“…Moreover, CA125 was associated with increased 6-month mortality independently of evidence of fluid overload, leading us to conclude that in addition of being a surrogate for systemic fluid congestion, its elevation may also be an indication for its involvement in other pathogenic processes. Turgut et al, in a recent letter [8], proposed that increased ventricular wall stress with concomitant overexpression of some cytokines would lead to an increased secretion of CA125 by mesothelial cells. Within the same line of thinking, Kosar et al reported in a case-control study, that CA125 was highly correlated with tumour necrosis factor (TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10) in 35 hospitalized HF patients with left ventricular systolic dysfunction [9].…”