ABSTRACT
Pentoxifylline (Ptx) (1-/5-oxohexyl)-3,7-dimethylxantine) has been widely used for the treatment of chronic occlusive arterial disease because of its rheological action. The effectiveness of this drug has been attributed to its influence on erythrocyte deformability, platelet reactivity and plasma viscosity, and prostacycline release (1). Like other methylxanthines, Ptx inhibits phosphodiesterase, resulting in a significant increase of intracellular cyclic adenosine monophosphate (cAMP), which is known to modulate a number of cellular immune functions (2,3). It has been reported that Ptx is able to inhibit inflammatory processes including phagocytosis and superoxide anion and nitric oxide (NO) production by polymorphonuclear granulocytes and monocytes (4,5). This drug has also been reported to affect T lymphocytes by modulating production of various cytokines involved in immune and autoimmune reactions (6-9). Recently, the immunomodulating effects of Ptx were investigated in a randomized double-blind study comparing Ptx with placebo in 140 patients receiving cadaveric kidney grafts under cyclosporine and prednisolone treatment. Ptx weakened the consequences of rejection on graft survival and this phenomenon was mediated by reduction of tumor necrosis factor α (TNF-α) in sera of patients receiving transplants (10-12). Furthermore, Ptx influenced cytokine-induced fibroblast proliferation. Ptx exerted a robust inhibitory effect on fibroblast proliferation, extracellular matrix synthesis, and myofibroblast differentiation (13).
