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2010 | 5 | 1 | 36-40
Tytuł artykułu

Plasma level of myeloperoxidase in children with juvenile idiopathic arthritis (a pilot study)

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
To examine the plasma levels of MPO in oligoarthritis and polyarthritis subtypes of JIA in comparison with healthy age-matched controls. Thirty-eight JIA patients (25 girls and 13 boys) aged 9.1–11.8 years and 23 healthy controls (8 girls and 15 boys) participated in the study. Twenty-one patients had oligoarthritis (8 with extended oligoarthritis) and 17 had polyarthritis (among them three were seropositive). The plasma concentration of MPO was measured by the ELISA technique (OxisResearchTM, BIOXYTECH® MPO-EIATM, Portland, OR USA). The mean plasma concentration of MPO in the JIA group was significantly higher than in the control group (76.6±24.8 µg/L versus 62.7±15.6 µg/L; p=0.01). Patients with polyarthritis presented a significantly higher mean plasma MPO level than patients with oligoarthritis (81.3±25.6 µg/L and 62.1±27.1 µg/L, respectively; p=0.02). Different subtypes of JIA may have different MPO-related backgrounds. MPO is a new potent inflammatory marker. Patients with polyarthritis have higher mean plasma MPO levels than patients with oligoarthritis and may therefore have an enhanced risk for subclinical oxidative stress-related atherogenic promotion.
Wydawca

