Multiple skleroz hastalarında C-reaktif protein/albümin oranı ve hastalık alt tipi ve disabilite ile ilişkisi

Öz

Amaç: Oksidatif stres ve inflamasyon Multiple Skleroz (MS) hastalarında demiyelinizasyon ve aksonal hasarın sebebidir. Serum C-reaktif protein (CRP) ve albümin düzeyleri birçok hastalıkta sistemik inflamasyon ve oksidatif stresin belirteci olarak kullanılmaktadır. Bu çalışmada, MS hastalığında CRP/albümin düzeyinin saptanması, hastalık alt tipi ve dizabilite ile ilişkisini değerlendirilmesi amaçlanmıştır. Yöntemler: Bu kesitsel çalışma MS hastalığı nedeniyle tedavi edilen hastalarda yapıldı. Çalışmaya 120 MS hastası ve 62 sağlıklı kontrol alındı. Sosyodemografik özellikler sorgulandı. MS subtipi belirlendi. Dizabilite genişletilmiş özürlülük durum ölçeği (EDSS) ile hesaplandı. Hastalar EDSS 0-3 (hafif), 3,5-4,5 (orta) ve 5,0 veya üzeri (ağır) olmak üzere 3 gruba ayrıldı. Atak sıklığı belirlendi. Albümin ve CRP serum seviyesi belirlendi. Hemogram floresans akış sitometrisi ile ölçüldü. Bulgular: Çalışmada 71 (%59,2) kadın ve 49 (%40,8) erkek hasta vardı. Yaş ortalamaları 39,49 (11,47) idi. MS hastalarında lökosit değeri daha yüksek, albümin ise düşüktü (P=0,046; 0,006). Progresif MS hastalarında relapsing remitting alt tipine göre CRP ve CRP/albümin oranı daha yüksek, albümin seviyesi daha düşüktü (P<0,01). EDSS yüksek olan hastalarda CRP ve CRP/albümin oranı daha yüksek, albümin seviyesi daha düşüktü (P<0,01). Atak sayısı ile CRP/albümin oranı arasında zayıf korelasyon saptandı (P=0,032; r=0,196). Sonuç: Bu çalışmada albümin seviyesi ve CRP/albümin oranının MS hastalığında hastalık alt tipi ve aktivitesi ile ilişkili olduğu ortaya konulmuştur.

Anahtar Kelimeler

• Multiple skleroz
• Hipoalbüminemi
• CRP/albümin oranı

C-reactive protein/albumin ratio in patients with multiple sclerosis and its relationship with disease subtype and disability

Abstract

Aim: Oxidative stress and inflammation are the cause of demyelination and axonal damage in patients with Multiple Sclerosis (MS). Serum C-reactive protein (CRP) and albumin levels are used as a marker of systemic inflammation and oxidative stress for many diseases. In this study, we aimed to determine the level of CRP/albumin ratio in patients with MS and its relationship with disease subtype and disability. Methods: This cross-sectional study was conducted in patients treated for MS disease. One hundred twenty MS patients and 62 healthy controls were included. Sociodemographic characteristics were questioned. MS subtype was determined. Disability was calculated with Expanded Disability Status Scale (EDSS). Patients were divided into 3 groups: EDSS 0-3 (minor), 3.5-4.5 (moderate) and 5.0 or higher (major). Attack frequency, albumin and CRP serum levels were noted, and hemogram was analyzed with fluorescence flow cytometry. Results: There were 71 (59.2%) female and 49 (40.8%) male patients in the study, and their mean age was 39.49 (11.47) years. Leukocyte value was higher and albumin was lower in patients with MS (P=0.046, P=0.006). In progressive MS patients, CRP and CRP/albumin ratio was higher and albumin level was lower compared to the relapse remitting subtype (P<0.01). Patients with high EDSS had higher CRP and CRP/albumin ratio and lower albumin levels (P<0.01). A low correlation was detected between the number of attacks and CRP/albumin ratio (P=0.032; r=0.196). Conclusion: We detected that albumin level and CRP/albumin ratio are related with subtype and activity of MS disease.

