Figure 2 – Main 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
|