@article{MTMT:34745209, title = {Natural Autoantibodies in Biologic-Treated Rheumatoid Arthritis and Ankylosing Spondylitis Patients: Associations with Vascular Pathophysiology}, url = {https://m2.mtmt.hu/api/publication/34745209}, author = {Simon, Diána and Kacsándi, Dorottya and Karancsiné Pusztai, Anita and Soós, Boglárka and Végh, Edit and Kerekes, György and Czókolyová, Monika and Szamosi, Szilvia and Szűcs, Gabriella and Prohászka, Zoltán and Németh, Péter and Berki, Tímea and Szekanecz, Zoltán}, doi = {10.3390/ijms25063429}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {25}, unique-id = {34745209}, issn = {1661-6596}, abstract = {Cardiovascular (CV) morbidity and mortality have been associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Natural autoantibodies (nAAb) are involved in innate immunity, as well as autoimmunity, inflammation, and atherosclerosis. There have not been any studies assessing the effects of biologics on nAAbs in RA and AS, also in relation to vascular pathophysiology. Fifty-three anti-TNF-treated RA and AS patients were included in a 12-month follow-up study. Anti-citrate synthase (CS) and anti-topoisomerase I fragment 4 (TOPO-F4) IgM and IgG levels were determined by ELISA. Ultrasonography was performed to assess brachial artery flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT), and arterial pulse-wave velocity (PWV). Other variables were also evaluated at baseline and 6 and 12 months after treatment initiation. Anti-TNF therapy improved FMD in RA and PWV in AS and stabilized ccIMT. TNF inhibition increased anti-CS IgM and IgG, and possibly also anti-TOPO-F4 IgG levels. Various correlation analyses revealed that nAAbs might be independently involved in autoimmunity as well as changes in inflammation and vascular pathology over time in biologic-treated patients (p < 0.05). We also found associations between anti-TOPO-F4 IgG and anti-Hsp60 IgG (p < 0.05). Baseline nAAb levels or nAAb level changes might determine changes in CRP, disease activity, FMD, PWV, and ccIMT over time (p < 0.05). The interplay between arthritis and inflammatory atherosclerosis, as well as the effects of anti-TNF biologics on these pathologies, might independently involve nAAbs.}, year = {2024}, eissn = {1422-0067}, orcid-numbers = {Prohászka, Zoltán/0000-0003-1761-7982; Berki, Tímea/0000-0002-0134-8127} } @article{MTMT:34775337, title = {AB0237 EFFECTS OF ONE-YEAR TOFACITINIB THERAPY ON ANGIOGENIC BIOMARKERS IN RHEUMATOID ARTHRITIS}, url = {https://m2.mtmt.hu/api/publication/34775337}, author = {Kerekes, György and Bodoki, Levente and Hamar, Attila and Karancsiné Pusztai, Anita and Tajti, Gábor and Katkó, Mónika and Végh, Edit and Pethő, Zsófia and Bodnár, Nóra and Horváth, Ágnes and Soós, B. and Szamosi, Szilvia and Hascsi, Z. and Harangi, Mariann and Panyi, György and Szűcs, Gabriella and Szekanecz, Zoltán}, doi = {10.1136/annrheumdis-2023-eular.2331}, journal-iso = {ANN RHEUM DIS}, journal = {ANNALS OF THE RHEUMATIC DISEASES}, volume = {82}, unique-id = {34775337}, issn = {0003-4967}, year = {2023}, eissn = {1468-2060}, pages = {1303-1303}, orcid-numbers = {Panyi, György/0000-0001-6227-3301} } @article{MTMT:34215318, title = {Effects of 1-year tofacitinib therapy on angiogenic biomarkers in rheumatoid arthritis}, url = {https://m2.mtmt.hu/api/publication/34215318}, author = {Kerekes, György and Czókolyová, Monika and Hamar, Attila and Karancsiné