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Indian Journal of Dermatology
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CORRESPONDENCE
Year : 2020  |  Volume : 65  |  Issue : 2  |  Page : 154-155
Tumor necrosis factor-alpha polymorphisms in the pathogenesis of chronic spontaneous urticaria


1 Department of Internal Diseases, Allergology and Clinical Immunology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Poland
2 Department of Internal Diseases, Diabetology and Nephrology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Poland
3 Clinic of Allergology, Rybnik, Poland
4 Department of Internal Diseases and Nephrodiabetology, Medical University of Lodz, Lodz, Poland

Date of Web Publication25-Feb-2020

Correspondence Address:
Zenon Brzoza
Department of Internal Diseases, Allergology and Clinical Immunology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice
Poland
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijd.IJD_73_18

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How to cite this article:
Brzoza Z, Rymarczyk B, Grzeszczak W, Trautsolt W, Oles-Krykowska A, Pluta-Kubicz M, Moczulski D. Tumor necrosis factor-alpha polymorphisms in the pathogenesis of chronic spontaneous urticaria. Indian J Dermatol 2020;65:154-5

How to cite this URL:
Brzoza Z, Rymarczyk B, Grzeszczak W, Trautsolt W, Oles-Krykowska A, Pluta-Kubicz M, Moczulski D. Tumor necrosis factor-alpha polymorphisms in the pathogenesis of chronic spontaneous urticaria. Indian J Dermatol [serial online] 2020 [cited 2020 Nov 28];65:154-5. Available from: https://www.e-ijd.org/text.asp?2020/65/2/154/279205




Sir,

Recent reports highlight the possible genetic background of chronic spontaneous urticaria (CSU). According to eligible published papers, polymorphisms in genes related to inflammation and autoimmunity may predispose to CSU.[1],[2] Tumor necrosis factor (TNF) is secreted mainly by macrophages and mast cells and acts as a multifunctional pro-inflammatory cytokine. Its synthesis is augmented on mast cell activation. A few controlled studies showed that TNF-α is upregulated in patients with CSU.[3] Moreover, a few trials in small series gave promising results with TNF-α inhibitors as an effective tool in controlling recalcitrant CSU. Since the role of TNF-α in CSU is suspected, the role of certain polymorphisms of TNF-α can be hypothesized.

In our study, patients' group was composed of 153 unrelated CSU patients (91 females and 62 males, mean age: 36.4 years, range: 19–61) with positive autologous serum skin test (ASST) result. The control group was composed of 106 unrelated healthy volunteers (70 females and 36 males, mean age: 38.9 years, range: 18–59). All individuals were Caucasian and came from the Polish population. Disease severity was analyzed by a 7-day assessment with the Urticaria Activity Score. The age of disease onset was also analyzed. In all the examined subjects, we studied TNF1α rs1799964, rs1799724, and rs1800629 polymorphisms. In statistical analyses, we used Chi-square, odds ratio, and ANOVA tests. The study was approved by the Bioethics Committee of the Medical University of Silesia in Katowice, Poland.

Hardy–Weinberg equilibrium assay revealed no deviation in the examined groups. The allele or genotype distribution analysis resulted in no statistically significant differences between CSU patients and controls [Table 1]. There were no differences in haplotype frequencies [Table 2]. In addition, no relation was proved between TNF1α polymorphisms and urticaria severity or the age of disease onset.
Table 1: Tumor necrosis factor 1-α genotypes and allele distribution in chronic spontaneous urticaria patients and healthy controls

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Table 2: Tumor necrosis factor 1-alpha haplotype distribution in chronic spontaneous urticaria patients and healthy controls

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The contribution of autoimmunity to the pathogenesis of CSU is obvious; however, the exact mechanisms involved are still open to debate. Therefore, patients with positive ASST were enrolled in our study. One of the genes considered in CSU pathogenesis is TNF-α gene. Choi et al .[4] demonstrated that TNF-α polymorphisms at –1031T/C and –863C/A as well as their haplotypes were significantly associated with aspirin-induced urticaria in the Korean population. Tavakol et al .[5] showed in the Iranian population that G allele was significantly higher in CSU patients at locus –238G/A and –308G/A of TNF-α gene and concluded that this polymorphism can affect susceptibility to this disorder. Our data did not confirm the observation of a potent link between TNF-α polymorphisms at –1031 T/C, –857C/T, and –308G/A and CSU in the Polish population. To the best of our knowledge, this is the first study considering the role of the above-mentioned polymorphisms in the pathogenesis of CSU. Further analyses should be conducted on large population stratified by ethnicity. Genetics seem to be a promising direction in further search for CSU pathogenesis.

Financial support and sponsorship

This study was supported by a research grant from the Medical University of Silesia (KNW-1-067/N/5/0).

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Brzoza Z, Grzeszczak W, Rogala B, Trautsolt W, Moczulski D. PTPN22 polymorphism presumably plays a role in the genetic background of chronic spontaneous autoreactive urticaria. Dermatology 2012;224:340-5.  Back to cited text no. 1
    
2.
Brzoza Z, Grzeszczak W, Rogala B, Trautsolt W, Moczulski D. Possible contribution of chemokine receptor CCR2 and CCR5 polymorphisms in the pathogenesis of chronic spontaneous autoreactive urticaria. Allergol Immunopathol (Madr) 2014;42:302-6.  Back to cited text no. 2
    
3.
Atwa MA, Emara AS, Youssef N, Bayoumy NM. Serum concentration of IL-17, IL-23 and TNF-α among patients with chronic spontaneous urticaria: Association with disease activity and autologous serum skin test. J Eur Acad Dermatol Venereol 2014;28:469-74.  Back to cited text no. 3
    
4.
Choi JH, Kim SH, Cho BY, Lee SK, Kim SH, Suh CH, et al. Association of TNF-α promoter polymorphisms with aspirin-induced urticaria. J Clin Pharm Ther 2009;34:231-8.  Back to cited text no. 4
    
5.
Tavakol M, Amirzargar AA, Movahedi M, Aryan Z, Bidoki AZ, Gharagozlou M, et al. Interleukin-6 and tumor necrosis factor-α gene polymorphisms in chronic idiopathic urticaria. Allergol Immunopathol (Madr) 2014;42:533-8.  Back to cited text no. 5
    



 
 
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