@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: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}
}

@article{MTMT:32440947,
	title = {Associations of vascular and bone status in arthritis patients},
	url = {https://m2.mtmt.hu/api/publication/32440947},
	author = {Karancsiné Pusztai, Anita and Hamar, Attila and Czókolyová, Monika and Gulyás, Katalin and Horváth, Ágnes and Vegh, Edit and Pethő, Zsófia and Szamosi, Szilvia and Balogh, Emese and Bodnár, Nóra and Bodoki, Levente and Szentpetery, Agnes and Bhattoa Harjit, Pál and Kerekes, György and Juhász, Balázs and Szekanecz, Éva and Hodosi, Katalin and Domjan, Andrea and Szántó, Sándor Zoltán and Raterman, Hennie G. and Lems, Willem F. and Szekanecz, Zoltán and Szűcs, Gabriella},
	doi = {10.1038/s41598-021-99071-9},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {11},
	unique-id = {32440947},
	issn = {2045-2322},
	abstract = {Cardiovascular (CV) disease and osteoporosis (OP) have been associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Bone and vascular biomarkers and parameters along with the effect of 1-year anti-TNF therapy on these markers were assessed in order to determine correlations between vascular pathophysiology and bone metabolism in RA and AS. Thirty-six patients treated with etanercept or certolizumab pegol and 17 AS patients treated with ETN were included in a 12-month follow-up study. Bone and vascular markers were previously assessed by ELISA. Bone density was measured by DXA and quantitative CT (QCT). Flow-mediated vasodilation (FMD), common carotid intima-media thickness (IMT) and pulse-wave velocity (PWV) were assessed by ultrasound. Multiple correlation analyses indicated associations between bone and vascular markers. Osteoprotegerin, sclerostin and cathepsin K were significantly associated with FMD, IMT and PWV, respectively (p < 0.05). Moreover, total and trabecular BMD determined by QCT inversely correlated with IMT (p < 0.05). On the other hand, among vascular parameters, platelet-derived growth factor BB and IMT correlated with DXA femoral and QCT total BMD, respectively (p < 0.05). In the RM-ANOVA analysis, anti-TNF treatment together with baseline osteocalcin, procollagen 1 N-terminal propeptide (P1NP) or vitamin D3 levels determined one-year changes in IMT (p < 0.05). In the MANOVA analysis, baseline disease activity indices (DAS28, BASDAI), the one-year changes in these indices, as well as CRP exerted effects on multiple correlations between bone and vascular markers (p < 0.05). As the pattern of interactions between bone and vascular biomarkers differed between baseline and after 12 months, anti-TNF therapy influenced these associations. We found a great number of correlations in our RA and AS patients undergoing anti-TNF therapy. Some of the bone markers have been associated with vascular pathophysiology, while some vascular markers correlated with bone status. In arthritis, systemic inflammation and disease activity may drive both vascular and bone disease.},
	year = {2021},
	eissn = {2045-2322},
	orcid-numbers = {Bhattoa Harjit, Pál/0000-0002-4909-0065; Szántó, Sándor Zoltán/0000-0001-5030-6292}
}

