Evaluation of the Relationship Between Vitamin D Levels and Inflammation Markers

Yıl 2022, , 268 - 274, 28.02.2022

Eren Vurgun

https://doi.org/10.20515/otd.922247

Öz

The aim of this study was to investigate the relationships between 25-hydroxyvitamin D (25(OH)D) levels and inflammation markers such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), leukocyte count and neutrophil/lymphocyte (N/L) ratio parameters. In addition, it was aimed to investigate the frequency of elevation of inflammation markers in vitamin D deficient population and thus frequency of vitamin D deficiency in the population with elevated inflammation markers. Simultaneously requested 25(OH)D, CRP, ESR, leukocyte count and N/L ratio results of 49166 adult patients between September 2017 and March 2020 were retrospectively analyzed. The correlations between parameters and the frequencies of 25(OH)D deficiency and elevated inflammation markers were evaluated. Weak inverse correlations were observed between 25(OH)D and inflammation markers such as CRP, ESR, leukocyte count and NLR (r=-0.077, p<0.01; r=-0.036, p<0.01; r=-0.074, p<0.01 and r=-0.074, p<0.01, respectively). When <30 ng/mL considered as the cut-off value for vitamin D deficiency; CRP levels were normal in 63.2% of those with 25(OH)D deficiency, while 85.6% of those with elevated CRP levels had 25(OH)D deficiency (p<0.001). Similarly, while the leukocyte count was normal in 85.3% of those with 25(OH)D deficiency, 86.6% of those with elevated leukocyte deficiency had 25(OH)D deficiency (p<0.001). In addition, while ESR levels were normal in 42.7% of those with 25 (OH) D deficiency, it was found that 84.1% of those with elevated ESR had 25(OH)D deficiency (p<0.001). The findings of this study support the hypothesis that vitamin D levels are low as a result of inflammation rather than the lower vitamin D levels causes inflammation.

Anahtar Kelimeler

vitamin D, inflammation, inflammation markers, C-reactive protein

D Vitamini Düzeyleri ile İnflamasyon Belirteçleri Arasındaki İlişkinin Değerlendirilmesi

Öz

25-hidroksivitamin D (25(OH)D) düzeyleri ile inflamasyon belirteçleri olan C-reaktif protein (CRP), eritrosit sedimantasyon hızı (ESR), lökosit sayısı ve nötrofil/lenfosit (N/L) oranı parametreleri arasındaki ilişkinin incelenmesi amaçlandı. Ek olarak, D vitamini eksikliği olan popülasyondaki inflamasyon belirteçlerinin yüksekliğinin ve eş zamanlı olarak inflamasyon belirteçleri yüksek olan popülasyondaki D vitamini eksikliğinin araştırılması amaçlandı. Eylül 2017 – Mart 2020 tarihleri arasında 18 yaş ve üzerindeki 49166 erişkin hastaya ait eş zamanlı olarak istenmiş olan 25(OH)D, CRP, ESR, lökosit sayısı ve N/L oranı sonuçları retrospektif olarak incelendi. Parameteler arasındaki korelasyonlar ve 25(OH)D eksikliği ve inflamasyon belirteçleri yükseklikleri arasındaki ilişkiler değerlendirildi. İnflamasyon belirteçleri olan CRP, ESR, lökosit sayısı ve NLR ile 25(OH)D arasında zayıf düzeyde ters yönlü korelasyonlar tespit edildi (sırasıyla; r=-0,077, p<0.01; r=-0,036, p<0.01; r=-0,074, p<0.01 ve r=-0,074, p<0.01). D vitamini eksiklik sınır değeri olarak 30 ng/mL kabul edildiğinde, 25(OH)D eksikliği olanların %63,2’sinde CRP düzeyleri normal iken, CRP yüksekliği olanların %85,6’sında 25(OH)D eksikliği olduğu saptandı (p<0,001). Benzer olarak 25(OH)D eksikliği olanların %85,3’ünde lökosit sayısı normal iken, lökosit yüksekliği olanların %86,6’sında 25(OH)D eksikliği olduğu saptandı (p<0,001). Ek olarak, 25(OH)D eksikliği olanların %42,7’sinde ESR düzeyleri normal iken, ESR yüksekliği olanların %84,1’inde 25(OH)D eksikliği olduğu saptandı (p<0,001). Çalışmanın bulguları, D vitamini düşüklüğünün inflamasyona neden olmasından ziyade D vitamini düzeylerinin inflamasyonun sonucu olarak düşük olduğu hipotezini desteklemektedir.

