Journal Article Review Epublish 2 citations
PubMed: 39463646 DOI: 10.7759/cureus.70148
Shared Pathophysiology of Inflammatory Bowel Disease and Psoriasis: Unraveling the Connection.
Cureus 16(9):e70148
Authors: Shadi Tabbarah, Hakam Sulaiman, Frank Ansah Owusu, Megha Rajeev Joshi, Nitheesha Reddy Marepalli, Nohelia Pino, Samra Saleem Azam, Aaliya Ali Ahmed, José Abraham Suárez Álvarez
Affiliations
- Department of Medicine, Lebanese American University School of Medicine, Beirut, LBN.
- Department of Medicine, American University of the Caribbean School of Medicine, Cupecoy, SXM.
- Department of Medicine, Stavropol State Medical University, Stavropol, RUS.
- Department of Medicine, West Pine Medical, St. Louis, USA.
- Department of Medicine, Smt. Nathiba Hargovandas Lakhmichand (NHL) Municipal Medical College, Ahmedabad, IND.
- Department of Medicine, Dr. Patnam Mahender Reddy (PMR) Institute of Medical Sciences, Hyderabad, IND.
- Department of Medicine, University of Manizales, Manizales, COL.
- Department of Medicine, Dow Medical College, Karachi, PAK.
- Department of Internal Medicine, Aga Khan Hospital Mombasa, Mombasa, KEN.
- Department of General Surgery, Tijuana General Hospital, Tijuana, MEX.
Abstract
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.
MeSH
Cells, Interleukin-23, Tumor Necrosis Factor-Alpha, Genetic Predisposition To Disease, Neoplasms, Inflammatory Bowel Diseases, Autoimmune Diseases, Necrosis, Therapeutics, Psoriasis, Interleukin-17