Triggers for the onset and recurrence of psoriasis: a review and update

Abstract

Psoriasis is an immune-mediated inflammatory skin disease, involving a complex interplay between genetic and environmental factors. Previous studies have demonstrated that genetic factors play a major role in the pathogenesis of psoriasis. However, non-genetic factors are also necessary to trigger the onset and recurrence of psoriasis in genetically predisposed individuals, which include infections, microbiota dysbiosis of the skin and gut, dysregulated lipid metabolism, dysregulated sex hormones, and mental illness. Psoriasis can also be induced by other environmental triggers, such as skin trauma, unhealthy lifestyles, and medications. Understanding how these triggers play a role in the onset and recurrence of psoriasis provides insights into psoriasis pathogenesis, as well as better clinical administration. In this review, we summarize the triggers for the onset and recurrence of psoriasis and update the current evidence on the underlying mechanism of how these factors elicit the disease.

Risk Factors for Psoriasis Flares: A Narrative Review

“… 9 Furthermore, in patients with psoriasis, a higher presence of Firmicutes was observed in the skin lesions than Actinobacteria, which was higher in the skin of healthy subjects. 9 Although the significance of these alterations in the microbiota is unknown, it is believed that leads to an increase in skin T-cells conducted by IL-17 and IL-22, a hypothesis similar to that of the role of the intestinal microbiota in Crohn’s disease. 17 Regarding mycoses, the literature indicates a higher OR of colonisation by Candida in patients with psoriasis compared to controls; 18 in addition, a meta-analysis observed that in patients with psoriasis, Candida colonization of the oral mucosa is greater than in controls.…”

“… 16 Dysregulation of the skin microbiota is another factor related to psoriasis, as evidenced by the presence of S. Aureus in the psoriatic lesions of 60% of the affected population, compared with 5–30% of the population with healthy skin. 9 The increased presence of this bacterium is associated with a reduction in S. epidermidis and Propionibacterium acnes, compared to healthy patients. 9 Furthermore, in patients with psoriasis, a higher presence of Firmicutes was observed in the skin lesions than Actinobacteria, which was higher in the skin of healthy subjects.…”

“… 9 The increased presence of this bacterium is associated with a reduction in S. epidermidis and Propionibacterium acnes, compared to healthy patients. 9 Furthermore, in patients with psoriasis, a higher presence of Firmicutes was observed in the skin lesions than Actinobacteria, which was higher in the skin of healthy subjects. 9 Although the significance of these alterations in the microbiota is unknown, it is believed that leads to an increase in skin T-cells conducted by IL-17 and IL-22, a hypothesis similar to that of the role of the intestinal microbiota in Crohn’s disease.…”

“… 3 The former include external mechanical stress, infections, medications, lifestyle, environment and pollution; the intrinsic include psychological stress, hormonal and metabolic alterations, and dysbiosis of the skin and intestinal microbiota. 9 However, another possible classification is between classic and emerging risk factors for psoriasis flare-ups. Classic risk factors have long been known to be responsible for worsening and/or reoccurrence of psoriatic manifestations; emerging risk factors are defined as those newly identified risk factors being represented by newly developed drugs and vaccines or newly identified infectious agents.…”

“…The underlying mechanism is not fully elucidated, but undoubtedly, as a result of the trauma, there is an increased production of cathelicidin LL-37, an antimicrobial peptide that increases in response to damage and forms complexes with genetic material from the damaged cells themselves, which in turn stimulate plasmacytoid dendritic cells to secrete type 1 interferons (IFN), such as IFN-α and IFN-β. 9 These are crucial for the proliferation of basal keratinocytes and in increasing Nerve Growth Factor (NGF) with consequent angiogenesis and activation of memory T-cells resident in the affected tissue, which is followed by the development of the psoriatic lesion. 10 A characteristic example that can induce this phenomenon is tattooing.…”