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1.

001-es BibID:BIBFORM015816
Első szerző:Gerlag, Danielle M.
Cím:Preclinical and clinical investigation of a CCR5 antagonist, AZD5672, in patients with rheumatoid arthritis receiving methotrexate / Gerlag, D. M., Hollis, S., Layton, M., Vencovsky, J., Szekanecz, Z., Braddock, M., Tak, P. P., The ESCAPE Study Group
Dátum:2010
ISSN:1529-0131 (Electronic)
Megjegyzések:To investigate both the preclinical effects of blocking the chemokine receptor CCR5 and the clinical effects of this approach on the signs and symptoms of rheumatoid arthritis (RA) in patients with active disease. METHODS: Preclinical evaluations of AZD5672, a small-molecule antagonist of CCR5, were performed, including studies of ligand binding and chemotaxis. The pharmacokinetics of AZD5672 were assessed in both single- and multiple-dose studies in healthy volunteers. A randomized, placebo-controlled, phase IIb study was conducted in patients with active RA receiving methotrexate. Treatment arms were AZD5672 (20, 50, 100, or 150 mg orally, once daily), matched placebo, or open-label etanercept (50 mg subcutaneously, once weekly). The primary end point was the proportion of patients achieving a 20% improvement response on the American College of Rheumatology improvement criteria (ACR20) at week 12. Secondary end points included the ACR20 over time, as well as 50% (ACR50) and 70% (ACR70) improvement responses, changes in individual components of the ACR improvement criteria, and disease activity measured with the Disease Activity Score based on the 28-joint count. RESULTS: AZD5672 was a highly potent and selective antagonist of CCR5, displaying nonproportional steady-state pharmacokinetics while inhibiting internalization of CCR5 in an ex vivo macrophage inflammatory protein 1beta stimulation assay in which AZD5672 was evaluated over the 20-150-mg dose range. In the phase IIb study testing this dose range in patients with RA (n = 371 patients randomized to received treatment), AZD5672 was generally well tolerated, with no unexpected adverse events. There was no statistically significant difference in the proportion of patients achieving an ACR20 response at week 12 between those receiving any dose of AZD5672 and those receiving placebo; etanercept was significantly more efficacious than AZD5672 and placebo. CONCLUSION: Despite a clear rationale for targeting CCR5, this clinical study showed that AZD5672, administered orally, did not have any clinical benefit, suggesting that CCR5 antagonism alone is unlikely to be a viable therapeutic strategy in RA.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Antirheumatic Agents/therapeutic use
Arthritis, Rheumatoid/*drug therapy
Benzeneacetamides/*therapeutic use
Chi-Square Distribution
Double-Blind Method
Drug Therapy, Combination
Female
Humans
Male
Methotrexate/*therapeutic use
Receptors, CCR5/*antagonists & inhibitors
Sulfonamides/*therapeutic use
Treatment Outcome
Megjelenés:Arthritis and Rheumatism. - 62 : 11 (2010), p. 3154-3160. -
További szerzők:Hollis, Sally Layton, Mark Vencovsky, Jiri Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Braddock, Martin Tak, Paul P. The ESCAPE Study Group
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2.

001-es BibID:BIBFORM050381
035-os BibID:PMID:23653330
Első szerző:Glant Tibor T.
Cím:Differentially expressed epigenome modifiers, including aurora kinases A and B, in immune cells in rheumatoid arthritis in humans and mouse models / Tibor T. Glant, Timea Besenyei, András Kádár, Júlia Kurkó, Beata Tryniszewska, János Gál, Györgyi Soós, Zoltán Szekanecz, Gyula Hoffmann, Joel A. Block, Robert S. Katz, Katalin Mikecz, Tibor A. Rauch
Dátum:2013
ISSN:0004-3591
Megjegyzések:To identify epigenetic factors that are implicated in the pathogenesis of rheumatoid arthritis (RA), and to explore the therapeutic potential of the targeted inhibition of these factors. METHODS: Polymerase chain reaction (PCR) arrays were used to investigate the expression profile of genes that encode key epigenetic regulator enzymes. Mononuclear cells from RA patients and mice were monitored for gene expression changes, in association with arthritis development in murine models of RA. Selected genes were further characterized by quantitative reverse transcription-PCR, Western blot, and flow cytometry methods. The targeted inhibition of the up-regulated enzymes was studied in arthritic mice. RESULTS: A set of genes with arthritis-specific expression was identified by the PCR arrays. Aurora kinases A and B, both of which were highly expressed in arthritic mice and treatment-naive RA patients, were selected for detailed analysis. Elevated aurora kinase expression was accompanied by increased phosphorylation of histone H3, which promotes proliferation of T lymphocytes. Treatment with VX-680, a pan-aurora kinase inhibitor, promoted B cell apoptosis, provided significant protection against disease onset, and attenuated inflammatory reactions in arthritic mice. CONCLUSION: Arthritis development is accompanied by changes in expression of a number of epigenome-modifying enzymes. Drug-induced down-regulation of the aurora kinases, among other targets, seems to be sufficient to treat experimental arthritis. Development of new therapeutics that target aurora kinases can potentially improve RA management.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
epigenome modifiers
rheumatoid arthritis
Megjelenés:Arthritis and Rheumatism. - 65 : 7 (2013), p. 1725-1735. -
További szerzők:Besenyei Tímea (1980-) (reumatológus, belgyógyász) Kádár András (1977-) (belgyógyász) Kurkó Júlia Emese (1979-) (reumatológus) Tryniszewska Beáta Gál János Soós Györgyike (1959-) (pathológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Hoffmann Gyula Block, Joel A. Katz, Robert S. Mikecz Katalin Rauch Tibor A.
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3.

