- 期刊
新型活性維生素D2在臨床腎臟病之運用
The Application of New Active Vitamin D2 in Clinical Renal Medicine
摘要
慢性腎臟病患者相關的骨骼病變其主要原因為鈣、磷、維生素D3、副甲狀腺素等代謝異常所致；而續發性副甲狀腺素過高或過低及血中鈣、磷的異常所導致的血管鈣化，是造成長期透析病人死亡的重要因素。慢性腎衰竭的病人常使用傳統的活性維生素D3（1,25(OH)2D3; calcitriol）來治療其續發性副甲狀腺素亢進症。但使用calcitriol後，常發生副甲狀腺素受到過度抑制，骨骼成無力骨（Adynamic bone disease）的狀態，亦或是血鈣、磷的升高，這些情況均會增加血管鈣化的風險，而增加病人的死亡率。在慢性腎臟病初期階段，由於其腎小管1α-hydroxylase仍有活性，且1α-hydroxylase為受質依賴性（substrate-dependent），只要給予足夠量生理性維生素（25(OH)D），即會有calcitriol的產生。另近年來有新型活性維生素D2的問世，除能有效降低副甲狀腺素亢進，其血鈣、磷的上升只有傳統calcitriol的十分之一。另新型活性維生素D2尚且有骨骼外的益處，如心臟，降蛋白尿，改善免疫，腫瘤等方面均有其益處。本文除探討續發性副甲狀腺亢進治療外，擬將介紹新型活性維生素D2其在腎臟醫學使用所帶來優點。
並列摘要
The main problem of chronic kidney disease - mineral bone disorder (CKD-MBD) is the metabolic abnormalities of calcium, phosphate, vitamin D and parathyroid hormone. Then, vessel calcification, mostly caused by secondary hyperparathyroidism, hypoparathyroidism, or abnormal serum calcium and phosphate level, is the major cause of death for long term dialysis patients. Usually, CKD patients receive active vitamin D3 to treat secondary hyperparathyroidism. However, active vitamin D3 may over suppress parathyroid to induce adynamic bone disorder, and brings hypercalcemia, or hyperphosphatemia problems. These may further increase the risks of vessel calcification and mortality. In early CKD, renal tubular 1α-hydroxylase is still active and is substrate-dependent. Therefore, the enough amount of native vitamin D can produce active vitamin D3 by the patient himself as needed. Recently, the new active vitamin D2 not only efficiently decreases hyperparathyroidism but also has less increase in serum calcium and phosphate than traditional active vitamin D3. In addition, new active Vitamin D2 has extra-skeletal benefits, such as heart disease, proteinuria, immune, cancer etc. This review article will discuss the treatment of hyperparathyroidism and the other advantages of new active vitamin D2 in clinical practice.
延伸閱讀
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