Pusztai, Anita and Tajti, Gábor and Katkó, Mónika and Végh, Edit and Pethő, Zsófia and Bodnár, Nóra and Horváth, Ágnes and Soós, Boglárka and Szamosi, Szilvia and Hascsi, Zsolt and Harangi, Mariann and Hodosi, Katalin and Panyi, György and Seres, Tamás and Szűcs, Gabriella and Szekanecz, Zoltán}, doi = {10.1093/rheumatology/kead502}, journal-iso = {RHEUMATOLOGY}, journal = {RHEUMATOLOGY (UNITED KINGDOM)}, volume = {62}, unique-id = {34215318}, issn = {1462-0324}, year = {2023}, eissn = {1462-0332}, pages = {SI304-SI312}, orcid-numbers = {Panyi, György/0000-0001-6227-3301} } @article{MTMT:33457576, title = {Effects of tofacitinib therapy on arginine and methionine metabolites in association with vascular pathophysiology in rheumatoid arthritis: A metabolomic approach}, url = {https://m2.mtmt.hu/api/publication/33457576}, author = {Soos, Boglarka and Hamar, Attila and Karancsiné Pusztai, Anita and Czókolyová, Monika and Végh, Edit and Szamosi, Szilvia and Pethő, Zsófia and Gulyás, Katalin and Kerekes, György and Szántó, Sándor Zoltán and Szűcs, Gabriella and Christians, Uwe and Klawitter, Jelena and Seres, Tamas and Szekanecz, Zoltán}, doi = {10.3389/fmed.2022.1011734}, journal-iso = {FRONT MED}, journal = {FRONTIERS IN MEDICINE}, volume = {9}, unique-id = {33457576}, abstract = {IntroductionRheumatoid arthritis (RA) has been associated with changes in lipid, arginine and NO metabolism with increased cardiovascular (CV) risk. The aim of this study is to evaluate the effect of tofacitinib, a Janus kinase (JAK) inhibitor, on arginine and methionine metabolism in correlation with inflammation, functional and pathological vascular changes during one-year treatment of patients with RA. Materials and methodsThirty RA patients with active disease were treated with either 5 mg bid or 10 mg bid tofacitinib for 12 months. We determined DAS28, CRP, IgM rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP) levels. We assessed brachial artery flow-mediated vasodilation (FMD), carotid intima-media thickness (IMT) and pulse-wave velocity (PWV) by ultrasound at baseline and after 6 and 12 months. We also determined plasma L-arginine, L-citrulline, L-ornithine, inducible nitric oxide synthase (iNOS), asymmetric (ADMA) and symmetric dimethylarginine (SDMA), L-N-monomethyl-arginine (L-NMMA), cysteine, homocysteine, and methionine levels at these time points. ResultsTwenty-six patients (13 on each arm) completed the study. CRP, ESR and DAS28 decreased significantly during one-year treatment with tofacitinib. Arginine and ADMA showed a negative univariate correlation with CRP but not with FMD, PWV or IMT. Tofacitinib at 10 mg bid significantly increased L-arginine, L-ornithine, iNOS and methionine levels after 12 months. ADMA and SDMA levels did not change in our study. Methionine showed negative correlation with FMD at baseline and positive correlation with PWV after 12 months. No change was observed in FMD and PWV but a significant increase was measured in IMT at 6 and 12 months. Multivariate analysis indicated variable correlations of L-arginine, L-citrulline, ADMA, L-NMMA, homocysteine and methionine with DAS28, CRP, ESR and RF but not with anti-CCP after one-year treatment. With respect to vascular pathophysiology, only PWV and methionine correlated with each other. ConclusionOne-year tofacitinib treatment suppressed systemic inflammation and improved functional status in RA. FMD, PWV have not been affected by one-year tofacitinib treatment., while IMT increased further despite treatment. Increased arginine and methionine might contribute to the anti-inflammatory effects of tofacitinib. Increased arginine availability with no changing ADMA may protect FMD and PWV from deterioration. The increase of IMT in the anti-inflammatory environment cannot be explained by arginine or methionine metabolism in this study.