@article{MTMT:34784014,
	title = {A felső végtagok mélyvénás thrombosisának diagnosztikája és akut ellátása},
	url = {https://m2.mtmt.hu/api/publication/34784014},
	author = {Kerekes, György and Kovács, Beáta},
	doi = {10.33616/lam.34.0101},
	journal-iso = {LEGE ART MED},
	journal = {LEGE ARTIS MEDICINAE},
	volume = {34},
	unique-id = {34784014},
	issn = {0866-4811},
	abstract = {A felső végtagot érintő mélyvénás thrombosisok a vénás thromboemboliás betegségek szerény hányadát teszik ki, így az orvosi köztudatnak nem képezi szerves részét ezek patofiziológiai alapokon nyugvó speciális kezelése. Az összefoglaló közleményben ismertetésre kerülnek a betegség patofiziológiájának részletei, melyek alapján a kezelés szempontjából fontos szubcsoportok kialakítására van lehetőség. A diagnosztikus lehetőségek bemutatását követően részletesen kitér a közlemény a szubcsoport specifikus ellátási lehetőségeire, algoritmusszerûen kerül bemutatásra a fenti betegcsoportok akut ellátási sémája. Remény szerint ezen információk birtokában javítható a mellkaskimeneti szindrómán alapuló felső végtagi mélyvénás thrombosisban szenvedő betegek ellátásszervezése, mely egyre több megfelelő funkcionális állapotú felső végtagban, akár professzionális sportkarrierek eredményes folytatásában is megnyilvánulhat. Mind a centrális vénás kanülökhöz, mind a pacemaker-elektródákhoz társuló felső végtagi vénás thromboemboliás események is bemutatásra kerülnek az eszközök fenntartási igényének, az antikoaguláció és a vénás keringés szempontjainak is a figyelembevételével.},
	year = {2024},
	eissn = {2063-4161},
	pages = {101-109}
}

@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:34441246,
	title = {Elevated level of serum human epididymis protein 4 (HE4) predicts disease severity and mortality in COVID-19 pneumonia},
	url = {https://m2.mtmt.hu/api/publication/34441246},
	author = {Sütő, Renáta and Pócsi, Marianna and Szabó, Zsolt and Fejes, Zsolt and Ivády, Gergely and Kerekes, György and Fagyas, Miklós and Nagy, Attila Csaba and Szentkereszty, Zoltán and Kappelmayer, János and Nagy, Béla},
	doi = {10.1186/s12890-023-02811-y},
	journal-iso = {BMC PULM MED},
	journal = {BMC PULMONARY MEDICINE},
	volume = {23},
	unique-id = {34441246},
	issn = {1471-2466},
	year = {2023},
	eissn = {1471-2466},
	orcid-numbers = {Nagy, Attila Csaba/0000-0002-0554-7350}
}

@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:34185575,
	title = {Effect of tofacitinib therapy on angiotensin converting enzyme activity in rheumatoid arthritis},
	url = {https://m2.mtmt.hu/api/publication/34185575},
	author = {Kacsándi, Dorottya and Fagyas, Miklós and Horváth, Ágnes and Végh, Edit and Pusztai, Anita and Czókolyová, Monika and Soós, Boglárka and Szabó, Attila Ádám and Hamar, Attila and Pethő, Zsófia and Bodnár, Nóra and Kerekes, György and Hodosi, Katalin and Szamosi, Szilvia and Szűcs, Gabriella and Papp, Zoltán and Szekanecz, Zoltán},
	doi = {10.3389/fmed.2023.1226760},
	journal-iso = {FRONT MED},
	journal = {FRONTIERS IN MEDICINE},
	volume = {10},
	unique-id = {34185575},
	year = {2023},
	eissn = {2296-858X}
}

@article{MTMT:34129873,
	title = {One step back from bedside to the bench - How do different arterial stiffness parameters behave in relation to peripheral resistance?},
	url = {https://m2.mtmt.hu/api/publication/34129873},
	author = {Nóra, Obajed Al-Ali and Sára, Rebeka Tóth and Váróczy, László and Pinczés, László Imre and Soltész, Pál and Szekanecz, Zoltán and Kerekes, György},
	doi = {10.3390/diagnostics13182897},
	journal-iso = {DIAGNOSTICS},
	journal = {DIAGNOSTICS},
	volume = {13},
	unique-id = {34129873},
	issn = {2075-4418},
	year = {2023},
	eissn = {2075-4418},
	orcid-numbers = {Pinczés, László Imre/0000-0003-0453-1709}
}

@article{MTMT:34084596,
	title = {Atherosclerosis in autoimmune rheumatic diseases},
	url = {https://m2.mtmt.hu/api/publication/34084596},
	author = {Szekanecz, Zoltán and Kerekes, György and Shoenfeld, Yehuda},
	doi = {10.1016/j.ejim.2023.07.032},
	journal-iso = {EUR J INTERNAL MED},
	journal = {EUROPEAN JOURNAL OF INTERNAL MEDICINE},
	volume = {115},
	unique-id = {34084596},
	issn = {0953-6205},
	year = {2023},
	eissn = {1879-0828},
	pages = {46-47}
}

@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}
}