Demir Eksikliği Kronik Inflamasyonun Bir Nedeni midir?

Yıl 2022, Cilt: 44 Sayı: 2, 199 - 203, 28.02.2022

Mehmet Bankir , Didar Yanardağ Açık

https://doi.org/10.20515/otd.980423

Cited By: 1

Öz

Demir, çeşitli hayati biyolojik işlevler için gerekli olan temel bir mineraldir. C-reaktif protein, kronik veya akut inflamasyonun rutin bir belirteci olarak yaygın şekilde kullanılmaktadır. Hem demir eksikliği hem de fazlalığı vücutta proinflamatuar bir duruma neden olur. Demir tedavisi öncesi yüksek olan C-reaktif proteinin, demir tedavisi sonrası düştüğünü klinik olarak gözlemledik. Bu klinik gözlemin gerçekliğini araştırmayı ve sonuçlarımızı literatürle karşılaştırmayı amaçladık.Tek merkezli, prospektif planlanmış bu çalışmaya etik kurul onayı alınarak, 2001 WHO demir eksikliği kriterlerine göre demir eksikliği anemisi saptanan reprodüktif çağda 170 kadın hasta dahil edildi. Hastaların ilk başvuru sırasındaki ve tedaviden 4-8 hafta sonraki hemoglobin, hematokrit, ortalama eritrosit hacmi, lökosit, trombosit, ferritin, folat, C-reaktif protein değerleri kaydedildi. Tüm hastalarda tedavi sonrası tedavi öncesine kıyasla ortalama hemoglobin (11,7±1,4 vs 9,5±1,7; p<0,001), ortalama HCT (36,0±3,6 vs 30,7±4,7; p<0,001), ortalama MCV (76,7±7,8 vs 70,0±9,2; p<0,001) ve ortanca ferritin (43 vs 3,6; p<0,001) düzeylerinde artış saptandı, ortanca platelet (273 vs 302; p<0,001) ve ortanca CRP (0,9 vs 1,3; p<0,001) düzeylerinde düşüş saptandı. Çalışmamızın sonuçları ve literatür bilgileri ışığında demir eksikliğinin kronik inflamatuar bir sürece yol açtığını söyleyebiliriz.

Anahtar Kelimeler

demir;, demir eksikliği;, inflamasyon, C-reaktif protein

Destekleyen Kurum

Yok

Proje Numarası

Yok

Is Iron Deficiency a Cause of Chronic Inflammation?

Öz

Iron is an essential mineral required for a variety of vital biological functions. C-reactive protein (CRP) is widely used as a routine marker of chronic or acute inflammation. Both iron deficiency and excess induce proinflammatory activity in the body. We clinically observed that C-reactive protein, which was high before iron treatment, decreased after iron treatment. We aimed to investigate the authenticity of this clinical observation and compare our results with the literature. In this single-center, prospective study, 170 female patients of reproductive age who were found to have iron deficiency anemia according to the 2001 WHO iron deficiency criteria were included in this study, with the approval of the ethics committee. Hemoglobin, hematocrit, mean corpuscular volume, leukocyte, platelet, ferritin, folate, C-reactive protein values were recorded at the time of first admission and 4-8 weeks after the treatment. An increase in the levels of mean hemoglobin (11.7±1.4 vs 9.5±1.7; p<0.001), mean HCT (36.0±3.6 vs 30.7±4.7; p<0.001), mean MCV (76.7±7.8 vs 70.0±9.2; p<0.001), and median ferritin (43 vs 3.6; p<0.001) was observed in addition to a decrease in the levels of median platelet (273 vs 302; p<0.001) and median CRP (0.9 vs 1.3; p<0.001) in all patients after the treatment versus baseline.In the light of the results of our study and the literature, we can say that iron deficiency causes a chronic inflammatory process.