@article{MTMT:32274642,
	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/32274642},
	author = {Juhász, Balázs and Gulyás, Katalin and Horvath, Agnes and Vegh, Edit and Karancsiné Pusztai, Anita and Szentpetery, Agnes and Pethő, Zsófia and Bodnár, Nóra and Hamar, Attila and Bodoki, Levente and Bhattoa Harjit, Pál and Szekanecz, Éva and Hodosi, Katalin and Domjan, Andrea and Szamosi, Szilvia and Horváth, Csaba and Szántó, Sándor Zoltán and Szűcs, Gabriella and Raterman, Hennie G. and Lems, Willem F. and FitzGerald, Oliver and Szekanecz, Zoltán},
	doi = {10.1186/s12891-021-04708-5},
	journal-iso = {BMC MUSCULOSKEL DIS},
	journal = {BMC MUSCULOSKELETAL DISORDERS},
	volume = {22},
	unique-id = {32274642},
	issn = {1471-2474},
	abstract = {Introduction Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are associated with osteoporosis. There have not been many peripheral quantitative computed tomography (QCT) studies in patients receiving biologics. We assessed volumetric and areal bone mineral density (BMD) by forearm QCT and dual-energy X-ray absorptiometry (DXA), respectively in addition to laboratory biomarkers in these arthritides. Methods Forty RA and AS patients treated with either etanercept (ETN) or certolizumab pegol (CZP) were undergoing follow-ups for one year. Volumetric and areal BMD, as well as parathyroid hormone (PTH), osteocalcin, RANKL, 25-hydroxyvitamin D (VITD), P1NP, CTX, sclerostin (SOST), Dickkopf 1 (DKK-1) and cathepsin K (CATHK) were determined. Results We did not observe any further bone loss during the 12-month treatment period. Volumetric and areal BMD showed significant correlations with each other (p<0.017 after Bonferroni's correction). Trabecular QCT BMD at baseline (p=0.015) and cortical QCT BMD after 12 months (p=0.005) were inversely determined by disease activity at baseline in the full cohort. Trabecular QCT BMD at baseline also correlated with CTX (p=0.011). In RA, CRP negatively (p=0.014), while SOST positively (p=0.013) correlated with different QCT parameters. In AS, RANKL at baseline (p=0.014) and after 12 months (p=0.007) correlated with cortical QCT BMD. In the full cohort, 12-month change in QTRABBMD was related to TNF inhibition together with elevated VITD-0 levels (p=0.031). Treatment and lower CATHK correlated with QCORTBMD changes (p=0.006). In RA, TNF inhibition together with VITD-0 (p<0.01) or CATHK-0 (p=0.002), while in AS, treatment and RANKL-0 (p<0.05) determined one-year changes in QCT BMD. Conclusions BMD as determined by QCT did not change over one year of anti-TNF treatment. Disease activity, CATHK, RANKL and VITD may be associated with the effects of anti-TNF treatment on QCT BMD changes. RA and AS may differ in this respect.},
	keywords = {Bone Density; osteoporosis; rheumatoid arthritis; ankylosing spondylitis; Biologics; Peripheral quantitative computed tomography},
	year = {2021},
	eissn = {1471-2474},
	orcid-numbers = {Bhattoa Harjit, Pál/0000-0002-4909-0065; Horváth, Csaba/0000-0002-0490-7932; Szántó, Sándor Zoltán/0000-0001-5030-6292}
}

@article{MTMT:31878487,
	title = {Effects of one-year tofacitinib therapy on bone metabolism in rheumatoid arthritis},
	url = {https://m2.mtmt.hu/api/publication/31878487},
	author = {Hamar, Attila and Szekanecz, Zoltán and Karancsiné Pusztai, Anita and Czókolyová, Monika and Végh, E. and Pethő, Zoltán Dénes and Bodnár, Nóra and Gulyás, Katalin and Horváth, Á. and Soós, B. and Bodoki, Levente and Bhattoa Harjit, Pál and Nagy, Gábor and Tajti, Gábor and Panyi, György and Szekanecz, Éva and Domján, A. and Hodosi, K. and Szántó, Sándor Zoltán and Szűcs, Gabriella and Szamosi, Szilvia},
	doi = {10.1007/s00198-021-05871-0},
	journal-iso = {OSTEOPOROSIS INT},
	journal = {OSTEOPOROSIS INTERNATIONAL},
	volume = {32},
	unique-id = {31878487},
	issn = {0937-941X},
	year = {2021},
	eissn = {1433-2965},
	pages = {1621-1629},
	orcid-numbers = {Bhattoa Harjit, Pál/0000-0002-4909-0065; Nagy, Gábor/0000-0002-2943-2750; Panyi, György/0000-0001-6227-3301; Szántó, Sándor Zoltán/0000-0001-5030-6292}
}