001-es BibID:BIBFORM046367
Első szerző:Halloran, Margaret M.
Cím:Cellular adhesion molecules in rat adjuvant arthritis / Halloran M. M., Szekanecz Z., Barquin N., Haines G. K., Koch A. E.
Dátum:1996
ISSN:0004-3591
Megjegyzések:To examine adhesion molecule expression during the progression of inflammation in a rheumatoid arthritis model of adjuvant-induced arthritis (AIA) in rats. METHODS: Immunohistochemical analysis was used to determine the distribution of the following adhesion molecules: lymphocyte function-associated antigen 1 (LFA-1; CD11a/CD18), Mac-1 and p150/95 (CD11bc/CD18), intercellular adhesion molecule 1 (ICAM-1), and CD44 in tissue sections from the ankle joints of rats with AIA. Control animals and those with AIA were killed at intervals over a 54-day period after injection with mineral oil and Mycobacterium butyricum, respectively. RESULTS: CD44 and LFA-1 were expressed on lymphocytes, macrophages, and synovial (ST) lining cells. CD44 expression on macrophages was found to be increased compared with control animals by day 18, and was significantly increased by day 41. CD44 expression on lymphocytes significantly increased earlier, on days 11-18. Increased LFA-1 expression on macrophages occurred late, on day 41. LFA-1 expression on lymphocytes was significantly increased on days 25, 47, and 54. ST lining cells exhibited two distinct periods of increased expression, one early, on days 11-25 and one later, on days 41-54. CD11b/c was expressed on macrophages and ST lining cells, showing a significant increase on AIA rat ST lining cells compared with control animals on day 4. No differences in ICAM-1 expression on endothelial cells between rats with AIA and controls were found on any of the days examined. CONCLUSION: CD44 expression is up-regulated on macrophages and lymphocytes during the early development of AIA, while LFA-1 expression is up-regulated later in the development of AIA. The up-regulation of CD44 and LFA-1 at different times in the development of AIA suggests an important role for these adhesion molecules in establishing and sustaining an inflammatory response in the AIA joint.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arthritis and Rheumatism. - 39 : 5 (1996), p. 810-819. -
További szerzők:Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Barquin, Nora Haines, G. Kenneth Koch, Alisa E.
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4.

001-es BibID:BIBFORM105027
035-os BibID:(cikkazonosító)152109 (WoS)001042945400005 (Scopus)85140434684
Első szerző:Hartman, Linda
Cím:Cost-effectiveness and cost-utility of add-on, low-dose prednisolone in patients with rheumatoid arthritis aged 65+ : the pragmatic, multicenter, placebo-controlled GLORIA trial / L. Hartman, M. El Alili, M. Cutolo, D. Opris, J. A. P. Da Silva, Z. Szekanecz, F. Buttgereit, P. Masaryk, R. Bos, M. R. Kok, S. Paolino, V. M. H. Coupè, W. F. Lems, M. Boers, GLORIA consortium
Dátum:2022
ISSN:0049-0172
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Seminars In Arthritis And Rheumatism. - 57 (2022), p. 1-8. -
További szerzők:El Alili, M. Cutolo, Maurizio Opris, Daniela (1976-) (reumatológus) Da Silva, J. A. P. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Buttgereit, Frank Masaryk, Pavol Bos, Reinhard Kok, Marc R. Paolino, Sabrina Coupé, V. M. H. Lems, Willem F. Boers, Maarten GLORIA Trial consortium
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DOI
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5.

