Comparison of the Multiple Sclerosis Patients Attack and Non-Attack Period Findings

Abstract

It is thought that the loss of conduction that causes clinical findings in multiple sclerosis (MS) attack may be the result of loss and damage of myelin, as well as the substances that activate autoimmune cascades affect axonal conductivity. Only some of the inflammatory processes that occur are manifesting and are reflected as an attack. The effects of these changes can also be seen in the serum of the patients during the attack period, when the inflammatory changes are intense. In this study, we aimed to compare the laboratory findings of MS patients during the attack and non-attack periods. The data of 61 patients between 18-65 years of age, who had liver function tests, lipid parameters, vitamin D levels, thyroid function tests, ferritin, folate and vitamin B12 levels studied both during and after the attack, were analyzed retrospectively. The attack period and non-attack data of the patients whose age, gender, height, weight, duration of diagnosis and EDSS (expanded-disability status scale) scores were recorded were compared. There was no significant difference in lipid parameters, ferritin, folate, vitamin B12 levels and liver function tests measured in the attack period and in the non-attack period, while the patients had significantly lower vitamin D levels and high thyroid function tests. VitD, Thyroid function tests and changes in cholesterol levels, which are easily accessible laboratory tests, are thought to give an idea about disease activity and attack status. More specific studies with the greater number of samples are needed to evaluate the possible effects of thyroid hormone on remyelination.

Keywords

• multiple sclerosis,attack,vitamin d,thyroid,lipid

Multipl Skleroz Hastalarının Atak ve Atak Dışı Dönem Bulgularının Karşılaştırılması

Abstract

Multipl skleroz (MS) atağında klinik bulguların ortaya çıkmasına neden olan ileti kayıplarının; myelin kaybı ve hasarlanması sonucu olabileceği gibi, otoimmünkaskadları aktive eden maddelerin aksonal iletkenliği etkilemesiyle de ortaya çıkabileceği düşünülmektedir. Ortaya çıkan inflamatuar süreçlerin yalnızca bir kısmı bulgu vermekte ve atak olarak kliniğe yansımaktadır. İnflamatuar değişikliklerin yoğun görüldüğü atak döneminde hastaların serumlarında da bu değişikliklerin yansımaları görülebilmektedir. Bu çalışmada, MS hastalarının atak döneminde ve atak dışı dönemdeki laboratuvar bulgularını karşılaştırmayı amaçladık. Hem atak döneminde hem de atak dışı dönemde karaciğer fonksiyon testleri, lipit parametreleri, D vitamini düzeyleri, tiroid fonksiyon testleri, ferritin, folat ve vitamin B12 düzeyleri kayıtlı olan, 18-65 yaş aralığında, 61 hastanın verileri retrospektif olarak incelendi. Yaş, cinsiyet, boy, kilo, tanı süresi ve hastalık şiddetini gösteren EDSS (expanded disability status scale) skorları kayıt edilen hastaların atak dönemi ve atak dışındaki verileri karşılaştırıldı. Hastaların atak döne-minde ve atak dışı dönemde ölçülen lipid parametreleri, ferritin, folat, vitamin B12 düzeyi ve karaciğer fonksiyon testlerinde anlamlı farklılık saptanmazken hastaların atak döneminde Vitamin D düzeylerinin anlamlı olarak daha düşük, tiroid fonksiyonlarının da yüksek olduğu gözlendi. Hastaların takip sürecinde, kolay ulaşılabilir laboratuvar tetkikleri olan vitamin D, tiroid fonksiyon testleri ve kolesterol seviyelerinde-ki değişikliklerin hastalık aktivitesi ve atak durumu ile ilgili fikir verebileceği düşünülmektedir. Tiroid hormonunun remiyelinizasyon üzerine olası etkilerini değerlendirecek örneklem sayısının daha fazla olduğu daha spesifik çalışmalara ihtiyaç vardır.

Keywords

• Multiple skleroz,atak,vitamin d,tiroid,lipid

References

1. Dutta, R. and B.D. Trapp, Pathogenesis of axonal and neuronal damage in multiple sclerosis. Neurology, 2007. 68(22 Suppl 3): p. S22-31; discussion S43-54.10.1212/01.wnl.0000275229.13012.32
2. Kalincik, T., Multiple Sclerosis Relapses: Epidemiology, Outcomes and Management. A Systematic Review. Neuroepidemiology, 2015. 44(4): p. 199-214.10.1159/000382130
3. Steinman, L., Immunology of relapse and remission in multiple sclerosis. Annu Rev Immunol, 2014. 32: p. 257-81.10.1146/annurev-immunol-032713-120227
4. Cantorna, M.T., Vitamin D and multiple sclerosis: an update. Nutr Rev, 2008. 66(10 Suppl 2): p. S135-8.10.1111/j.1753-4887.2008.00097.x
5. Sassi, F., C. Tamone, and P. D'Amelio, Vitamin D: Nutrient, Hormone, and Immunomodulator. Nutrients, 2018. 10(11).10.3390/nu10111656
6. Correale, J., M.C. Ysrraelit, and M.I. Gaitan, Immunomodulatory effects of Vitamin D in multiple sclerosis. Brain, 2009. 132(Pt 5): p. 1146-60.10.1093/brain/awp033
7. Giubilei, F., G. Antonini, S. Di Legge, M.P. Sormani, P. Pantano, R. Antonini, M. Sepe-Monti, F. Caramia, and C. Pozzilli, Blood cholesterol and MRI activity in first clinical episode suggestive of multiple sclerosis. Acta Neurol Scand, 2002. 106(2): p. 109-12.10.1034/j.1600-0404.2002.01334.x
8. Smolders, J., O. Torkildsen, W. Camu, and T. Holmoy, An Update on Vitamin D and Disease Activity in Multiple Sclerosis. CNS Drugs, 2019. 33(12): p. 1187-1199.10.1007/s40263-019-00674-8