Keywords

• Multiple sclerosis
• Hypoalbuminemia
• CRP/albumin ratio

Kaynakça

1. 1. Coleman M. Axon degeneration mechanisms: commonality amid diversity. Nat Rev Neurosci. 2005;6(11):889-98. doi: 10.1038/nrn1788.
2. 2. Coleman MP, Perry VH. Axon pathology in neurological disease: a neglected therapeutic target. Trends Neurosci. 2002;25(10):532-7. doi: 10.1016/s0166-2236(02)02255-5.
3. 3. Lassmann H. Pathogenic mechanisms associated with different clinical courses of multiple sclerosis. Fronti Immunol. 2019;9:3116. doi: 10.3389/fimmu.2018.03116.
4. 4. Su KG, Banker G, Bourdette D, Forte M. Axonal degeneration in multiple sclerosis: the mitochondrial hypothesis. Curr Neurol Neurosci Rep. 2009;9(5):411-7. doi: 10.1007/s11910-009-0060-3.
5. 5. Rojo AI, McBean G, Cindric M, Egea J, López MG, Rada P, et al. Redox control of microglial function: Molecular mechanisms and functional significance. Antioxid Redox Signal. 2014;21(12):1766-801. doi: 10.1089/ars.2013.5745.
6. 6. Moretti M, Fraga DB, Rodrigues A. Preventive and therapeutic potential of ascorbic acid in neurodegenerative diseases. CNS Neurosci Ther. 2017;23(12):921-9. doi: 10.1111/cns.12767.
7. 7. Carvalho C, Moreira PI. Oxidative Stress: A Major player in cerebrovascular alterations associated to neurodegenerative events. Front Physiol. 2018;9:806. doi: 10.3389/fphys.2018.00806.
8. 8. Lutton EM, Farney SK, Andrews AM, Shuvaev VV, Chuang GY, Muzykantov VR, et al. Endothelial targeted strategies to combat oxidative stress: Improving outcomes in traumatic brain injury. Front Neurol. 2019;10:582. doi: 10.3389/fneur.2019.00582.

