Increased plasma lipocalin-2 levels correlate with disease severity and may be a marker of acute inflammatory response in patients with psoriasis
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More than a skin disease, psoriasis is also considered a systemic disorder. Lipocalin-2, an adipokine, may be a link between psoriasis and systemic inflammation. We conducted this study to measure the plasma level of lipocalin-2 and investigate its relationship with the clinical manifestations in patients with psoriasis. We assessed 62 patients with psoriasis and 31 healthy controls. Their demographic information and clinical characteristics were determined by physical examination and review of the recorded medical history. Plasma lipocalin-2 levels were measured using an enzyme-linked immunosorbent assay. Plasma lipocalin-2 concentration was significantly higher in patients with psoriasis than in the control group (P<0.001). Patients with acute psoriatic subgroups, including psoriatic erythroderma and pustular psoriasis, had significantly higher plasma lipocalin-2 levels than those with the chronic plaque type. In addition, plasma lipocalin-2 concentration positively correlates with the disease severity index, including the psoriasis area severity index, body surface area, high-sensitivity C-reactive protein, nail psoriasis severity index, and pustular severity index. In patients with psoriasis, increased plasma lipocalin-2 levels correlated with severity and indicated an active disease state. These findings suggest that lipocalin-2 may play an important role in determining the pathogenesis of acute psoriasis and may serve as a valuable clinical biomarker of this disease.
Sewon Kang, Masayuki Amagai, Anna L. Bruckner, et al. Psoriasis. Fitzpatrick's Dermatology. 1. 9th ed. United States: Mc Graw Hill Education; 2019. p. 457-97.
Lynde CW, Poulin Y, Vender R, et al. Interleukin 17A: toward a new understanding of psoriasis pathogenesis. J Am Acad Dermatol 2014;71:141-50. DOI: https://doi.org/10.1016/j.jaad.2013.12.036
Gisondi P, Fostini AC, Fossa I, et al. Psoriasis and the metabolic syndrome. Clin Dermatol 2018;36:21-8. DOI: https://doi.org/10.1016/j.clindermatol.2017.09.005
Coimbra S., Catarino C., Santos-Silva A. The triad psoriasis-obesity-adipokine profile. J Eur Acad Dermatol Venereol 2016;30:1876-85. DOI: https://doi.org/10.1111/jdv.13701
Boehncke WH, Boehncke S, Tobin AM, Kirby B. The 'psoriatic march': a concept of how severe psoriasis may drive cardiovascular comorbidity. Experim Dermatol 2011;20:303-7. DOI: https://doi.org/10.1111/j.1600-0625.2011.01261.x
Padhi T, Garima. Metabolic syndrome and skin: psoriasis and beyond. Indian J Dermatol 2013;58:299-305. DOI: https://doi.org/10.4103/0019-5154.113950
Ouchi N, Parker JL, Lugus JJ, Walsh K. Adipokines in inflammation and metabolic disease. Nat Rev Immunol 2011;11:85-97. DOI: https://doi.org/10.1038/nri2921
Bai F, Zheng W, Dong Y, et al. Serum levels of adipokines and cytokines in psoriasis patients: a systematic review and meta-analysis. Oncotarget 2018;9:1266-78. DOI: https://doi.org/10.18632/oncotarget.22260
Romani J, Caixas A, Ceperuelo-Mallafre V, et al. Circulating levels of lipocalin-2 and retinol-binding protein-4 are increased in psoriatic patients and correlated with baseline PASI. Arch Dermatol Res 2013;305:105-12. DOI: https://doi.org/10.1007/s00403-012-1306-5
Abella V, Scotece M, Conde J, et al. The potential of lipocalin-2/NGAL as biomarker for inflammatory and metabolic diseases. Biomarkers 2015;20:565-71. DOI: https://doi.org/10.3109/1354750X.2015.1123354
Kamata M, Tada Y, Tatsuta A, et al. Serum lipocalin-2 levels are increased in patients with psoriasis. Clin Exp Dermatol 2012;37:296-9. DOI: https://doi.org/10.1111/j.1365-2230.2011.04265.x
Ataseven A, Kesli R, Kurtipek GS, Ozturk P. Assessment of lipocalin 2, clusterin, soluble tumor necrosis factor receptor-1, interleukin-6, homocysteine, and uric acid levels in patients with psoriasis. Dis Markers 2014;2014:541709. DOI: https://doi.org/10.1155/2014/541709
