Spustová V, Dzúrik R
Vedeckovýskumná základna Slovenskej zdravotníckej univerzity-Ustav preventívnej a klinickej medicíny, Bratislava, Slovenská republika.
Vnitr Lek. 2004 Jul;50(7):537-43.
The main source of vitamin D in a man is its synthesis in human skin. 7-Dehydrocholesterol converts into cholecalciferol--vitamin D3--as a result of UV radiation. Cholecalciferol hydroxylates in liver into 25-hydroxyvitamin D3 [25(OH)D, calcidiol], which concentration in blood is a relevant indicator of the total of vitamin D in a human body. 25(OH)D hydroxylates in kidneys into 1,25-dihydroxyvitamin D3 [1,25(OH)2D, calcitriol], which is considered an active metabolite of vitamin D. Epidemiological studies showed high prevalence of low concentrations of 25(OH)D especially in older population and people with chronic diseases. 25(OH)D concentrations were defined at which rise parathormone levels, increases bone conversion, impairs bone mineralization and develops osteomalacia. Based on these results a deficiency of vitamin D was defined. Patients with chronic renal disease experience development of serious bone impairments described as renal osteodystrophy. These disorders are caused by secondary hyperparathyroidism which develops as a result of mineral metabolism impairment, especially of hypocalemia, 25(OH)D deficiency, and insufficient synthesis of 1,25(OH)2D. Presently published guidelines K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification and Stratification define processes of vitamin D supplementation, particularly 1,25(OH)2D according to a degree of renal disease. Early prevention and treatment of hypovitaminosis D is a treatment goal in order to reduce or stop development of secondary hyperparathyroidism with its consequences for bone metabolism.
男性维生素D的主要来源是人体皮肤中的合成。7-脱氢胆固醇在紫外线辐射作用下转化为胆钙化醇——维生素D3。胆钙化醇在肝脏中羟化成为25-羟维生素D3[25(OH)D，骨化二醇]，其血液浓度是人体维生素D总量的一个相关指标。25(OH)D在肾脏中羟化成为1,25-二羟维生素D3[1,25(OH)2D，骨化三醇]，它被认为是维生素D的活性代谢产物。流行病学研究表明，低浓度25(OH)D的患病率很高，尤其是在老年人群和患有慢性病的人群中。确定了25(OH)D的浓度，在该浓度下甲状旁腺激素水平升高、骨转换增加、骨矿化受损并发展为骨软化症。基于这些结果定义了维生素D缺乏症。患有慢性肾病的患者会出现严重的骨损伤，称为肾性骨营养不良。这些疾病是由继发性甲状旁腺功能亢进引起的，继发性甲状旁腺功能亢进是由于矿物质代谢受损，尤其是低钙血症、25(OH)D缺乏以及1,25(OH)2D合成不足所致。目前发布的《K/DOQI慢性肾脏病临床实践指南：评估、分类和分层》根据肾病程度定义了维生素D补充的过程，尤其是1,25(OH)2D的补充过程。早期预防和治疗维生素D缺乏症是一个治疗目标，以减少或阻止继发性甲状旁腺功能亢进的发展及其对骨代谢的影响。