Anahtar Kelimeler

D vitamini, inflamasyon, inflamasyon belirteçleri, C-reaktif protein

Kaynakça

• Han QQ, Yu J. Inflammation: a mechanism of depression? Neurosci Bull. 2014;30(3):515-23.
• Christodoulidis G, Vittorio TJ, Fudim M, et al. Inflammation in coronary artery disease. Cardiol Rev. 2014;22(6):279-88.
• Taniguchi K, Karin M. IL-6 and related cytokines as the critical lynchpins between inflammation and cancer. Semin Immunol. 2014;26(1):54-74.
• Skapenko A, Leipe J, Lipsky PE, et al. The role of the T cell in autoimmune inflammation. Arthritis Res Ther. 2005;7(Suppl 2):S4-14.
• Cannell JJ, Grant WB, Holick MF. Vitamin D and inflammation. Dermatoendocrinol. 2015;6(1):e983401.
• Núñez J, Núñez E, Bodí V, et al. Usefulness of the neutrophil to lymphocyte ratio in predicting long-term mortality in ST segment elevation myocardial infarction. Am J Cardiol. 2008;101(6):747-52.
• Crowe FL, Jolly K, MacArthur C, et al. Trends in the incidence of testing for vitamin D deficiency in primary care in the UK: a retrospective analysis of The Health Improvement Network (THIN), 2005–2015. BMJ Open. 2019;9(6):e028355.
• Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Guidelines for preventing and treating vitamin D deficiency and insufficiency revisited. J Clin Endocrinol Metab. 2012;97(4):1153–8.
• Ross AC, Taylor CL, Yaktine AL, et al. Dietary reference intakes for calcium and vitamin D. Washington: National Academy of Sciences. 2010. 0-309-16394-3.
• Autier P, Boniol M, Pizot C, et al. Vitamin D status and ill health: a systematic review. Lancet Diabetes Endocrinol. 2014;2(1):76-89.
• Henriksen VT, Rogers VE, Rasmussen GL, et al. Proinflammatory cytokines mediate the decrease in serum 25(OH)D concentrations after total knee arthroplasty? Med Hypotheses. 2014;82(2):134-7.
• Mangge H, Weghuber D, Prassl R, et al. The role of vitamin D in atherosclerosis inflammation revisited: more a bystander than a player? Curr Vasc Pharmacol. 2015;13(3):392-8.
• Guillot X, Semerano L, Saidenberg-Kermanac’h N, et al. Vitamin D and inflammation. Joint Bone Spine. 2010;77(6):552-7.
• Adorini L, Penna G. Control of autoimmune diseases by the vitamin D endocrine system. Nat Clin Pract Rheumatol. 2008;4(8):404-12.
• Marcotorchino J, Gouranton E, Romier B, et al. Vitamin D reduces the inflammatory response and restores glucose uptake in adipocytes. Mol Nutr Food Res. 2012;56(12):1771-82.
• Mangin M, Sinha R, Fincher K. Inflammation and vitamin D: the infection connection. Inflamm Res. 2014;63(10):803-19.
• Amer M, Qayyum R. Relation between serum 25-hydroxyvitamin D and C-reactive protein in asymptomatic adults (from the continuous National Health and Nutrition Examination Survey 2001 to 2006). Am J Cardiol. 2012;109(2):226-230.
• Hyppönen E, Berry D, Cortina-Borja M, et al. 25-Hydroxyvitamin D and pre-clinical alterations in inflammatory and hemostatic markers: a cross sectional analysis in the 1958 British Birth Cohort. PLoS One. 2010;5(5):e10801.
• Ghashut RA, Talwar D, Kinsella J, et al. The effect of the systemic inflammatory response on plasma vitamin 25(OH)D concentrations adjusted for albumin. PLoS One. 2014;9(3):e92614.
• Mellenthin L, Wallaschofski H, Grotevendt A, et al. Association between serum vitamin D concentrations and inflammatory markers in the general adult population. Metabolism. 2014;63(8):1056-62.
• Murr C, Pilz S, Grammer TB, et al. Vitamin D deficiency parallels inflammation and immune activation, the Ludwigshafen Risk and Cardiovascular Health (LURIC) study. Clin Chem Lab Med. 2012;50(12):2205-12.
• Kruit A, Zanen P. The association between vitamin D and C-reactive protein levels in patients with inflammatory and non-inflammatory diseases. Clin Biochem. 2016;49(7-8):534-7.
• Osei-Bimpong A, Meek JH, Lewis SM. ESR or CRP? A comparison of their clinical utility. Hematology. 2007;12(4):353-7.
• Akbas EM, Gungor A, Ozcicek A, et al. Vitamin D and inflammation: evaluation with neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio. Arch Med Sci. 2016;12(4):721-7.