■Molidustat是一种新型药物,用于治疗透析依赖性(DD)和非透析依赖性(NDD)患者的贫血。其疗效和安全性尚不清楚。
■我们搜索了五个数据库,以确定将墨利司他与红细胞生成刺激剂(ESA)或安慰剂在贫血患者中进行比较的随机对照试验。
■确定了六项包含2025名合格参与者的研究。对于NDD患者,与基线相比,molidustat的Hb水平变化(ΔHb)显着高于安慰剂[平均差(MD)=1.47(95%CI:1.18至1.75),P<0.00001]和ΔHb也明显高于ESA[MD=0.25(95%CI0.09至0.40),P=0.002]。对于NDD患者,molidustat的Δhepcidin显着低于安慰剂[MD=-20.66(95%CI:-31.67至-9.66),P=0.0002]和Δhepcidin也明显低于ESA[MD=-24.51(95%CI:-29.12至-19.90),P<0.00001]。对于NDD患者,molidustat的Δ铁显着低于ESA[MD=-11.85(95%CI:-15.52至-8.18),P<0.00001],和ΔTSAT也明显低于ESA[MD=-5.29(95%CI:-6.81至-3.78),P<0.00001]。对于NDD患者,molidustat的Δ铁蛋白显着低于安慰剂[MD=-90.01(95%CI:-134.77至-45.25),P<0.00001]。然而,对于DD-CKD患者,moleidustat对增加Hb水平的作用与ESA相似[MD=-0.18(95%CI:-0.47至0.11),P=0.23],Δ铁水平[MD=3.78(95%CI:-7.21至14.76),P=0.5],Δ铁蛋白水平[MD=25.03(95%CI:-34.69至84.75),P=0.41],和Δhepcidin水平[MD=1.20(95%CI:-4.36至6.76),P=0.67]。对于DD-CKD患者,与安慰剂组或ESA组相比,molidustat在ΔTSAT上显示出明显较高的水平[MD=3.88(95%CI:2.10至5.65),P<0.0001]和ΔTIBC水平上的水平略有增加[MD=1.08(95%CI:-0.07至2.23),P=0.07]。严重不良事件(SAEs)的发生率没有显着差异,死亡,Molidustat组和ESA组之间的心脏相关不良事件。
■Moricizine可以有效改善NDD患者的Hb水平,并纠正DD患者的贫血,而不会增加不良事件的发生率。
UNASSIGNED: Molidustat is a novel agent investigated for the treatment of anemia in both dialysisdependent (DD) and non-dialysis-dependent (NDD) patients. Its efficacy and safety are still unclear.
UNASSIGNED: We searched five databases to identify randomized controlled trials comparing molidustat to erythropoiesis-stimulating agents (ESAs) or placebo in patients with anemia.
UNASSIGNED: Six studies containing 2025 eligible participants were identified. For NDD patients, the change in Hb levels from baseline (ΔHb) was significantly higher for
molidustat than for placebo [mean difference (MD) = 1.47 (95 % CI: 1.18 to 1.75), P < 0.00001] and ΔHb was also significantly higher for molidustat than for ESAs [MD = 0.25 (95 % CI 0.09 to 0.40), P = 0.002]. For NDD patients, Δhepcidin was significantly lower for
molidustat than for placebo [MD = -20.66 (95 % CI: -31.67 to -9.66), P = 0.0002] and Δhepcidin was also significantly lower for
molidustat than for ESAs [MD = -24.51 (95 % CI: -29.12 to -19.90), P < 0.00001]. For NDD patients, Δiron was significantly lower for
molidustat than for ESAs [MD = -11.85 (95 % CI: -15.52 to -8.18), P < 0.00001], and ΔTSAT was also significantly lower for molidustat than for ESAs [MD = -5.29 (95 % CI: -6.81 to -3.78), P < 0.00001]. For NDD patients, Δferritin was significantly lower for molidustat than for placebo [MD = -90.01 (95 % CI: -134.77 to -45.25), P < 0.00001]. However, for DD-CKD patients, molidustat showed an effect similar to that of ESAs on increasing the Hb level [MD = -0.18 (95 % CI: -0.47 to 0.11), P = 0.23], Δiron level [MD = 3.78 (95 % CI: -7.21 to 14.76), P = 0.5], Δferritin level [MD = 25.03 (95 % CI: -34.69 to 84.75), P = 0.41], and Δhepcidin level [MD = 1.20 (95 % CI: -4.36 to 6.76), P = 0.67]. For DD-CKD patients, compared with the placebo or ESA group, molidustat showed a significantly higher level on ΔTSAT[MD = 3.88 (95 % CI: 2.10 to 5.65), P < 0.0001] and a slightly increased level on ΔTIBC level [MD = 1.08 (95 % CI: -0.07 to 2.23), P = 0.07]. There was no significant difference in the incidence of severe adverse events (SAEs), death, and cardio-related adverse events between molidustat and the ESAs groups.
UNASSIGNED: Moricizine can effectively improves Hb levels in NDD patients and corrects anemia in DD patients without increasing adverse event incidence.