Salt - More adverse effects
Salt - More adverse effects
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DOI：
10.1016/s0140-6736(96)01463-8
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发表时间：
1996-07-27
期刊：
影响因子：
168.9
通讯作者：
MacGregor, GA
中科院分区：
文献类型：
--
作者：
Antonios, TFT;MacGregor, GA
Lancet约900毫克。当绝经后妇女盐摄入量增加时，不仅尿钙排泄量增加，而且甲状旁腺激素浓度和羟脯氨酸排泄量也增加，这表明骨钙的动员。在另一项研究中，将绝经后妇女的每日钠摄入量从170 mmol降至70 mmol，钙排泄量和1，25-二羟麦角钙化醇及血清骨钙素浓度均大幅降低，表明骨动员减少。此外，Matkovic等人21认为，在少女快速生长期间，钙摄入量低和高盐摄入引起的尿中钙的高强制性损失可能会减少骨骼中的钙潴留，同时降低峰值骨量。特发性高钙尿症患者的骨矿物质含量低于正常人，其异常程度与盐摄入量直接相关。22此外，在高钙尿症中适度减少盐的摄入量在减少钙排泄方面与噻嗪类利尿剂一样有效。23对于给定的尿钠排泄量，高血压患者的尿钙排泄量高于血压正常的人，并且有低离子钙和高甲状旁腺激素和1，25-二羟麦角钙化醇浓度的趋势;这些因素表明，尿钙排泄量的增加不能通过钙吸收的增加来补偿，并且存在钙从骨中的动员。24对于给定的钠摄入量，原发性高血压患者比血压正常的受试者有更大的潜在骨脱矿风险。24自发
THE LANCET about 900 mg. When salt intake was increased in postmenopausal women there was an increase not only in urinary calcium excretion, but also in parathyroid hormone concentrations and hydroxyproline excretion which indicated mobilisation of calcium from bone. 20 In a separate study where daily sodium intake was reduced in postmenopausal women from 170 mmols to 70 mmols, there was a large reduction in both calcium excretion and 1, 25-dihydroxyergocalciferol and serum osteocalcin concentrations, indicating a decrease in bone mobilisation. In addition, Matkovic et al21 suggested that during rapid growth in young girls, a low calcium intake and a high obligatory calcium loss in urine caused by high salt intake may reduce calcium retention in the skeleton, with a concomitant reduction in peak bone mass. Patients with idiopathic hypercalciuria have lower bone mineral mass than normal people, and the extent of the abnormality is directly related to salt intake. 22 Furthermore, a moderate reduction in salt intake in hypercalciuria is as effective in reducing calcium excretion as a thiazide diuretic. 23Patients with high blood pressure have higher urinary calcium excretion for a given urinary sodium excretion than normotensive people, as well as a tendency for lower ionised calcium and higher parathyroid hormone and 1, 25-dihydroxyergocalciferol concentrations; these factors show that the increased urinary calcium excretion is not compensated for by an increase in calcium absorption, and that there is mobilisation of calcium from bone. 24 Patients with essential hypertension are potentially at greater risk of bone demineralisation for a given sodium intake than normotensive subjects. 24 In spontaneously