Povezanost između vrednosti C-reaktivnog proteina i normotenzivnog glaukoma
Sažetak
Uvod/Cilj. C-reaktivni protein (CRP) je sistemski inflamatorni marker koji je povezan sa rizikom od nastanka kardiovaskularnih bolesti (KVB). Određeni faktori rizika od KVB su ujedno i faktori rizika od razvoja normotenzivnog glaukoma (NTG), ali povezanost između CRP I NTG još uvek nije jasno definisana. Cilj ove studije bio je da se ispita povezanost između vrednosti visokosenzitivnog CRP u plazmi kod bolesnika sa NTG i u kontrolnoj grupi. Metode. Ispitano je ukupno 20 bolesnika sa NTG (4 muškaraca i 16 žena) i 25 osoba iz kontrolne grupe (5 muškaraca i 20 žena). Obe grupe ispitanika imale su približno iste demografske karakteristike (godine, pol i indeks telesne mase) i kod obe grupe bili su prisutni vaskularni faktori rizika u istom procentu. Rezultati. Vrednosti CRP u plazmi bolesnika sa NTG i u kontrolnoj grupi bile su poredive: srednja vrednost iznosila je 4.99 ± 0.77 mg/L, mediana 4.50 mg/L, opseg 2.50–18.90 mg/L kod bolesnika sa NTG, dok su te vrednosti u kontrolnoj grupi bile: 4.19 ± 0.30 mg/L, 3.50 mg/L, odnosno 2.20–8.50. Zaključak. Rezultati dobijeni u ovoj studiji pokazuju da vrednosti CRP nisu povećene kod bolesnika sa NTG.
Reference
Casson JR, Chidlow G, Wood PMJ, Crowston GJ, Goldberg I. Defini-tion of glaucoma: Clinical and experimental concepts. Clin Experiment Ophthalmol 2012; 40(4): 341−9.
Kamal D, Hitchings R. Normal tension glaucoma: A practical approach. Br J Ophthalmol 1998; 82(7): 835−40.
Shields BM. Normal-tension glaucoma: Is it different from pri-mary open-angle glaucoma?. Curr Opin Ophthalmol 2008; 19(2): 85−8.
Flammer J, Konieczka K, Flammer AJ. The primary vascular dysregulation syndrome: Implications for eye diseases. EPMA J 2013; 4(1): 14.
Galassi F, Giambene B, Varriale R. Systemic vascular dysregula-tion and retrobulbar hemodynamics in normal-tension glau-coma. Invest Ophthalmol Vis Sci 2011; 52(7): 4467−71.
Drance SM. What can we learn from the disc appearance about the risk factors in glaucoma?. Can J Ophthalmol 2008; 43(3): 322−7.
Sugiyama T, Moriya S, Oku H, Azuma I. Association of endo-thelin-1 with normal tension glaucoma: Clinical and funda-mental studies. Surv Ophthalmol 1995; 39(Suppl 1): S49−56.
Shoshani YZ, Harris A, Shoja MM, Rusia D, Siesky B, Arieli Y, et al.. Endothelin and its suspected role in the pathogenesis and possible treatment of glaucoma. Curr Eye Res 2012; 37(1): 1−11.
Pepys MB, Hirschfield GM. C-reactive protein: A critical update. J Clin Invest 2003; 111(12): 1805−12.
Mazer SP, Rabbani LE. Evidence for C-reactive protein's role in (CRP) vascular disease: Atherothrombosis, immuno-regulation and CRP. J Thromb Thrombolysis 2004; 17(2): 95−105.
Ridker PM. High-sensitivity C-reactive protein: Potential ad-junct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 2001; 103(13): 1813−8.
Leibovitch I, Kurtz S, Kesler A, Feithliher N, Shemesh G, Sela BA. C-reactive protein levels in normal tension glaucoma. J Glau-coma 2005; 14(5): 384−6.
Stefan C, Nenciu A, Melinte D, Malcea C, Nae I, Afanasiuc O. Pro-tein C reactive and glaucoma. Oftalmologia 2006; 50(4): 82−5. (Romanian)
Voogd S, Wolfs RC, Jansonius NM, Witteman JC, Hofman A, de Jong PT. Atherosclerosis, C-reactive protein, and risk for open-angle glaucoma: The Rotterdam study. Invest Ophthalmol Vis Sci 2006; 47(9): 3772−6.
Su WW, Ho WJ, Cheng ST, Chang SH, Wu SC. Systemic high-sensitivity C-reactive protein levels in normal-tension glauco-ma and primary open-angle glaucoma. J Glaucoma 2007; 16(3): 320−3.
Choi J, Joe SG, Seong M, Choi JY, Sung KR, Kook MS. C-reactive Protein and Lipid Profiles in Korean Patients With Normal Tension Glaucoma. Korean J Ophthalmol 2009; 23(3): 193−7.
Lee NY, Park NY, Park CK, Ahn MD. Analysis of systemic en-dothelin-1, matrix metalloproteinase-9, macrophage chemoat-tractant protein-1, and high-sensitivity C-reactive protein in normal tension glaucoma. Curr Eye Res 2012; 37: 1121−6.
Torzewski M, Rist C, Mortensen RF, Zwaka PT, Bienek M, Walten-berger J, at al. C- reactive protein in the arterial intima: Role of C – reactive protein receptor-dependent monocyte recruitment in atherogenesis. Arterioscler Thromb Vacs Biol 2000; 20(9): 2094−9.
Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation 2000; 102(18): 2165−8.
Pache M, Flammer J. A sick eye in a sick body?, Systemic find-ings in patients with primary open - angle glaucoma. Surv Ophthalmol 2006; 51(3): 179−212.
Levene RZ. Low tension glaucoma: A critical review and new material. Surv Ophthalmol 1980; 24(6): 621−64.
Gasser P. Why study vascular factors in glaucoma?. Int Oph-thalmol 1998; 22(4): 221−5.
Hayreh SS. The role of age and cardiovascular disease in glau-comatous optic neuropathy. Surv Ophthalmol 1999; 43(Suppl 1): S27−42.
Gherghel D, Hosking SL, Orgul S. Autonomic nervous system, circadian rhythms, and primary open-angle glaucoma. Surv Ophthalmol 2004; 49(5): 491−508.
Hayreh SS. Retinal and optic nerve head ischemic disorders and atherosclerosis: Role of serotonin. Prog Retin Eye Res 1999; 18(2): 191−221.
Grieshaber MC, Flammer J. Blood flow in glaucoma. Curr Opin Ophthalmol 2005; 16(2): 79−83.
Harris A, Jonescu-Cuypers C, Martin B, Kagemann L, Zalish M, Garzozi HJ. Simultaneous management of blood flow and IOP in glaucoma. Acta Ophthalmol Scand 2001; 79(4): 336−41.
Flammer J, Orgül S, Costa VP, Orzalesi N, Krieglstein GK, Serra LM, et al. The impact of ocular blood flow in glaucoma. Prog Retin Eye Res 2002; 21(4): 359−93.