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 |
|---|---|---|---|
â‘ Competitively inhibit the conversion of seemed to be more severe to HMG-COA reductase â‘¡Block important isoprenoid intermediates in the cholesterol biosynthetic pathway â‘¢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) â‘£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 | |
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 Myopathy | 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] | â‘ Inhibits glycerin esterase activity in adipose tissue â‘ 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 |
Binds to LDLR, mediates LDLR to enter liver cells, and is finally degraded by lysosomes | Respiratory tract infection | —— |