001-es BibID:BIBFORM102339
Első szerző:Kerekes György (belgyógyász, kardiológus, angiológus)
Cím:Adalimumab improves endothelial function and microcirculation in rheumatoid arthritis as determined by simultaneous assessment of brachial artery flow-mediated vasodilation and laser Doppler flowmetry / G. Kerekes, V. Pongrácz, O. Timár, Z. Csiki, P. Soltész, Z. Szekanecz
Dátum:2011
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Arthritis and rheumatism. - 63 : 10 (2011), p. S74. -
További szerzők:Pongrácz Vanda Tímár Orsolya (1980-) (belgyógyász) Csiki Zoltán (1962-) (belgyógyász, allergológus, klinikai immunológus, reumatológus) Soltész Pál (1961-) (belgyógyász, kardiológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
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6.

001-es BibID:BIBFORM033048
Első szerző:Kerekes György (belgyógyász, kardiológus, angiológus)
Cím:Adalimumab improves endothelial function and microcirculation in rheumatoid arthritisas determined by simultaneous assessment of brachial artery flow-mediated vasodilation and laser doppler flowmetry / György Kerekes, Vanda Pongrácz, Szilvia Szamosi, Gabriella Szücs, Andrea Váncsa, Orsolya Tímár, Zoltán Csiki, Edit Végh, Pál Soltész, Zoltan Szekanecz
Dátum:2011
ISSN:0004-3591
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:Arthritis and rheumatism. - 63 : 10 (2011), p. S74. -
További szerzők:Pongrácz Vanda Szamosi Szilvia (1975-) (belgyógyász, reumatológus) Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Váncsa Andrea (1972-) (orvos) Tímár Orsolya (1980-) (belgyógyász) Csiki Zoltán (1962-) (belgyógyász, allergológus, klinikai immunológus, reumatológus) Végh Edit (1978-) (reumatológus, belgyógyász) Soltész Pál (1961-) (belgyógyász, kardiológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM035348
Első szerző:Lakos Gabriella (laboratóriumi szakorvos, transzfúziológus, immunológus)
Cím:Anti-cyclic citrullinated peptide antibody isotypes in rheumatoid arthritis : association with disease duration, rheumatoid factor production and the presence of the shared epitope / Gabriella Lakos, Lilla Soós, Andrea Fekete, Zoltán Szabó, Margit Zeher, Ildikó F. Horváth, Katalin Dankó, Anikó Kapitány, Ágnes Gyetvai, Gyula Szegedi, Zoltán Szekanecz
Dátum:2007
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
egyetemen (Magyarországon) készült közlemény
Megjelenés:Arthritis and Rheumatism. Supplement. - 56 : 9 (2007), p. S438. -
További szerzők:Soós Lilla Fekete Andrea (immunológus) Szabó Zoltán (1970-) (belgyógyász, reumatológus) Zeher Margit (1957-2018) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Horváth Ildikó Fanny (1980-) (belgyógyász, allergológus, klinikai immunológus) Dankó Katalin (1952-2021) (belgyógyász, allergológus és klinikai immunológus) Kapitány Anikó (1979-) (molekuláris biológus) Gyetvai Ágnes Szegedi Gyula (1936-2013) (belgyógyász, immunológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
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8.

