The Importance of Early Treatment in Psoriasis and Management of Disease Progression
July 2018 | Volume 17 | Issue 7 | Original Article | 737 | Copyright © July 2018
Francisco Kerdel MD,a,b Frank Don DOa
aFlorida Academic Dermatology Center, Coral Gables, FL bFlorida International University, Miami, FL
Psoriasis is a chronic, immune-mediated, inflammatory disease that if left untreated can result in prolonged subclinical inflammation
that affects a variety of organs, including the heart, liver, kidney, and intestines, as well as joints and muscles. Relatedly, psoriasis significantly
increases patients’ risks for developing certain comorbidities. Disease progression in psoriasis is unpredictable, and some patients
have mild disease that is stable for many years, while in others, mild disease quickly progresses to moderate-to-severe psoriasis.
Adding to the complexity of this disease, subclinical systemic inflammation is present in patients with either mild or moderate-to-severe
psoriasis. In this review, key factors in psoriasis progression, including the role that systemic inflammation has in psoriasis pathogenesis
and the development of comorbidities, are highlighted along with the ability of various therapies to potentially stop or slow the
progression of psoriasis and its associated comorbidities. Additionally, practical guidance is provided for physicians regarding treatment
and monitoring of disease progression based on psoriasis severity and the risk of comorbidities.
J Drugs Dermatol. 2018;17(7):737-742.
Psoriasis is a chronic, immune-mediated, inflammatory disease that affects more than 7 million adults in the United States.1 In recent years, tremendous progress has been made in understanding disease pathogenesis and these findings have informed the development of new systemic therapies associated with a more targeted approach, leading to highly effective results. Despite these substantial advances in research, there is still more to elucidate and a gap exists in understanding and evaluating disease progression in psoriasis.2 Some patients experience chronic, persistent lesions for decades, while others experience periods of short- or long-term remission.3 In some cases, patients develop only mild disease that is relatively stable over many years, while in other cases, mild disease can quickly progress to moderate-to-severe psoriasis.4 There is no evidence that psoriasis follows a predictable stepwise progression that is dependent on previous events.5Reports by the American Academy of Dermatology and the US Centers for Disease Control and Prevention have identified understanding of disease progression in psoriasis as a major research gap that limits our knowledge about factors affecting prognosis, treatment response, and development of comorbid conditions.2,6,7 Research efforts are needed to understand the natural history of psoriasis in order to better predict disease triggers, progression, and the relationship between psoriasis and various comorbidities.2,6 If disease progression can be anticipated, healthcare providers can improve quality of care by utilizing early and aggressive treatment strategies for more severe disease that can alleviate symptoms, prevent permanent damage associated with comorbidities, and improve patients’ quality of life.This review discusses key factors in psoriasis progression, including the role of systemic inflammation in both psoriasis pathogenesis and development of comorbidities, along with the potential role of systemic therapy in halting or slowing progression of psoriasis and associated comorbidities. Practical guidance is provided for treatment and monitoring of disease progression based on psoriasis severity and risk factors for comorbidities.
Psoriasis Progression and Comorbidities
Psoriasis immunopathogenesis is characterized by upregulation of inflammatory pathways that stimulate abnormal/excessive growth of skin cells. These immune responses are mediated by T helper (Th) cells that release numerous different pro-inflammatory cytokines; for instance, interleukin (IL)-23 stimulates Th17 cells to produce tumor necrosis factor-α (TNFα), IL-17, and IL-22.8 IL-17 subsequently promotes keratinocyte hyperproliferation and stimulates production of cytokines. Additionally, the actions of IL-17 affect other organs beyond the skin.9,10 In patients with uncontrolled psoriasis, elevated levels of pro-inflammatory cytokines are found not only in skin lesions, but also in plasma,11,12 which may lead to subclinical systemic inflammation. As psoriasis progresses in patients with chronic disease, the risk for prolonged inflammation affecting other organs, including the heart, liver, kidneys, and intestines, as well as joints and muscles, significantly increases.13,14