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Table 2 Lipid-lowering drugs after allo-HSCT

From: Management of dyslipidemia after allogeneic hematopoietic stem cell transplantation

Lipid-lowering drugs Mechanism Side effect Drug interaction
Statins [41,42,43,44] Competitively inhibit the conversion of seemed to be more severe to HMG-COA reductase
Block important isoprenoid intermediates in the cholesterol biosynthetic pathway
Reduce and regulate immune function. (Reduce T cell activation and co-stimulatory molecules on APCs by reducing MHC-II. Increase levels of interleukin 10, an anti-inflammatory cytokine with TH2 phenotypic characteristics)
Others: improve endothelial function, enhance and stabilize atherosclerotic plaques, reduce oxidative stress and inflammation, and inhibit thrombosis response
Elevated transaminases, myositis, and rhabdomyolysis Cyclosporine can increase the serum level of statins through effects on the cell membrane transporter multidrug-resistant protein 2
Inhibitors of CYP3A4 such as azole antifungals, non-dihydropyridine calcium channel blockers (verapamil and diltiazem), and macrolide antibiotics increase the risk of toxicity of statins
Ezetimibe [45, 46] Reduces intestinal cholesterol absorption by inhibiting small intestinal cholesterol transporter, lowers plasma cholesterol level and liver cholesterol reserves by selectively inhibiting small intestinal cholesterol transporter Elevated transaminases Increase the serum level of cyclosporine
Fibrates [47] Increase the expression of apolipoprotein genes linked to the stimulus, enhance lipoprotein lipase activity Cholelithiasis
Gastrointestinal upset
The risk of myopathy is increased when fibrates are given with statins, particularly in patients with impaired kidney function or those on cyclosporine
Niacin [41] Inhibits glycerin esterase activity in adipose tissue
Enhances LPL activity and promotes the hydrolysis of plasma TGs
Exacerbate hyperglycemia and hyperuricemia, flushing, and gastrointestinal intolerance, enhance the blood pressure Lower effect of ganglion blockers, calcium channel blockers, and adenoid inhibitors
PCSK9 inhibitor [48, 49] Binds to LDLR, mediates LDLR to enter liver cells, and is finally degraded by lysosomes Respiratory tract infection ——
  1. Abbreviations: HMG-COA 3-hydroxy-3-methylglutaryl-coenzyme A, APCs Antigen-presenting cells, MHC-II Major histocompatibility complex II expression, TH2 T helper 2, LPL Lipoprotein lipase, LDLR LDL receptor