What Factors Affect a Sufficient Calcitriol Dose?

Dihydroxycholcalciferol is one of the most important active metabolites of vitamin 1, 25-D3. This metabolite is usually formed in the kidney. In recent years, it has been found that calcitriol can also be produced outside the kidney. It has been confirmed that placenta, monocytes, macrophages, tumor cell supernatants, lymph nodes and keratinocytes in patients with sarcoidosis have 1 hydroxylase to produce calcium triol alcohol. The precursor of calcitriol is 25-hydroxycholcalciferol (Alfacalciferol). Dihydroxycholcalciferol has the effects of promoting calcium absorption in the small intestine and regulating the transport of inorganic salts in bone. In patients with obvious renal insufficiency, especially those who need long-term hemodialysis, endogenous calcitriol synthesis can be greatly reduced, or even almost stopped, resulting in renal osteodystrophy. Oral dihydroxycholcalciferol can make the intestine absorb calcium normally, so it can correct hypocalcemia, reduce bone and muscle pain, reduce or tend to normalized alkaline phosphatase, and increase the elevated plasma parathyroid gland. The concentration makes it normal, which promotes bone mineralization. Dihydroxycholcalciferol also has the effect of accelerating skeletal collagen maturation. In recent years, it has also been found that it has important effects on cell proliferation, differentiation, and the immune system. It has begun to be used in clinical practice as a new immunoregulatory hormone in foreign countries.