Shared Pathophysiology of Inflammatory Bowel Disease and Psoriasis: Unraveling the Connection.

Autor:	Tabbarah S; Department of Medicine, Lebanese American University School of Medicine, Beirut, LBN., Sulaiman H; Department of Medicine, American University of the Caribbean School of Medicine, Cupecoy, SXM., Ansah Owusu F; Department of Medicine, Stavropol State Medical University, Stavropol, RUS.; Department of Medicine, West Pine Medical, St. Louis, USA., Rajeev Joshi M; Department of Medicine, Smt. Nathiba Hargovandas Lakhmichand (NHL) Municipal Medical College, Ahmedabad, IND., Marepalli NR; Department of Medicine, Dr. Patnam Mahender Reddy (PMR) Institute of Medical Sciences, Hyderabad, IND., Pino N; Department of Medicine, University of Manizales, Manizales, COL., Saleem Azam S; Department of Medicine, Dow Medical College, Karachi, PAK., Ali Ahmed A; Department of Internal Medicine, Aga Khan Hospital Mombasa, Mombasa, KEN., Abraham Suárez Álvarez J; Department of General Surgery, Tijuana General Hospital, Tijuana, MEX.
Jazyk:	angličtina
Zdroj:	Cureus [Cureus] 2024 Sep 25; Vol. 16 (9), pp. e70148. Date of Electronic Publication: 2024 Sep 25 (Print Publication: 2024).
DOI:	10.7759/cureus.70148
Abstrakt:	Inflammatory bowel disease (IBD) and psoriasis are both chronic autoimmune diseases with a unique set of characteristics. Interestingly, both conditions share considerable overlap in their pathophysiological mechanisms and immune dysregulation. Epidemiological studies validate the relationship by showing a greater prevalence of co-occurrence of the two disorders. At the genetic level, there is a confirmation of a link between shared susceptibility loci and DNA polymorphism, particularly interleukin-23 receptor (IL23R), interleukin-12 subunit beta (IL12B), tumor necrosis factor (ligand) superfamily member 15 (TNFSF15), and signal transducer and activator of transcription 3 (STAT3). In addition, epigenetic factors have a role in genetic predisposition in the development and progression through processes such as DNA methylation and histone modification adding another layer of genetic susceptibility. The relationship between psoriasis and IBD is emphasized by a comparable immunopathogenesis, which involves delicate relationships between the innate and adaptive immune responses. The primary interest is on the T-helper 17 (Th17) cell pathway and the cytokines interleukin-17 (IL-17), interleukin-23 (IL-23), and tumor necrosis factor-alpha (TNF-α). Consequently, both disorders exhibit chronic inflammation and tissue restructuring, resulting from similar cellular and molecular processes. The presence of overlapping pathophysiology highlights the significance of implementing integrated management strategies and employing multidisciplinary techniques for both diagnosis and therapy. Hence, understanding the mutual processes might facilitate the advancement of precise biologic treatments that aim at these commonly shared inflammatory pathways. Competing Interests: Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work. (Copyright © 2024, Tabbarah et al.)
Databáze:	MEDLINE
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