Background Chronic inflammation might be involved in the pathogenesis of different types of pulmonary hypertension (PH) . Serum amyloid A (SAA) is an evolutionarily conserved, inflammatory protein expressed in the liver in a manner analogous to that of C-reactive protein (CRP). SAA is also expressed by several extrahepatic cells, including vascular smooth muscle, macrophages and endothelial cells in response to different stimuli, such as interleukin 6 (IL-6) . Data on potential roles of SAA in PH are scarce. We recently reported that increased SAA is associated with pulmonary arterial hypertension (PAH) in patients with systemic sclerosis . Furthermore, children with idiopathic PAH experiencing non-response to specific drugs and a worse prognosis, had significantly elevated SAA .
Objectives To check associations of SAA with CRP, IL-6 and noninvasive markers of disease severity in PH referral patients.
Methods Seventy five consecutive patients were evaluated in the PH out-patient clinic within one year. Serum SAA and CRP were measured by nephelometry and IL-6 by routine ELISA. Markers of PH severity were evaluated with serum troponin I (TnI), N-terminal pro-B-type natriuretic peptide (NTproBNP), tricuspid annular plane systolic excursion (TAPSE), cardiac index (CI) and systolic pulmonary arterial pressure (sPAP), as assessed by routine echocardiography, and the six minute walk test (6MWT) in the whole group of patients, as well as in subgroups of 60 patients with PAH specifically, group I (n=17) or IV (n=43) according to WHO classification.
Results Within the whole group of 75 PH patients (64% females, 36% males, mean age 63, range 29-89 years), we found significant correlations of SAA with CRP, diffusing capacity for CO, TnI (r=0.75, r=-0.36, r=0.23, respectively, all p<0.05) and NTproBNP (0.23, p=0.057). In the subgroup of patients with PAH type IV, SAA strongly correlated with CRP, IL-6, TnI, NTproBNP (r=0.93, r=0.53, r=0.91, r=0.90, respectively, all p<0.000), as well as with sPAP (r=0.39, p=0.03), while in patient subgroup PAH type I, SAA correlations were less strong. No significant correlations were found between SAA and CI, TAPSE or 6MWT, either in the whole patient group or in the subgroups.
Conclusions We showed for the first time, that SAA is associated with markers of chronic inflammation and disease severity in unselected adult patients with PH. In subgroup PAH type IV, where increased SAA might indicate non-responsiveness to specific drugs and worse prognosis, this association is even stronger. These new findings are pending further evaluation.
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Disclosure of Interest None declared