Specifici markers di infiammazione sistemica in pazienti con Scompenso cardiaco o Broncopneumopatia cronica ostruttiva

INTRODUCTION: Chronic Heart failure (CHF) and Chronic obstructive pulmonary disease (COPD) are widespread diseases that often relate to smoking history and age. Low-grade systemic inflammation is considered a possible pathogenic mechanism common to both conditions. AIMS: To investigate whether specific inflammation mediators, both known (hs-CRP and IL-1β) and the less known [soluble form receptor for advanced glycation end product (sRAGE), advanced glycation end product (AGE), N-(carboxymethyl) lysine (CML), pentraxin 3 and soluble IL-1 receptor (SIL - 1RII)] are involved in these two diseases. MATERIALS AND METHODS: In order to evaluate the AGE/RAGE system patients aged 50 years or older and with a ≥ 10 packs-years, with COPD diagnosis (n=70) or CHF (n=124) were recruited. Moreover, in order to evaluate the expression of the putative markers Hs-CRP, PTX3, IL- 1β, SIL-1RII, 143 patients aged 65 years or older were recruited and divided into five groups: 58 with CHF, 23 with COPD, 27 with CHF+COPD and 35 controls (17 healthy smokers and 18 healthy non-smokers). Diabetic subjects were excluded from both populations. All patients underwent routine echocardiography, brain natriuretic peptide dosage (NT-proBNP), spirometry tests and blood sampling. sRAGE, CML, Hs-CRP, PTX3, IL- 1β and SIL-1RII plasma levels were determined using an enzyme-linked immunosorbent assay test (ELISA). RESULTS: CHF subjects, but not COPD subjects, had higher sRAGE and CML plasma levels compared to controls [sRAGE:0,48 ( 0,37-0,83) vs 0,42(0,29-0,52) ng/mL, p=0.0; CML:1,95(1,58-2,38) vs 1.68 (1,43-2,00) ng/mL, p=0,01]. NT-pro-BNP, diagnostic and prognostic CHF Specifici markers di infiammazione in pazienti con SC e BPCO 3 marker, positively correlated to sRAGe, but not to CML, in all patients. Nevertheless COPD subjects showed increased Hs -CRP, IL- 1β, and sIL-1RII plasma levels compared to CHF patients and controls(p<0.05). CONCLUSIONS: These data support the hypothesis for a low-grade systemic inflammation underlying both CHF and COPD. Nevertheless, the expression of specific inflammation-related biomarkers differs in these two conditions. In fact, systemic inflammation involves the AGE/RAGE axis for CHF patients, whereas in COPD patients, both proinflammatory cytokines and their receptors are involved.