9. 9. Miller E, Wachowicz B, Majsterek I. Advances in antioxidative therapy of multiple sclerosis. Curr Med Chem. 2013;20(37):4720-30. doi: 10.2174/09298673113209990156.
10. 10. Danesh J, Wheeler JG, Hirschfield GM, Eda S, Eiriksdottir G, Rumley A, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med. 2004;350(14):1387-97. doi: 10.1056/NEJMoa032804.
11. 11. Kaptoge S, Di Angelan¬tonio E, Lowe G, Pepys MB, Thompson SG, Collins R, et al. C-reactive protein concentration and risk of cor¬onary heart disease, stroke, and mortality: an individual par¬ticipant meta-analysis. Lancet 2010;375(9709):132-40. doi: 10.1016/S0140-6736(09)61717-7.
12. 12. Matsuo R, Ago T, Hata J, Wakisaka Y, Kuroda J, Kuwashiro T, et al. Plasma C-reactive protein and clinical outcomes after acute ischemic stroke: a prospective observational study. PLoS One. 2016;11(6):e0156790. doi: 10.1371/journal.pone.0156790.
13. 13. Windgassen EB, Funtowicz L, Lunsford TN, Harris LA, Mulvagh SL. C-reactive protein and high-sensitivity C-reactive protein: an update for clinicians. Postgrad Med. 2011;123(1):114-9. doi: 10.3810/pgm.2011.01.2252.
14. 14. Oliveira SR, Kallaur AP, Reiche EMV, Kaimen-Maciel DR, Panis C, Lozovoy MAB, et al. Albumin and protein oxidation are predictors that differentiate relapsing-remitting from progressive clinical forms of multiple sclerosis. Mol Neurobiol. 2017;54(4):2961-8. doi: 10.1007/s12035-016-9860-z.
15. 15. Yazar HO, Yazar T, Aygün A, Kaygisiz Ş, Kirbaş D. Evaluation of simple inflammatory blood parameters in patients with migraine. Ir J Med Sci. 2020;189(2):677-83. doi: 10.1007/s11845-019-02136-y.
16. 16. Ju SY, Ma SJ. High C-reactive protein to albumin ratio and the short-term survival prognosis within 30 days in terminal cancer patients receiving palliative care in a hospital setting: A retrospective analysis. Medicine 2020;99(9). e19350. doi: 10.1097/MD.0000000000019350.
17. 17. Yazar T, Yazar HO. Evaluation of C-reactive protein/albumin ratio according to stage in patients with idiopathic parkinson disease. Turkish J Neurol. 2019;25(3):123-8. doi: 10.4274/tnd.galenos.2019.13334.
18. 18. Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi G, et al. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. 2018;17(2):162-73. doi: 10.1016/S1474-4422(17)30470-2.
19. 19. Kurtzke JF. Rating neurologic impairment in multiple sclerosis: an expanded disability status scale (EDSS). Neurology 1983;33(11):1444-52. doi: 10.1212/wnl.33.11.1444.
20. 20. Frati A, Cerretani D, Fiaschi AI, Frati P, Gatto V, La Russa R, et al. Diffuse axonal injury and oxidative stress: A comprehensive review. Int J Mol Sci. 2017;18(12). pii: E2600. doi: 10.3390/ijms18122600.
21. 21. Siotto M, Filippi MM, Simonelli I, Landi D, Ghazaryan A, Vollaro S, et al. Oxidative stress related to iron metabolism in relapsing remitting multiple sclerosis patients with low disability. Front Neurosci. 2019;13:86. doi: 10.3389/fnins.2019.00086.
22. 22. Choi IY, Lee P, Adany P, Hughes AJ, Belliston S, Denney DR, et al. In vivo evidence of oxidative stress in brains of patients with progressive multiple sclerosis. Mult Scler. 2018;24(8):1029-38. doi: 10.1177/1352458517711568.
23. 23. Luan YY, Yao YM. The clinical significance and potential role of C-reactive protein in chronic inflammatory and neurodegenerative diseases. Front Immunol. 2018;9:1302. doi: 10.3389/fimmu.2018.01302.
24. 24. Vachatova S, Andrys C, Krejsek J, Salavec M, Ettler K, Rehacek V, et al. Metabolic syndrome and selective inflammatory markers in psoriatic patients. J Immunol Res. 2016;2016:5380792. doi: 10.1155/2016/5380792.
25. 25. Yasojima K, Schwab C, McGeer EG, McGeer PL. Human neurons generate C-reactive protein and amyloid P: upregulation in Alzheimer’s disease. Brain Res. 2000;887(1):80-9. doi: 10.1016/s0006-8993(00)02970-x.
26. 26. Mancinella A, Mancinella M, Carpinteri G, Bellomo A, Fossati C, Gianturco V, et al. Is there a relationship between high C-reactive protein (CRP) levels and dementia? Arch Gerontol Geriatr. 2009;49(1):185-94. doi: 10.1016/j.archger.2009.09.028.
27. 27. Shu Y, Li R, Qiu W, Chang Y, Sun X, Fang L, Kermode AG. Association of serum gamma-glutamyltransferase and C-reactive proteins with neuromyelitis optica and multiple sclerosis. Mult Scler Relat Disord. 2017;18:65-70. doi: 10.1016/j.msard.2017.09.021.
28. 28. Hon G, Hassan M, van Rensburg SJ, Abel S, Marais DW, van Jaarsveld P, et al. Immune cell membrane fatty acids and inflammatory marker, C-reactive protein, in patients with multiple sclerosis. Br J Nutr. 2009;102(9):1334-40. doi: 10.1017/S0007114509382185.
29. 29. Guzel I, Mungan S, Oztekin ZN, Ak F. Is there an association between the Expanded Disability Status Scale and inflammatory markers in multiple sclerosis?. J Chin Med Assoc. 2016;79(2):54-7. doi: 10.1016/j.jcma.2015.08.010.
30. 30. Yeun JY, Levine RA, Mantadilok V, Kaysen GA. C-Reactive protein predicts all-cause and cardiovascular mortality in hemodialysis patients. Am J Kidney Dis. 2000;35(3):469-76. doi: 10.1016/s0272-6386(00)70200-9.