Raya Sánchez J M, Hernández Nieto L, Brito Barroso M L, Hernández García M T
Departamento de Medicina Interna, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife.
Med Clin (Barc). 1994 Mar 19;102(10):380-2.
The active metabolite of vitamin D3 1.25 dehydroxycholecalciferol (1.25DHCC) is a potent inducer of monocytic differentiation of the myeloid blasts "in vitro". Likewise the inhibiting role of vitamin D3 on bone marrow fibrosis by, among others, a stimulating effect of macrophagic activity is known. However, these actions have seldom been clinically demonstrated. Two cases of chronic myeloproliferative syndromes in which treatment with 1.25DHCC was effective are presented. In the first case, one patient with polycythemia vera with myelofibrosis and focal blastosis in the bone marrow achieved disappearance of the excess of blasts and a reduction in the fibrosis (grade III to grade I) upon treatment. In the second case, idiopathic myelofibrosis, also with focal blastosis in the bone marrow biopsy, there was no regression of the fibrosis but the blastosis did disappear. It was concluded that 1.25DHCC may constitute an interesting treatment in this group of diseases through the following two mechanisms: limitation of the fibrosis and delay of blast transformation.
维生素D3的活性代谢产物1,25-二羟胆钙化醇(1,25DHCC)在“体外”是骨髓母细胞单核细胞分化的有效诱导剂。同样,维生素D3通过巨噬细胞活性的刺激作用等对骨髓纤维化具有抑制作用也为人所知。然而,这些作用很少在临床上得到证实。本文介绍了两例慢性骨髓增殖性综合征患者,用1,25DHCC治疗有效。第一例,一名真性红细胞增多症合并骨髓纤维化及骨髓局灶性母细胞化的患者,治疗后幼稚细胞过多现象消失,纤维化程度减轻(从III级降至I级)。第二例,特发性骨髓纤维化患者,骨髓活检也有局灶性母细胞化,纤维化无消退,但母细胞化确实消失了。得出的结论是,1,25DHCC可能通过以下两种机制成为这类疾病一种有意义的治疗方法:限制纤维化和延缓母细胞转化。