}, keywords = {ATHEROSCLEROSIS; arginine; rheumatoid arthritis; metabolomics; METHIONINE; Tofacitinib}, year = {2022}, eissn = {2296-858X}, orcid-numbers = {Szántó, Sándor Zoltán/0000-0001-5030-6292} } @article{MTMT:33153228, title = {Effects of One-Year Tofacitinib Therapy on Lipids and Adipokines in Association with Vascular Pathophysiology in Rheumatoid Arthritis}, url = {https://m2.mtmt.hu/api/publication/33153228}, author = {Czókolyová, Monika and Hamar, Attila and Karancsiné Pusztai, Anita and Tajti, Gábor and Végh, Edit and Pethő, Zsófia and Bodnár, Nóra and Horváth, Ágnes and Boglárka, Soós and Szamosi, Szilvia and Szentpéteri, Anita and Seres, Ildikó and Harangi, Mariann and Paragh, György and Kerekes, György and Bodoki, Levente and Katalin, Hodosi and Tamás, Seres and Panyi, György and Szekanecz, Zoltán and Szűcs, Gabriella}, doi = {10.3390/biom12101483}, journal-iso = {BIOMOLECULES}, journal = {BIOMOLECULES}, volume = {12}, unique-id = {33153228}, issn = {2218-273X}, abstract = {Background: Cardiovascular (CV) morbidity, mortality and metabolic syndrome are associated with rheumatoid arthritis (RA). A recent trial has suggested increased risk of major CV events (MACE) upon the Janus kinase (JAK) inhibitor tofacitinib compared with anti-tumor necrosis factor α (TNF-α) therapy. In our study, we evaluated lipids and other metabolic markers in relation to vascular function and clinical markers in RA patients undergoing one-year tofacitinib therapy. Patients and methods: Thirty RA patients treated with either 5 mg or 10 mg bid tofacitinib were included in a 12-month follow-up study. Various lipids, paraoxonase (PON1), myeloperoxidase (MPO), thrombospondin-1 (TSP-1) and adipokine levels, such as adiponectin, leptin, resistin, adipsin and chemerin were determined. In order to assess flow-mediated vasodilation (FMD), common carotid intima-media thickness (IMT) and arterial pulse-wave velocity (PWV) ultrasonography were performed. Assessments were carried out at baseline, and 6 and 12 months after initiating treatment. Results: One-year tofacitinib therapy significantly increased TC, HDL, LDL, APOA, APOB, leptin, adipsin and TSP-1, while significantly decreasing Lp(a), chemerin, PON1 and MPO levels. TG, lipid indices (TC/HDL and LDL/HDL), adiponectin and resistin showed no significant changes. Numerous associations were found between lipids, adipokines, clinical markers and IMT, FMD and PWV (p < 0.05). Regression analysis suggested, among others, association of BMI with CRP and PWV (p < 0.05). Adipokines variably correlated with age, BMI, CRP, CCP, FMD, IMT and PWV, while MPO, PON1 and TSP-1 variably correlated with age, disease duration, BMI, RF and PWV (p < 0.05). Conclusions: JAK inhibition by tofacitinib exerts balanced effects on lipids and other metabolic markers in RA. Various correlations may exist between metabolic, clinical parameters and vascular pathophysiology during tofacitinib treatment. Complex assessment of lipids, metabolic factors together with clinical parameters and vascular pathophysiology may be utilized in clinical practice to determine and monitor the CV status of patients in relation with clinical response to JAK inhibition.