Figure 2Main pathogenic mechanisms and causative drugs involved in peripheral edema. The four main mechanisms are illustrated: lymphedema (impaired lymphatic drainage that overcomes transcapillary filtration), permeability edema (loss of protein-rich fluid from the intravascular to the interstitial space due to decreased oncotic reflection coefficient), renal edema (fluid overload due to antinatriuretic and/or antiaquaretic effects is transmitted to the capillary bed, leading to increased capillary hydrostatic pressure) and vasodilatory edema (preferential precapillary arteriolar vasodilatation rising capillary hydrostatic pressure). ALK, anaplastic lymphoma kinase; ATRA, All-trans retinoic acid; BCR-Abl, breakpoint cluster region and Abelson; CCB, calcium channel blockers; CNI, calcineurin inhibitors; G-CSF, granulocyte colony-stimulating factor; GnRH, gonadotropin releasing hormone; IL-2, interleukin 2; MAOI-B, monoamine oxidase inhibitors type B; mTOR, mammalian target of rapamycin; PGI2, prostacyclin; PI3K, phosphoinositide 3-kinase; πc, oncotic capillary pressure; πi, oncotic interstitial pressure; Pc, capillary hydrostatic pressure; Pi, capillary interstitial pressure; Qλ, lymphatic flow