Gul FC, Cicek D, Kaman D, et al. Changes of serum lipocalin-2 and retinol binding protein-4 levels in patients with psoriasis and Behcet's disease. Eur J Dermatol 2015;25:195-7. DOI: https://doi.org/10.1684/ejd.2014.2490
Baran A, Swiderska M, Mysliwiec H, Flisiak I. Effect of psoriasis activity and topical treatment on serum lipocalin-2 levels. J Dermatol Treat 2017;28:136-40. DOI: https://doi.org/10.1080/09546634.2016.1180340
Aizawa N, Ishiuji Y, Tominaga M, et al. Relationship between the Degrees of Itch and Serum Lipocalin-2 Levels in Patients with Psoriasis. J Immunol Res 2019;2019:8171373. DOI: https://doi.org/10.1155/2019/8171373
El-Hadidi H, Samir N, Shaker OG, Otb S. Estimation of tissue and serum lipocalin-2 in psoriasis vulgaris and its relation to metabolic syndrome. Arch Dermatol Res 2014;306:239-45. DOI: https://doi.org/10.1007/s00403-013-1414-x
Conrad C, Gilliet M. Psoriasis: from Pathogenesis to Targeted Therapies. Clin Rev Allergy Immunol 2018;54:102-13. DOI: https://doi.org/10.1007/s12016-018-8668-1
Chakraborty S, Kaur S, Guha S, Batra SK. The multifaceted roles of neutrophil gelatinase associated lipocalin (NGAL) in inflammation and cancer. Biochim Biophys Acta 2012;1826:129-69. DOI: https://doi.org/10.1016/j.bbcan.2012.03.008
Fujita H, Terui T, Hayama K, et al. Japanese guidelines for the management and treatment of generalized pustular psoriasis: The new pathogenesis and treatment of GPP. J Dermatol 2018;45:1235-70. DOI: https://doi.org/10.1111/1346-8138.14523
Beygi S, Lajevardi V, Abedini R. C-reactive protein in psoriasis: a review of the literature. J Eur Acad Dermatol Venereol 2014;28:700-11. DOI: https://doi.org/10.1111/jdv.12257
Chiang CC, Cheng WJ, Korinek M, et al. Neutrophils in Psoriasis. Front Immunol 2019;10:2376. DOI: https://doi.org/10.3389/fimmu.2019.02376
Schroll A, Eller K, Feistritzer C, et al. Lipocalin-2 ameliorates granulocyte functionality. Eur J Immunol 2012;42:3346-57. DOI: https://doi.org/10.1002/eji.201142351
Shao S, Cao T, Jin L, et al. Increased Lipocalin-2 Contributes to the Pathogenesis of Psoriasis by Modulating Neutrophil Chemotaxis and Cytokine Secretion. J Invest Dermatol 2016;136:1418-28. DOI: https://doi.org/10.1016/j.jid.2016.03.002
Ferreira MC, Whibley N, Mamo AJ, et al. Interleukin-17-induced protein lipocalin 2 is dispensable for immunity to oral candidiasis. Infect Immun 2014;82:1030-5. DOI: https://doi.org/10.1128/IAI.01389-13
Hau CS, Kanda N, Tada Y, et al. Lipocalin-2 exacerbates psoriasiform skin inflammation by augmenting T-helper 17 response. J Dermatol 2016;43:785-94. DOI: https://doi.org/10.1111/1346-8138.13227
Mallbris L, O'Brien KP, Hulthen A, et al. Neutrophil gelatinase-associated lipocalin is a marker for dysregulated keratinocyte differentiation in human skin. Exp Dermatol 2002;11:584-91. DOI: https://doi.org/10.1034/j.1600-0625.2002.110611.x
Wolk K, Frambach Y, Jacobi A, et al. Increased levels of lipocalin 2 in palmoplantar pustular psoriasis. J Dermatol Sci 2018;90:68-74. DOI: https://doi.org/10.1016/j.jdermsci.2017.12.018
Kabashima K. Langerhans Cells and Dermal Dendritic Cells. Immunology of the Skin. Japan: Springer; 2016. p. 47-8.
Morizane S, Gallo RL. Antimicrobial peptides in the pathogenesis of psoriasis. J Dermatol 2012;39:225-30. DOI: https://doi.org/10.1111/j.1346-8138.2011.01483.x
Yan QW, Yang Q, Mody N, et al. The adipokine lipocalin 2 is regulated by obesity and promotes insulin resistance. Diabetes 2007;56:2533-40. DOI: https://doi.org/10.2337/db07-0007
Wang Y. Small lipid-binding proteins in regulating endothelial and vascular functions: focusing on adipocyte fatty acid binding protein and lipocalin-2. Br J Pharmacol 2012;165:603-21. DOI: https://doi.org/10.1111/j.1476-5381.2011.01528.x
Sultan S, Pascucci M, Ahmad S, et al. LIPOCALIN-2 is a major acute-phase protein in a rat and mouse model of sterile abscess. Shock (Augusta, Ga) 2012;37:191-6. DOI: https://doi.org/10.1097/SHK.0b013e31823918c2
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