Czasopismo
Rocznik
Tom
5
Numer
1
Strony
36-40
Opis fizyczny
Daty
wydano
2010-02-01
online
2010-01-29
Twórcy
  • Department of Pediatrics, Tartu University, Lunini 6, Tartu, 51014, Estonia
  • Department of Biochemistry, Tartu University, Ravila 19, Tartu, 50411, Estonia
autor
  • Tallinn Children’s Hospital, Tervise 28, Tallinn, 13419, Estonia
  • Children’s Clinic, Tartu University Hospital, Lunini 6, Tartu, 51014, Estonia
autor
  • Department of Pediatrics, Tartu University, Lunini 6, Tartu, 51014, Estonia
  • Department of Biochemistry, Tartu University, Ravila 19, Tartu, 50411, Estonia
  • Department of Pediatrics, Tartu University, Lunini 6, Tartu, 51014, Estonia
Bibliografia
  • [1] Fink CW. Proposal for the development of classification criteria for idiopathic arthritides of childhood. J Rheumatol 1995; 22:1566–1569
  • [2] Faith M, Sukumaran A, Pulimood AB, Jacob M. How reliable an indicator of inflammation is myeloperoxidase activity? Clin Chim Acta 2008; 396:23–25 http://dx.doi.org/10.1016/j.cca.2008.06.016[Crossref][WoS]
  • [3] Loria V, Dato I, Graziani F, Biasucci LM. Myeloperoxidase: A new biomarker of inflammation in ischemic heart disease and acute coronary syndromes. Mediators Inflamm 2008; 2008:135625 http://dx.doi.org/10.1155/2008/135625[WoS][Crossref]
  • [4] Klebanoff SJ. Myeloperoxidase: friend and foe. J Leukoc Biol 2005; 77:598–625 http://dx.doi.org/10.1189/jlb.1204697[Crossref]
  • [5] Ramos VA, Ramos PA, Dominguez MC. Role of oxidative stress in the maintenance of inflammation in patients with juvenile rheumatoid arthritis. J Pediatr 2000; 76:125–132
  • [6] Kampus P, Kals J, Ristimäe T, Muda P, Ulst K, Zilmer K, Salonen RM, Tuomainen TP, Teesalu R, Zilmer M. Augmentation index and carotid intima-media thickness are differently related to age, C-reactive protein and xidized low-density lipoprotein. J Hypertens 2007; 25:819–825 http://dx.doi.org/10.1097/HJH.0b013e328014952b[WoS][Crossref]
  • [7] Gaut JP, Byun J, Tran HD, Lauber WM, Carroll JA, Hotchkiss RS, Belaaouaj A, Heinecke JW. Myeloperoxidase produces nitrating oxidants in vivo. J Clin Invest 2002; 109:1287–1289
  • [8] Podrez EA, Abu-Soud HM, Hazen SL. Myeloperoxidase-generated oxidants and atherosclerosis. Free Radic Biol Med 2000; 28:1717–1725 http://dx.doi.org/10.1016/S0891-5849(00)00229-X[Crossref]
  • [9] Minohara M, Matsuoka T, Li W, Osoegawa M, Ishizu T, Ohyagi Y, Kira J. Upregulation of myeloperoxidase in patients with opticospinal multiple sclerosis: positive correlation with disease severity. J Neuroimmunol 2006; 178:156–160 http://dx.doi.org/10.1016/j.jneuroim.2006.05.026[Crossref]
  • [10] Lefkowitz DL, Lefkowitz SS. Microglia and myeloperoxidase: A deadly partnership in neurodegenerative disease. Free Radic Biol Med 2008; 45:726–731 http://dx.doi.org/10.1016/j.freeradbiomed.2008.05.021[Crossref]
  • [11] Lotito AP, Muscará MN, Kiss MH, Teixeira SA, Novaes GS, Laurindo IM, Silva Ca, Mello SB. Nitric oxide-derived species in synovial fluid from patients with juvenile idiopathic arthritis. J Rheumatol 2004; 31:992–997
  • [12] Liskmann S, Zilmer M, Vihalemm T, Salum O, Fischer K. Correlation of peri-implant health and myeloperoxidase levels: a cross-sectional clinical study. Clin Oral Implants Res 2004; 15:546–552 http://dx.doi.org/10.1111/j.1600-0501.2004.01061.x[Crossref]
  • [13] Renke J, Szlagatys A, Hansdorfer-Korzon R, Szumera M, Kamińska B, Knap N, Popadiuk S, Szarszewski A, Woźniak M. Persistence of protein oxidation products and plasma antioxidants in juvenile idiopathic arthritis. A one-year follow-up study. Clin Exp Rheumatol 2007; 25:112–114
  • [14] Bonomini F, Tengattini S, Fabiano A, Bianchi R, Rezzani R. Atherosclerosis and oxidative stress. Histol Histopathol 2008; 23:381–390
  • [15] Düzgünçinar O, Yavuz B, Hazirolan T, Deniz A, Tokgözoğlu SL, Akata D, Demirpençe E. Plasma myeloperoxidase is related to the severity of coronary artery disease. Acta Cardiol 2008; 63:147–152 http://dx.doi.org/10.2143/AC.63.2.2029520[Crossref][WoS]
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  • [17] Doi K, Noiri E, Maeda R, Nakao A, Kobayashi S, Tokunaga K, Fujita T. Functional polymorphism of the myeloperoxidase gene in hypertensive nephrosclerosis dialysis patients. Hypertens Res 2007; 30:1193–1198 http://dx.doi.org/10.1291/hypres.30.1193[Crossref][WoS]
  • [18] Hoi A, Leininger-Muller B, Poirier O, Siest G, Gautier M, Elbaz A, Amarenco P, Visvikis S. Myeloperoxidase polymorphisms in brain infarction. Association with infarct size and functional outcome. Atherosclerosis 2003; 167:223–230 http://dx.doi.org/10.1016/S0021-9150(02)00041-2[Crossref]
  • [19] Reynolds WF, Sermet-Gaudelus I, Gausson V, Feuillet MN, Bonnefont JP, Lenoir G, Descamps-Latscha B, Witko-Sarsat V. Myeloperoxidase promoter polymorphism −463G is associated with more severe clinical expression of cystic fibrosis pulmonary disease. Mediators Inflamm 2006; 2:36735
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_2478_s11536-009-0107-5
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