Discussion: Psoriasis Is A Chronic Inflammatory Proliferativ

Discussion 1psoriasis Is Chronic Inflammatory Proliferative Relapsin

Discussion 1psoriasis Is Chronic Inflammatory Proliferative Relapsin

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Psoriasis is a chronic, inflammatory, proliferative, and relapsing skin disorder affecting the skin, scalp, and nails. Its complex pathophysiology involves immune-mediated mechanisms, primarily characterized by abnormal epidermal differentiation and hyperproliferation of keratinocytes. Current research emphasizes the role of the immune system, especially T-cells, in the development and progression of psoriasis. Langerhans cells, antigen-presenting cells within the skin, play a pivotal role by migrating to regional lymph nodes and activating T-cells through interaction with cytokines and co-stimulatory signals involving CD2 and LFA-1 receptors, which bind to adhesion molecules like LFA-3 and ICAM-1 (Lui, 2022). Upon activation, T-cells release cytokines such as TNF-alpha, IFN-gamma, and IL-17, fostering a local inflammatory response that sustains and propagates the epidermal hyperplasia characteristic of psoriasis (Gottlieb et al., 2017). The inflammatory milieu results in keratinocyte proliferation and altered differentiation, leading to the formation of the thick, scaly plaques typical of the disease.

Clinically, psoriasis presents with raised, well-demarcated plaques that are often irregular or oval-shaped, ranging from a few millimeters to several centimeters in size. These lesions are typically found on extensor surfaces such as elbows, knees, and scalp, displaying a characteristic silvery-white or micaceous scale over a red or violaceous base. The lesions are usually symmetrically distributed and may involve the trunk and limbs. The diagnosis is primarily clinical, based on characteristic morphological features. In atypical cases, skin biopsy can confirm hyperkeratosis, acanthosis, and inflammatory infiltrates consistent with psoriasis (Lui, 2022).

Management of psoriasis involves a multidisciplinary approach, including topical therapies, phototherapy, and systemic agents. Topical corticosteroids are the first-line treatment and serve to reduce inflammation and scale. Vitamin D analogs such as calcipotriol, coal tar, and topical immunomodulators may also be used. Phototherapy, particularly narrowband UVB, is effective for moderate to severe cases. When topical treatments are insufficient, biological therapies targeting specific cytokines (e.g., anti-TNF agents, IL-17 inhibitors) have revolutionized management by addressing the underlying immune dysregulation (Gottlieb et al., 2017). These biologics interfere with T-cell activation or cytokine activity, leading to significant improvements in clinical severity and quality of life for many patients.

Lichen planus (LP) is another immune-mediated skin disorder, of which the pathophysiology remains incompletely understood. It involves a cell-mediated immune response where T-cells attack basal keratinocytes, leading to characteristic violaceous papules and plaques. It often coexists with other autoimmune or inflammatory conditions, such as ulcerative colitis and hepatitis C infection, suggesting a systemic immune derangement (Chuang, 2021). Clinically, LP presents with pruritic, polygonal, purple papules that may involve mucous membranes, nails, and scalp. Oral mucosal involvement appears as Wickham striae—lacy white lines—and may be asymptomatic or cause burning. Nail involvement can lead to pitting or ridging, while scalp lesions may result in alopecia. Diagnosis involves clinical examination complemented by histopathology and direct immunofluorescence, which reveals characteristic band-like lymphocytic infiltrates and deposits of immunoglobulins (Chuang, 2021). Treatment aims at symptom control, often with topical corticosteroids; severe or resistant cases may require systemic immunosuppressants like cyclosporine.

Seborrheic keratosis represents the most common benign epidermal tumor, predominantly affecting older adults. Its pathogenesis remains unknown but involves benign proliferation of basal keratinocytes, resulting in well-circumscribed, waxy, greasy lesions that appear 'stuck-on.' Clinically, these lesions are varied in color, from tan to dark brown or black, with sizes ranging from a few millimeters to centimeters. They often occur on seborrheic areas such as the face, chest, and back. Dermatoscopic examination reveals characteristic features such as keratin pseudocysts and comedo-like openings. Confirmatory diagnosis is via shave biopsy, which shows hyperkeratosis, acanthosis, and papillomatosis without atypia (Balin, 2021). These lesions are benign, requiring no treatment unless for cosmetic reasons, with options including cryotherapy or electrocautery.

Actinic keratosis (AK) is a premalignant lesion caused by prolonged ultraviolet (UV) exposure leading to mutations in critical tumor suppressor genes such as TP53 and deletion of p16. AK manifests as rough, scaly, erythematous or pink papules, often on sun-exposed areas like the face, ears, scalp, and dorsal hands (Spencer, 2021). The lesion’s appearance reflects dysplastic keratinocytes confined to the epidermis. Although AK has the potential to progress to invasive squamous cell carcinoma (SCC), progression risk varies depending on size, number, and histological features. Diagnosis involves dermoscopy and histopathology, which show keratinocyte atypia and partial loss of maturation. Management includes photoprotection, topical agents such as 5-fluorouracil (5-FU) or imiquimod, and ablative therapies like cryotherapy. Regular follow-up is essential to monitor for malignant transformation (McCance & Huether, 2014; Spencer, 2021).

References

  • Balin, A. K. (2021). Seborrheic Keratosis: Background, Pathophysiology, Etiology. In StatPearls.
  • Chuang, T. (2021). Lichen Planus: Practice Essentials, Background, Pathophysiology. Medscape.
  • Gottlieb, A. B., et al. (2017). Psoriasis: Pathogenesis and Therapy. Nature Reviews Disease Primers, 3, 17010.
  • Lui, H. (2022). Plaque Psoriasis: Practice Essentials, Background, Pathophysiology. In Medscape.
  • McCance, K. L., & Huether, S. E. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). Elsevier Mosby.
  • Spencer, J. M. (2021). Actinic Keratosis: Practice Essentials, Background, Pathophysiology. In Medscape.
  • Koya, H. H., & Paul, M. (2022). Shock. StatPearls.

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