral Disease Branch.
    Chinese Journal of Osteoporosis and Bone Mineral Disease, 2017, 10(5): 413-443.
    [2] Zhu Hanmin.
    Drug Evaluation, 2012 , 09(007):21-27.
    [3] Branch of Osteoporosis and Bone Mineral Diseases, Chinese Medical Association.
    Chinese Journal of Osteoporosis and Bone Mineral Diseases, 2018,11(1):1-19.
    [4 ] Child Health Branch of Chinese Preventive Medicine Association.
    China Maternal and Child Health Research, 2019, 30(03): 262-269.
    [5] Christakos S, Lieben L, et al.
    Bonekey Rep, 2014, 3: 496.
    [6] Fang AP, et al.
    Asia Pac J Clin Nutr, 2016, 25(4): 776-784.
    [7] Chan EL, et al.
    Clin Endocrinol(Oxf).
    1992, 36(4): 375-381.
    [8 ] Wang Jianzhi, et al.
    Pathophysiology (Ninth Edition).
    People's Health Publishing House.
    2018: 67.
    [9] Christakos S, et al.
    Bonekey Rep, 2014, 3: 496.
    [10] Diaz de Barboza G, et al.
    al.
    World J Gastroenterol, 2015, 21(23): 7142-7154.
    [11] Abe M.
    et al.
    Tokyo, Chugai Pharmaceuticals Co.
    , 2010 [12] Sasaki H, et al.
    Heterocycles, 2011, 83 (6 ): 1385.
    [13] Hirota Y, et al.
    PLoS One, 2018, 13(10): e0199856.
    [14] Uenishi K, et al.
    Osteoporos Int, 2018, 29(3): 723-732.
    [15 ]iang Y, et al.
    J Bone Miner Metab, 2019, 37(6): 1036-1047.
    [16] Matsumoto T, et al.
    Bone, 2011, 49(4): 605-612.
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