Maleeha Ahmad

Background: Psoriasis is a chronic, non-contagious skin condition characterized by sharply demarcated, erythematous, scaly plaques which commonly appear on extensor surfaces, such as the elbows, knees, scalp, and other areas of the body. It is estimated that 125 million people worldwide suffer from psoriasis, and it can occur in both children and adults.¹ Psoriasis manifestation is heterogenous and complex, with a wide range of presentations and a variety of comorbidities. The exact cause and mechanism of psoriasis is not known, but it is thought to be an autoimmune disorder triggered by environmental and genetic factors. Studies have identified several genetic loci associated with psoriasis, including the human leukocyte antigen (HLA) loci, as well as genes involved in the regulation of cytokine production.² Environmental factors, such as stress, trauma, smoking, and certain medications, have also been linked to psoriasis. Stress has been proposed to play a role in the pathogenesis of psoriasis, as it can lead to altered cytokine production and increased skin sensitivity. Certain medications, such as beta blockers and antimalarials, can also trigger or exacerbate psoriasis.

Objective: In this narrative review, we explored the mechanisms behind psoriatic symptomatology with a focus on changes in lymphatic activity.

Search Methods: An online search of the PubMed database was conducted from 2017 to 2023 with searchwords: “psoriasis”, “lymphatics”, “psoriasis pathogenesis”.

Results: Theories surrounding psoriatic pathophysiology include an inappropriate cascade of cellular and molecular events, including the activation of helper T cells and the production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-17 (IL-17) and interleukin-23 (IL-23). These cytokines play a role in the induction of keratinocyte proliferation and the formation of the red, scaly plaques that are characteristic of psoriasis.³

Approximately 30% of patients develop psoriatic arthritis in conjunction with extensor surface rash.⁴ Psoriatic arthritis manifestation occurs due to immune system attack upon the entheses, the lining around joints. Psoriatic arthritis can occur in any joint, and symptoms include swelling, pain, stiffness, tenderness, fatigue, psoriasis, nail changes, tophi, enthesitis, dactylitis, uveitis, spondylitis, synovitis, and arthropathy.

The primary objective of psoriasis treatment is to reduce the symptoms of the illness and to improve quality of life in patients. Treatments available include topical steroid therapies, phototherapy, systemic medications, and biologics.⁵ Recently, there has been increase focus on the use of biologics in severe psoriasis, which are disease-modifying drugs that target specific pathways of the immune system.

Conclusion: In conclusion, psoriasis is a complex disorder, with multiple factors contributing to its pathogenesis. It is believed to involve an altered immune system, as well as genetic and environmental factors. Further research is needed to understand the pathophysiology of psoriasis and to develop more effective treatments; however, changes in lymphatic activity and endothelial dysfunction remain primary suspects.

Works Cited.

1. Armstrong AW, Read C. Pathophysiology, Clinical Presentation, and Treatment of Psoriasis: A Review. JAMA. 2020;323(19):1945-1960. doi:10.1001/jama.2020.4006
2. Huang YW, Tsai TF. HLA-Cw1 and Psoriasis. Am J Clin Dermatol. 2021;22(3):339-347. doi:10.1007/s40257-020-00585-1
3. Furue K, Ito T, Tsuji G, Kadono T, Furue M. Psoriasis and the TNF/IL23/IL17 axis. G Ital Dermatol Venereol. 2019;154(4):418-424. doi:10.23736/S0392-0488.18.06202-8
4. Ocampo D V, Gladman D. Psoriatic arthritis. F1000Res. 2019;8:F1000 Faculty Rev-1665. Published 2019 Sep 20. doi:10.12688/f1000research.19144.1
5. Jiang Y, Chen Y, Yu Q, Shi Y. Biologic and Small-Molecule Therapies for Moderate-to-Severe Psoriasis: Focus on Psoriasis Comorbidities. BioDrugs. 2023;37(1):35-55. doi:10.1007/s40259-022-00569-z