001-es BibID:BIBFORM007088
Első szerző:Szabó Zoltán (belgyógyász, reumatológus)
Cím:Genetic control of experimental spondylarthropathy / Szabo, Z., Szanto, S., Vegvari, A., Szekanecz, Z., Mikecz, K., Glant, T. T.
Dátum:2005
ISSN:0004-3591 (Print)
Megjegyzések:To characterize experimentally induced spondylarthropathy (SpA) in arthritis-susceptible inbred mice and in their F(1) and F(2) hybrid generations of susceptible and resistant mouse strains. METHODS: SpA was induced in susceptible BALB/c and C3H/HeJCr (C3H) strains of mice, and in their F(1) and F(2) generations derived from intercrosses with arthritis- and/or spondylitis-resistant DBA/2 and DBA/1 parent strains, by systemic immunization with cartilage proteoglycan (PG) aggrecan. The incidence and severity of PG-induced spondylitis (PGIS) were scored histologically, and these scores for spine involvement were correlated with serum antibody and cytokine levels and with in vitro T cell responses to cartilage PG. RESULTS: PGIS was induced by systemic immunization with cartilage PG in adjuvant, and approximately 60-70% of susceptible mouse strains and their F(2) hybrids developed spondylitis either with or without arthritis. Adjuvants, particularly those activating the innate immune system and enforcing the Th1 dominance, had significant effects on the outcome and progression of SpA. The DBA/1 strain appeared to carry genes protecting this strain and its F(1) and F(2) hybrids from spondylitis, whereas the DBA/2 strain, although resistant to PGIS, harbored genes permitting PGIS in its hybrid generations. Arthritis- and/or spondylitis-susceptible BALB/c and C3H parent strains and their F(2) hybrids exhibited the highest incidence and severity of spondylitis. CONCLUSION: PGIS, a murine model of autoimmune spondylitis, shows similarities to ankylosing spondylitis. Segregation of susceptibility to PG-induced arthritis (PGIA) from that to PGIS in different genetic crosses suggests that PGIA and PGIS are separate diseases. Therefore, this model allows for the elucidation of genetic components involved in the etiology of SpA, independent of those controlling the susceptibility to PGIA.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Aggrecans
Animals
Arthritis
Extracellular Matrix Proteins
Female
Genetic Predisposition to Disease
Hybridization, Genetic
Incidence
Lectins, C-Type
Male
Mice
Mice, Inbred Strains
Proteoglycans
Severity of Illness Index
Species Specificity
Spondylarthropathies
Megjelenés:Arthritis and Rheumatism. - 52 : 8 (2005), p. 2452-2460. -
További szerzők:Szántó Sándor (1968-) (belgyógyász, reumatológus) Végvári Anikó (belgyógyász, III. sz. Belgyógyászati Klinika) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Mikecz Katalin Glant Tibor T.
Internet cím:elektronikus változat
DOI
elektronikus változat
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9.

001-es BibID:BIBFORM046369
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Differential distribution of intercellular adhesion molecules (ICAM-1, ICAM-2, and ICAM-3) and the MS-1 antigen in normal and diseased human synovia : their possible pathogenetic and clinical significance in rheumatoid arthritis / Szekanecz Z., Haines G. K., Lin T. R., Harlow L. A., Goerdt S., Rayan G., Koch A. E.
Dátum:1994
ISSN:0004-3591
Megjegyzések:Cellular adhesion and differentiation molecules (CAMs) may play a role in the recruitment and retention of inflammatory cells into rheumatoid arthritis synovial tissue (RA ST). In order to determine if certain CAMs are up-regulated in RA ST compared with normal ST, we studied the distribution of intercellular adhesion molecules (ICAMs) 1, 2, and 3 in ST. We also studied the MS-1 antigen since it is preferentially expressed on discontinuous endothelia, such as those found in RA ST; MS-1 is also expressed differentially upon cytokine activation of cells in vitro or in pathologic conditions in situ. Thus, we postulated a possible similarity between MS-1 and ICAM-1 expression in inflamed ST. METHODS. Immunohistochemical analysis was used to determine the distribution of ICAMs and MS-1 in ST from 10 patients with RA, 10 with osteoarthritis (OA), and 4 normal individuals. RESULTS. ICAM-1 expression was found on significantly more RA ST endothelial cells compared with normal cells, as well as on RA ST macrophages and lining cells. ICAM-2, also found on endothelial cells, showed no differential staining pattern. ICAM-3 was present on RA ST macrophages and lining cells as well as on some RA and OA endothelial cells. The MS-1 antigen was present on most RA and OA ST endothelia, lining cells, and macrophages. ICAM-1 expression and MS-1 expression in the lining layer were positively correlated in both RA and OA. CONCLUSION. ICAM-1, while found mainly on endothelial cells, is up-regulated on RA ST macrophages and lining cells, suggesting a role for these cells in the infiltration and tissue damage seen in the RA ST. ICAM-3, which is present mainly on normal resting leukocytes but not on normal endothelium, is expressed by some diseased ST leukocytes and endothelial cells. MS-1 is also found on the RA ST specialized, fenestrated endothelium, on macrophages, and in the lining layer. These results suggest that the differential expression of ICAMs and MS-1 in RA ST compared with normal ST might play a special role in the pathogenesis of RA.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arthritis and Rheumatism. - 37 : 2 (1994), p. 221-231. -
További szerzők:Haines, G. Kenneth Lin, Theodore R. Harlow, Lisa A. Goerdt, Sergij Rayan, Ghazi Koch, Alisa E.
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10.