9. Smolders, J., P. Menheere, A. Kessels, J. Damoiseaux, and R. Hupperts, Association of vitamin D metabolite levels with relapse rate and disability in multiple sclerosis. Mult Scler, 2008. 14(9): p. 1220-4.10.1177/1352458508094399
10. Soilu-Hanninen, M., M. Laaksonen, I. Laitinen, J.P. Eralinna, E.M. Lilius, and I. Mononen, A longitudinal study of serum 25-hydroxyvitamin D and intact parathyroid hormone levels indicate the importance of vitamin D and calcium homeostasis regulation in multiple sclerosis. J Neurol Neurosurg Psychiatry, 2008. 79(2): p. 152-7.10.1136/jnnp.2006.105320
11. Simpson, S., Jr., B. Taylor, L. Blizzard, A.L. Ponsonby, F. Pittas, H. Tremlett, T. Dwyer, P. Gies, and I. van der Mei, Higher 25-hydroxyvitamin D is associated with lower relapse risk in multiple sclerosis. Ann Neurol, 2010. 68(2): p. 193-203.10.1002/ana.22043
12. Hartley, M.D., T. Banerji, I.J. Tagge, L.L. Kirkemo, P. Chaudhary, E. Calkins, D. Galipeau, M.D. Shokat, M.J. DeBell, S. Van Leuven, H. Miller, G. Marracci, E. Pocius, T. Banerji, S.J. Ferrara, J.M. Meinig, B. Emery, D. Bourdette, and T.S. Scanlan, Myelin repair stimulated by CNS-selective thyroid hormone action. JCI Insight, 2019. 4(8).10.1172/jci.insight.126329
13. Marrie, R.A., N. Reider, J. Cohen, O. Stuve, P.S. Sorensen, G. Cutter, S.C. Reingold, and M. Trojano, A systematic review of the incidence and prevalence of autoimmune disease in multiple sclerosis. Mult Scler, 2015. 21(3): p. 282-93.10.1177/1352458514564490
14. van der Spek, A.H., O.V. Surovtseva, K.K. Jim, A. van Oudenaren, M.C. Brouwer, C. Vandenbroucke-Grauls, P.J.M. Leenen, D. van de Beek, A. Hernandez, E. Fliers, and A. Boelen, Regulation of Intracellular Triiodothyronine Is Essential for Optimal Macrophage Function. Endocrinology, 2018. 159(5): p. 2241-2252.10.1210/en.2018-00053
15. Marchiori, R.C., L.A. Pereira, A.A. Naujorks, D.L. Rovaris, D.F. Meinerz, M.M. Duarte, and J.B. Rocha, Improvement of blood inflammatory marker levels in patients with hypothyroidism under levothyroxine treatment. BMC Endocr Disord, 2015. 15: p. 32.10.1186/s12902-015-0032-3
16. Rozing, M.P., R.G. Westendorp, A.B. Maier, C.A. Wijsman, M. Frolich, A.J. de Craen, and D. van Heemst, Serum triiodothyronine levels and inflammatory cytokine production capacity. Age (Dordr), 2012. 34(1): p. 195-201.10.1007/s11357-011-9220-x
17. Nijampurkar, B., F. Qureshi, N. Jain, T. Banerjee, A. Kumar, and H.S. Parmar, Anti-Inflammatory Role of Thyroid Hormones on Rat Air Pouch Model of Inflammation. Inflamm Allergy Drug Targets, 2015. 14(2): p. 117-24.10.2174/1871528114666160105113342
18. Hodkinson, C.F., E.E. Simpson, J.H. Beattie, J.M. O'Connor, D.J. Campbell, J.J. Strain, and J.M. Wallace, Preliminary evidence of immune function modulation by thyroid hormones in healthy men and women aged 55-70 years. J Endocrinol, 2009. 202(1): p. 55-63.10.1677/JOE-08-0488
19. Kimball, S.M., M.R. Ursell, P. O'Connor, and R. Vieth, Safety of vitamin D3 in adults with multiple sclerosis. Am J Clin Nutr, 2007. 86(3): p. 645-51.10.1093/ajcn/86.3.645
20. Zhornitsky, S., K.A. McKay, L.M. Metz, C.E. Teunissen, and M. Rangachari, Cholesterol and markers of cholesterol turnover in multiple sclerosis: relationship with disease outcomes. Mult Scler Relat Disord, 2016. 5: p. 53-65.10.1016/j.msard.2015.10.005
21. Durfinova, M., L. Prochazkova, D. Petrlenicova, Z. Bystricka, K. Oresanska, L. Kuracka, and B. Liska, Cholesterol level correlate with disability score in patients with relapsing-remitting form of multiple sclerosis. Neurosci Lett, 2018. 687: p. 304-307.10.1016/j.neulet.2018.10.030
22. Weinstock-Guttman, B., R. Zivadinov, D. Horakova, E. Havrdova, J. Qu, G. Shyh, E. Lakota, K. O'Connor, D. Badgett, M. Tamano-Blanco, M. Tyblova, S. Hussein, N. Bergsland, L. Willis, J. Krasensky, M. Vaneckova, Z. Seidl, and M. Ramanathan, Lipid profiles are associated with lesion formation over 24 months in interferon-beta treated patients following the first demyelinating event. J Neurol Neurosurg Psychiatry, 2013. 84(11): p. 1186-91.10.1136/jnnp-2012-304740