Mawer E B, Backhouse J, Davies M, Hill L F, Taylor C M
Lancet. 1976 Jun 5;1(7971):1203-6. doi: 10.1016/s0140-6736(76)92157-7.
In four healthy controls and three patients with hypoparathyroidism serum-1,25-dihydroxycholecalciferol (1,25-D.H.C.C.) concentrations, after oral or intravenous administration, declined biphasically with a rapid-phase half-time of about 14 hours. Repeated oral doses of 1 mug 1,25-D.H.C.C. (2-4 nmol) produced serum concentrations well below the assayed normal range but were nevertheless effective in raising serum-calcium. It is suggested that orally administered 1,25-D.H.C.C. acts directly on the intestinal mucosal-cell nucleus to promote calcium absorption. 1,25-D.H.C.C. is more rapidly eliminated from the body than vitamin D, and it is predicted that any hypercalcaemia caused by 1,25-D.H.C.C. therapy should be of relatively short duration.
在4名健康对照者和3名甲状旁腺功能减退患者中,口服或静脉注射后,血清1,25-二羟胆钙化醇(1,25-D.H.C.C.)浓度呈双相下降,快速相半衰期约为14小时。重复口服1微克1,25-D.H.C.C.(2 - 4纳摩尔)所产生的血清浓度远低于检测到的正常范围,但仍能有效提高血清钙水平。提示口服1,25-D.H.C.C.直接作用于肠黏膜细胞核以促进钙吸收。1,25-D.H.C.C.比维生素D从体内消除得更快,预计1,25-D.H.C.C.治疗引起的任何高钙血症持续时间相对较短。