Psoriasis and inflammatory bowel disease (IBD), both chronic and inflammatory diseases, coexist in many patients and share genetic profiles. In a recent review, researchers explores and described the existing evidence connecting and distinguishing both diseases, from the immune response to the currently used treatments and known risk factors.
The review paper, titled “Psoriasis and inflammatory bowel disease: links and risks,” was published in Psoriasis: Targets and Therapy.
Psoriasis is a chronic, inflammatory skin condition that affects 2-3% of the population. Ulcerative colitis (UC) and Crohn’s disease (CD) are the main diseases constituting the IBD group. Immune system dysregulation, resulting from a combination of genetic predisposition and environmental factors, underlies all three conditions. Importantly, various clinical studies have suggested a coincidence of psoriasis and IBD in some patients. The relative risk of psoriasis is significantly increased in both UC and Crohn’s. Likewise, patients with psoriasis have an increased risk of developing IBD.
In the recent study, researchers reviewed the more relevant and recent literature on the role of microbiota, inflammatory cells and inflammation mediators in psoriasis and IBD development, and response to pharmacologic treatments.
The authors reported that a genetic susceptibility background is the probable cause of disease development and clinical overlap between psoriasis and IBD. To date, there are 13 psoriasis susceptibility genome regions (loci) described, 32 loci in the pathogenesis of CD, and 17 in UC. Some of the disease susceptibility loci are shared between the conditions, despite the genes being mostly different. Future research will likely bring better understanding of the common genetics involved in all three disorders.
The microbiota represents the community of beneficial and pathogenic microorganisms that exist in the human body. It is increasingly studied for its role in human health and disease development. The organisms can act as both triggers and inhibitors of inflammation; the balance of the effects have been studied more in the IBD context than in psoriasis.
According to researchers: “Alterations of the microbial flora in the gut and the skin may not only result from disease-associated tissue perturbations but may also exacerbate and maintain the disease state in a vicious self-perpetuating cycle.”
The role of both the innate immune system, the body’s primary line of defense, and the adaptive immune system in the pathogenesis of the conditions are also discussed. Both conditions share the disruption of the epithelial cell barriers, in the skin for psoriasis and in the lining of the intestinal tract. Such defects alter the structure of the protective barriers, leading to increased microorganism invasion and stimulation of inflammation. Many other cell types are also covered in the lengthy review.
Another factor that hints at the close proximity of the diseases is the overlap of approved pharmacologic treatments employed to treat psoriasis and IBD. But some core differences in response to the treatments highlight the different pathogenicity process of the conditions.
While the available data supports common disease traits at several fronts, the authors concluded: “Further studies may unravel the common mechanism that underlies these common chronic inflammatory diseases of skin and gut and may provide valuable insights for the development of innovative interventions for both conditions.”