001-es BibID:BIBFORM035341
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Disturbancies in T and B cell homeostasis are associated with disease duration and disease-specific autoantibody levels in rheumatoid arthritis / Zoltán Szekanecz, Andrea Fekete, Lilla Soós, Zoltán Szabó, Peter Szodoray, Sándor Baráth, Gabriella Lakos
Dátum:2007
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
egyetemen (Magyarországon) készült közlemény
Megjelenés:Arthritis and Rheumatism. Supplement. - 56 : 9 (2007), p. S760. -
További szerzők:Fekete Andrea (immunológus) Soós Lilla Szabó Zoltán (1970-) (belgyógyász, reumatológus) Szodoray Péter (1973-) (belgyógyász, orvos) Baráth Sándor (1977-) (biológus) Lakos Gabriella (1963-) (laboratóriumi szakorvos, transzfúziológus, immunológus)
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11.

001-es BibID:BIBFORM007107
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis / Szekanecz, Z., Halloran, M. M., Volin, M. V., Woods, J. M., Strieter, R. M., Kenneth Haines, G. 3rd, Kunkel, S. L., Burdick, M. D., Koch, A. E.
Dátum:2000
ISSN:0004-3591 (Print)
Megjegyzések:To examine cytokine and chemokine production during the evolution of rat adjuvant-induced arthritis (AIA), a model of rheumatoid arthritis. METHODS: Clinical and laboratory assessment of the course of AIA was performed over a 47-day period. Levels of the cytokines tumor necrosis factor a (TNFalpha), interleukin-1beta (IL-1beta), and IL-6, as well as levels of the chemokines macrophage inflammatory protein 1alpha (MIP-1alpha) and JE, the murine homolog of monocyte chemoattractant protein 1, were determined by enzyme-linked immunosorbent assay in the sera and joints of AIA and control rats. Synovia from AIA rats were (immuno)histochemically analyzed. Results of cytokine and chemokine measurements were correlated with clinical and laboratory markers of inflammation and histology. RESULTS: Early (before day 14 post adjuvant injection) and later phases of AIA could be distinguished. Cytokine and chemokine production was increased in AIA versus control rats. The production of TNFalpha, IL-1beta, MIP-1alpha, and, as determined earlier, epithelial neutrophil-activating peptide 78-like protein was abundant prior to and during the course of AIA, while that of IL-6 and JE was elevated in the late phase of AIA. Cytokine and chemokine levels were correlated with the clinical symptoms of arthritis and blood neutrophil counts. Joint levels of IL-1beta showed correlation with synovial lining proliferation and neutrophil ingress into AIA synovium. CONCLUSION: Cytokines and chemokines are involved in the clinical, laboratory, and histologic changes underlying AIA. The production of these mediators may be temporally and spatially regulated. These findings may be important for the optimal timing of cytokine and chemokine targeting.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Animals
Arthritis, Experimental
Chemokines
Cytokines
Enzyme-Linked Immunosorbent Assay
Female
Inflammation Mediators
Joints
Kinetics
Rats
Rats, Inbred Lew
Reference Values
Synovitis
Time Factors
Megjelenés:Arthritis and Rheumatism. - 43 : 6 (2000), p. 1266-1277. -
További szerzők:Halloran, Margaret M. Volin, Michael V. Woods, James M. Strieter, Robert M. Haines, Kenneth G. III. Kunkel, Steven L. Burdick, Marie D. Koch, Alisa E.
Internet cím:elektronikus változat
elektronikus változat
Szerző által megadott URL
DOI
Borító:

12.

001-es BibID:BIBFORM033046
Első szerző:Szentpétery Ágnes (reumatológus)
Cím:Circulating mediators of bone remodelling in patients with psoriatic and rheumatoid arthritis treated with anti-tnf-alpha therapy / Agnes Szentpetery, Harjit P. Bhattoa, Peter Antal-Szalmas, Zoltan Szekanecz, Oliver M. FitzGerald
Dátum:2011
ISSN:0004-3591
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
egyetemen (Magyarországon) készült közlemény
Megjelenés:Arthritis and rheumatism. - 63 : 10 (2011), p. S200. -
További szerzők:Bhattoa Harjit Pal (1973-) (laboratóriumi szakorvos) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) FitzGerald, Oliver
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