Anahtar Kelimeler

iron, iron deficiency, inflammation, C-reactive protein

Proje Numarası

Yok

Kaynakça

• Kobayashi M, Suhara T, Baba Y, Kawasaki NK, Higa JK, Matsui T. Pathological Roles of Iron in Cardiovascular Disease. Curr Drug Targets. 2018;19(9):1068-1076. doi: 10.2174/1389450119666180605112235.
• Petzer V, Theurl I, Weiss G. Established and Emerging Concepts to Treat Imbalances of Iron Homeostasis in Inflammatory Diseases. Pharmaceuticals (Basel). 2018 Dec; 11(4): 135.
• Gozzelino R, Arosio P. Iron Homeostasis in Health and Disease. Int J Mol Sci. 2016 Jan 20;17(1):130. doi: 10.3390/ijms17010130.
• Hussain T, Tan B, Yin Y, Blachier F, Tossou MC, Rahu N. Oxidative Stress and Inflammation: What Polyphenols Can Do for Us? Oxid Med Cell Longev. 2016;2016:7432797. doi: 10.1155/2016/7432797.
• Erichsen K, Hausken T, Ulvik RJ, Svardal A, Berstad A, Berge RK. Ferrous fumarate deteriorated plasma antioxidant status in patients with Crohn disease. Scand. J. Gastroenterol. 2003; 38: 543–8.
• World Health Organization, World Health Organization, Geneva. Iron deficiency anaemia: assessment, prevention and control. A guide for programme managers. Google Sch. 2001.
• Pasricha SR, Tye-Din J, Muckenthaler MU, Swinkels DW. Iron deficiency. Lancet. 2021 Jan 16;397(10270):233-248. doi: 10.1016/S0140-6736(20)32594-0.
• Iqbal T, Stein J, Sharma N, Kulnigg-Dabsch S, Vel S, Gasche C. Clinical Significance of C-Reactive Protein Levels in Predicting Responsiveness to Iron Therapy in Patients with Inflammatory Bowel Disease and Iron Deficiency Anemia. Dig. Dis. Sci. 2015, 60, 1375–1381.
• Merono T, Dauteuille C, Tetzlaff W, et al. Oxidative stress, HDL functionality and effects of intravenous iron administration in women with iron deficiency anemia. Clin Nutr. 2017 Apr;36(2):552-558. doi: 10.1016/j.clnu.2016.02.003.
• Cheng CF, Lian WS. Prooxidant mechanisms in iron overload cardiomyopathy. Biomed Res Int. 2013;2013:740573. doi: 10.1155/2013/740573.
• Zhou X, Xu W, Xu Y, Qian Z. Iron Supplementation Improves Cardiovascular Outcomes in Patients with Heart Failure. Am J Med. 2019 Aug;132(8):955-963. doi: 10.1016/j.amjmed.2019.02.018.
• Cohen-Solal A, Leclercq C, Deray G, et al. Iron deficiency: an emerging therapeutic target in heart failure. Heart. 2014;100:1414-20.
• Yambire KF, Rostosky C, Watanabe T et al. Impaired lysosomal acidification triggers iron deficiency and inflammation in vivo. eLife. 2019; 8: e51031.
• Fan Y, Wang J, Wei L, He B, Wang C, Wang B. Iron deficiency activates proinflammatory signaling in macrophages and foam cells via the p38 MAPKNF- kappaB pathway. Int J Cardiol 2011;152:49-55.
• Pagani A, Nai A, Corna G, Bosurgi L, Rovere-Querini P, Camaschella C, et al. Low hepcidin accounts for the proinflammatory status associated with iron deficiency. Blood 2011;118:736-46.
• Nemeth E, Tuttle MS, Powelson J, et al. Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization., Science, 2004, vol. 306 5704(pg. 2090-2093)
• Recalcati S, Pometta R, Levi S, Conte D, Cairo G. Response of monocyte iron regulatory protein activity to inflammation: abnormal behavior in genetic hemochromatosis. Blood. 1998;91(7):2565-2572.
• Robach P, Recalcati S, Girelli D, et al. Alterations of systemic and muscle iron metabolism in human subjects treated with low-dose recombinant erythropoietin. Blood. 2009;113(26): 6707-6715.
• Piperno A, Galimberti S, Mariani R, et al. Modulation of hepcidin production during hypoxia-induced erythropoiesis in humans in vivo: data from the HIGHCARE project. Blood. 2011;117(10):2953- 2959.