@article{MTMT:31789607,
	title = {Soluble vascular biomarkers in rheumatoid arthritis and ankylosing spondylitis: effects of one-year anti-TNF-α therapy},
	url = {https://m2.mtmt.hu/api/publication/31789607},
	author = {Karancsiné Pusztai, Anita and Hamar, Attila and Horváth, Ágnes and Gulyás, Katalin and Végh, Edit and Bodnár, Nóra and Kerekes, György and Czókolyová, Monika and Bodoki, Levente and Hodosi, Katalin and Domján, Andrea and Nagy, Gábor and Szöllősi, Ibolya and Lopez, Luis R. and Matsuura, Eiji and Prohászka, Zoltán and Szántó, Sándor Zoltán and Szűcs, Gabriella and Nagy, Zoltán and Shoenfeld, Yehuda and Szekanecz, Zoltán and Szamosi, Szilvia},
	doi = {10.3899/jrheum.200916},
	journal-iso = {J RHEUMATOL},
	journal = {JOURNAL OF RHEUMATOLOGY},
	volume = {48},
	unique-id = {31789607},
	issn = {0315-162X},
	abstract = {Objective. Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with cardiovascular disease. The treatment of arthritis by tumor necrosis factor-α (TNF-α) inhibitors may decrease the serum concentrations of vascular biomarkers. We determined circulating levels of oxidized low-density lipoprotein (oxLDL)/β2 glycoprotein I (β2-GPI) complexes, antibodies to 60 kDa heat shock protein (anti-Hsp60), soluble urokinase plasminogen activator receptor (suPAR), and B-type natriuretic peptide (BNP) fragment in sera of RA and AS patients undergoing anti-TNF treatment.
		
		Methods. Fifty-three patients with RA/AS were treated with etanercept or certolizumab pegol for 1 year. Circulating oxLDL/β2-GPI complex (AtherOx), anti-Hsp60 IgG, and BNP8-29 fragment levels were assessed by ELISA. suPAR levels were determined by suPARnostic Quick Triage test. Flow-mediated vasodilation (FMD), carotid intima-media thickness (CIMT), and arterial pulse wave velocity (PWV) were determined by ultrasound.
		
		Results. One-year anti-TNF treatment significantly decreased oxLDL/β2-GPI levels, as well as suPAR levels in patients with critically high suPAR levels at baseline. In RA, BNP levels were higher in seropositive vs seronegative patients. Serum levels of these vascular biomarkers variably correlated with lipids, anticitrullinated protein antibodies, rheumatoid factor, and C-reactive protein. CIMT positively correlated with BNP, and PWV with suPAR and anti-Hsp60, whereas FMD inversely associated with anti-Hsp60. In repeated measures ANOVA analysis, disease activity supported the effects of anti-TNF treatment on 12-month changes in oxLDL/β2-GPI. CIMT supported the effects of therapy on changes in anti-Hsp60 and suPAR.
		
		Conclusion. These biomarkers may be involved in the pathogenesis of atherosclerosis underlying RA/AS. TNF inhibition variably affects the serum levels of oxLDL/β2-GPI, suPAR, and BNP.},
	year = {2021},
	eissn = {1499-2752},
	pages = {821-828},
	orcid-numbers = {Nagy, Gábor/0000-0002-2943-2750; Prohászka, Zoltán/0000-0003-1761-7982; Szántó, Sándor Zoltán/0000-0001-5030-6292}
}

@article{MTMT:32120577,
	title = {Soluble Vascular Biomarkers in Rheumatoid Arthritis and Ankylosing Spondylitis: Effects of One-year Anti-TNF-alpha Therapy},
	url = {https://m2.mtmt.hu/api/publication/32120577},
	author = {Karancsiné Pusztai, Anita and Hamar, Attila and Horvath, Agnes and Gulyás, Katalin and Végh, Edit and Bodnár, Nóra and Kerekes, György and Czókolyová, Monika and Szamosi, Szilvia and Bodoki, Levente and Hodosi, Katalin and Presznerné Domján, Andrea and Nagy, Gabor and Lopez, Luis and Matsuura, Ejii and Prohászka, Zoltán and Szántó, Sándor Zoltán and Nagy, Zoltan and Shoenfeld, Yehuda and Szekanecz, Zoltán and Szűcs, Gabriella},
	journal-iso = {ARTHRITIS RHEUMATOL},
	journal = {ARTHRITIS & RHEUMATOLOGY},
	volume = {72},
	unique-id = {32120577},
	issn = {2326-5191},
	year = {2020},
	eissn = {2326-5205},
	orcid-numbers = {Presznerné Domján, Andrea/0000-0002-1557-2680; Prohászka, Zoltán/0000-0003-1761-7982; Szántó, Sándor Zoltán/0000-0001-5030-6292}
}