}, year = {2022}, eissn = {2218-273X}, orcid-numbers = {Panyi, György/0000-0001-6227-3301} } @article{MTMT:32634351, title = {Angiotensin Converting Enzyme Activity in Anti-TNF-Treated Rheumatoid Arthritis and Ankylosing Spondylitis Patients}, url = {https://m2.mtmt.hu/api/publication/32634351}, author = {Soós, Boglárka and Fagyas, Miklós and Horváth, Ágnes and Végh, Edit and Karancsiné Pusztai, Anita and Czókolyová, Monika and Csongrádi, Alexandra and Hamar, Attila and Pethő, Zsófia and Bodnár, Nóra and Kerekes, György and Hodosi, Katalin and Szekanecz, Éva and Szamosi, Szilvia and Szántó, Sándor Zoltán and Szűcs, Gabriella and Papp, Zoltán and Szekanecz, Zoltán}, doi = {10.3389/fmed.2021.785744}, journal-iso = {FRONT MED}, journal = {FRONTIERS IN MEDICINE}, volume = {8}, unique-id = {32634351}, abstract = {Introduction: Angiotensin-converting enzyme (ACE) and ACE2 have been implicated in the regulation of vascular physiology. Elevated synovial and decreased or normal ACE or ACE2 levels have been found in rheumatoid arthritis (RA). Very little is known about the effects of tumor necrosis factor α (TNF-α) inhibition on ACE or ACE2 homeostasis. In this study, we assessed the effects of one-year anti-TNF therapy on ACE and ACE2 production in RA and ankylosing spondylitis (AS) in association with other biomarkers. Patients and Methods: Forty patients including 24 RA patients treated with either etanercept (ETN) or certolizumab pegol (CZP) and 16 AS patients treated with ETN were included in a 12-month follow-up study. Serum ACE levels were determined by commercial ELISA, while serum ACE2 activity was assessed using a specific quenched fluorescent substrate. Ultrasonography was performed to determine flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT) and arterial pulse-wave velocity (PWV) in all patients. In addition, CRP, rheumatoid factor (RF) and ACPA were also measured. All assessments were performed at baseline and 6 and 12 months after treatment initiation. Results: Anti-TNF therapy increased ACE levels in the full cohort, as well as in the RA and AS subsets. ACE2 activity increased in the full cohort, while the ACE/ACE2 ratio increased in the full cohort and in the RA subset (p < 0.05). Uni- and multivariable regression analyses determined associations between ACE or ACE/ACE2 ratios at different time points and disease duration, CRP, RF, FMD and IMT (p < 0.05). ACE2 activity correlated with CRP. The changes of ACE or ACE2 over 12 months were determined by treatment together with either RF or FMD (p < 0.05). Conclusions: Anti-TNF treatment may increase ACE and ACE2 in the sera of RA and AS patients. ACE and ACE2 may be associated with disease duration, markers of inflammation and vascular pathophysiology. The effects of TNF inhibition on ACE and ACE2 may reflect, in part, the effects of these biologics on the cardiovascular system.