Malgorzata Jasiewicz1, Krzysztof Kowal2, Otylia Kowal-Bielecka3, Malgorzata Knapp4, Roman Skiepko5, Anna Bodzenta-Lukaszyk6, Bozena Sobkowicz7, Wlodzimierz Jerzy Musial8, Karol Adam Kaminski9. 1. Department of Cardiology, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: jasiewiczm@gmail.com. 2. Department of Allergology and Internal Medicine, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: kowalkmd@umb.edu.pl. 3. Department of Rheumatology and Internal Medicine, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: otylia@umb.edu.pl. 4. Department of Cardiology, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: malgo33@interia.pl. 5. Department of Allergology and Internal Medicine, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: roman_skiepko@op.pl. 6. Department of Allergology and Internal Medicine, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: abodzentalukaszyk@gmail.com. 7. Department of Cardiology, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: sobkowic@wp.pl. 8. Department of Cardiology, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: musialwj@wp.pl. 9. Department of Cardiology, Medical University of Bialystok, ul. M. Sklodowskiej-Curie 24 A, 15-276 Bialystok, Poland. Electronic address: fizklin@gmail.com.
Abstract
BACKGROUND: Inflammation may play a pivotal role in the pathogenesis of pulmonary arterial hypertension (PAH). We evaluated the concentrations of serum sTWEAK, its scavenger receptor sCD163 and sTWEAK/sCD163 ratio in patients with PAH. DESIGN: The study enrolled 26 stable patients with PAH confirmed by right heart catheterization and 24 healthy volunteers matched for age, sex and body weight. All patients underwent transthoracic echocardiography, cardiopulmonary exercise test, 6-min walk test, measurement of lung diffusing capacity for the carbon monoxide (DLCO) and venous blood tests. Concentrations of sTWEAK and sCD163 were determined using ELISA kits. RESULTS: The PAH patients were characterized by significantly higher median serum sCD163 levels (1072 vs 890ng/ml, p=0.04) together with lower serum sTWEAK concentrations (200 vs 278.1pg/ml, p=0.003) comparing to control subjects. sTWEAK/sCD163 ratio was therefore significantly lower in PAH group (0.18 vs 0.33, p=0.0005). No correlation was found between sTWEAK and sCD163 concentrations in both groups. We observed statistically significant inverse correlation between peak VO2 consumption and sCD163 concentrations (r=-0.52, p<0.05) and positive with sTWEAK/sCD163 ratio (r=0.45, p<0.05) in PAH group. Moreover, sTWEAK/sCD163 ratio positively correlated with % of predicted values of DLCO (r=0.42, p<0.05). CONCLUSIONS: Patients with PAH present altered serum sTWEAK and sCD163 levels. The sTWEAK/sCD163 ratio appears to be a better indicator of the severity of PAH as compared to sTWEAK or sCD163 alone. The exact role of sCD163 or interaction between CD163 and sTWEAK in the initiation or progression of PAH as well as their potential prognostic significance remains to be established.
BACKGROUND: Inflammation may play a pivotal role in the pathogenesis of pulmonary arterial hypertension (PAH). We evaluated the concentrations of serum sTWEAK, its scavenger receptor sCD163 and sTWEAK/sCD163 ratio in patients with PAH. DESIGN: The study enrolled 26 stable patients with PAH confirmed by right heart catheterization and 24 healthy volunteers matched for age, sex and body weight. All patients underwent transthoracic echocardiography, cardiopulmonary exercise test, 6-min walk test, measurement of lung diffusing capacity for the carbon monoxide (DLCO) and venous blood tests. Concentrations of sTWEAK and sCD163 were determined using ELISA kits. RESULTS: The PAH patients were characterized by significantly higher median serum sCD163 levels (1072 vs 890ng/ml, p=0.04) together with lower serum sTWEAK concentrations (200 vs 278.1pg/ml, p=0.003) comparing to control subjects. sTWEAK/sCD163 ratio was therefore significantly lower in PAH group (0.18 vs 0.33, p=0.0005). No correlation was found between sTWEAK and sCD163 concentrations in both groups. We observed statistically significant inverse correlation between peak VO2 consumption and sCD163 concentrations (r=-0.52, p<0.05) and positive with sTWEAK/sCD163 ratio (r=0.45, p<0.05) in PAH group. Moreover, sTWEAK/sCD163 ratio positively correlated with % of predicted values of DLCO (r=0.42, p<0.05). CONCLUSIONS:Patients with PAH present altered serum sTWEAK and sCD163 levels. The sTWEAK/sCD163 ratio appears to be a better indicator of the severity of PAH as compared to sTWEAK or sCD163 alone. The exact role of sCD163 or interaction between CD163 and sTWEAK in the initiation or progression of PAH as well as their potential prognostic significance remains to be established.
Authors: Hengdao Liu; Dan Lin; Hong Xiang; Wei Chen; Shaoli Zhao; Hui Peng; Jie Yang; Pan Chen; Shuhua Chen; Hongwei Lu Journal: Exp Ther Med Date: 2017-06-14 Impact factor: 2.447
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