}, year = {2022}, eissn = {2296-858X}, orcid-numbers = {Szántó, Sándor Zoltán/0000-0001-5030-6292} } @article{MTMT:32575467, title = {Prospective, simultaneous assessment of joint and vascular inflammation by PET/CT in tofacitinib-treated patients with rheumatoid arthritis: associations with vascular and bone status}, url = {https://m2.mtmt.hu/api/publication/32575467}, author = {Hamar, Attila and Hascsi, Zsolt and Karancsiné Pusztai, Anita and Czókolyová, Monika and Végh, Edit and Pethő, Zsófia and Gulyás, Katalin and Soós, Boglárka and Kerekes, György and Szekanecz, Éva and Hódosi, Katalin and Szántó, Sándor Zoltán and Szűcs, Gabriella and Seres, Tamás and Szekanecz, Zoltán and Szamosi, Szilvia}, doi = {10.1136/rmdopen-2021-001804}, journal-iso = {RMD OPEN}, journal = {RMD OPEN}, volume = {7}, unique-id = {32575467}, issn = {2056-5933}, keywords = {rheumatoid arthritis; PET-CT; JAK-gátló}, year = {2021}, eissn = {2056-5933}, pages = {1-10}, orcid-numbers = {Szántó, Sándor Zoltán/0000-0001-5030-6292} } @article{MTMT:32501310, title = {SIMULTANEOUS ASSESSMENT OF JOINT AND VASCULAR INFLAMMATION BY PET-CT IN TOFACITINIB-TREATED PATIENTS WITH RHEUMATOID ARTHRITIS: A PROSPECTIVE STUDY}, url = {https://m2.mtmt.hu/api/publication/32501310}, author = {Hamar, Attila and Hascsi, Z. and Karancsiné Pusztai, Anita and Czókolyová, Monika and Vegh, E. and Pethő, Zsófia and Gulyás, Katalin and Soos, B. and Kerekes, György and Szekanecz, Éva and Hodosi, K. and Szántó, Sándor Zoltán and Szűcs, Gabriella and Seres, T. and Szekanecz, Zoltán and Szamosi, Szilvia}, doi = {10.1136/annrheumdis-2021-eular.2473}, journal-iso = {ANN RHEUM DIS}, journal = {ANNALS OF THE RHEUMATIC DISEASES}, volume = {80}, unique-id = {32501310}, issn = {0003-4967}, year = {2021}, eissn = {1468-2060}, pages = {425-425}, orcid-numbers = {Szántó, Sándor Zoltán/0000-0001-5030-6292} } @article{MTMT:32500463, title = {EFFECTS OF TOFACITINIB THERAPY ON ARGININE AND METHIONINE METABOLITES IN ASSOCIATION WITH VASCULAR PATHOPHYSIOLOGY IN RHEUMATOID ARTHRITIS: A METABOLOMIC APPROACH}, url = {https://m2.mtmt.hu/api/publication/32500463}, author = {Soos, B. and Hamar, Attila and Karancsiné Pusztai, Anita and Czókolyová, Monika and Vegh, E. and Szamosi, Szilvia and Pethő, Zsófia and Gulyás, Katalin and Kerekes, György and Szekanecz, Éva and Szántó, Sándor Zoltán and Szűcs, Gabriella and Christians, U. and Klawitter, J. and Seres, T. and Szekanecz, Zoltán}, doi = {10.1136/annrheumdis-2021-eular.1697}, journal-iso = {ANN RHEUM DIS}, journal = {ANNALS OF THE RHEUMATIC DISEASES}, volume = {80}, unique-id = {32500463}, issn = {0003-4967}, year = {2021}, eissn = {1468-2060}, pages = {421-422}, orcid-numbers = {Szántó, Sándor Zoltán/0000-0001-5030-6292} } @article{MTMT:32499606, title = {Peripheral quantitative computed tomography in the assessment of bone mineral density in anti-TNF-treated rheumatoid arthritis and ankylosing spondylitis patients}, url = {https://m2.mtmt.hu/api/publication/32499606}, author = {Juhász, Balázs and Gulyás, Katalin and Horváth, Á. and Végh, E. and Karancsiné Pusztai, Anita and Szentpetery, A. and Pethő, Zsófia and Bodnár, Nóra and Hamar, Attila and Bodoki, Levente and Bhattoa Harjit, Pál and Szekanecz, Éva and Hodosi, K. and Domjan, A. and Szamosi, Szilvia and Horváth, C. and Szántó, Sándor Zoltán and Szűcs, Gabriella and Raterman, H. and Lems, W. and Fitzgerald, O. and Szekanecz, Zoltán}, doi = {10.1136/annrheumdis-2021-eular.1951}, journal-iso = {ANN RHEUM DIS}, journal = {ANNALS OF THE RHEUMATIC DISEASES}, volume = {80}, unique-id = {32499606}, issn = {0003-4967}, year = {2021}, eissn = {1468-2060}, pages = {226-227}, orcid-numbers = {Bhattoa Harjit, Pál/0000-0002-4909-0065; Szántó, Sándor Zoltán/0000-0001-5030-6292} }