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Psoriasis Risk Factors and Triggers

Cutis. 2018 November;102(5S):18-20
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Numerous factors contribute to the onset and exacerbation of psoriasis. Genetic risk factors include HLA-Cw6 and mutations in the caspase recruitment domain family member 14 gene, CARD14. Environmental risk factors, including infectious diseases, medications, and lifestyle, also have been implicated. It is important for clinicians to be aware of these risk factors and triggers because they might provide insight into the pathogenesis of psoriasis as well as help patients understand more about their disease.

Practice Points

  • HLA-Cw6 and CARD14 are genetic factors associated with psoriasis.
  • Psoriasis in the setting of human immunodeficiency virus infection may be treated with topical steroids, phototherapy, systemic retinoids, or apremilast.
  • Psoriasis is a potential adverse effect in patients taking lithium or tumor necrosis factor inhibitors.
  • Patients should be counseled about the role of obesity and smoking on psoriasis.

Medications

Numerous medications can trigger psoriasis, including lithium, nonsteroidal anti-inflammatory drugs, antimalarials, beta-blockers, and angiotensin-converting enzyme inhibitors.34 More recent literature suggests that TNF inhibitors also can paradoxically induce psoriasis in rare cases.35

Lithium
Psoriasis is the most common cutaneous adverse effect of lithium.34 It is more likely to exacerbate existing disease but also can induce onset of psoriasis; it also can cause disease that is more refractory to treatment.34,36 Current literature hypothesizes that lithium triggers psoriasis by interference of intracellular calcium channels through reduction of inositol, thereby affecting keratinocyte proliferation and differentiation.34 Lithium also inhibits glycogen synthase kinase-3 (GSK-3), a serine threonine kinase, which, in turn, induces human keratinocyte proliferation.37 However, it is unlikely lithium alone can induce psoriasis; genetic predisposition is necessary.

TNF Inhibitors
Tumor necrosis factor inhibitors such as adalimumab, etanercept, certolizumab pegol, golimumab, and infliximab are used in various inflammatory diseases, including psoriasis. Interestingly, there have been more than 200 reported cases of suspected TNF inhibitor–induced or –exacerbated psoriasis.38 This phenomenon appears to occur more frequently with infliximab and is most likely to occur in the first year of treatment of Crohn disease and rheumatoid arthritis.38 Plaque psoriasis is the most common form, but 15% to 26% of cases presented with 2 or more morphologies.38,39

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Treatment options include discontinuing therapy, though many patients experience resolution while continuing treatment or switching to another TNF inhibitor.38-40 Traditional topical therapies also have been used with success.40 The pathogenesis of this phenomenon is still unclear but is thought to involve both the IL-23/helper T cell 17 (TH17) axis and dysregulation of IFN-α in the setting of TNF suppression.38

Lifestyle

Obesity is a chronic low-grade inflammatory state that can contribute to the onset of psoriasis or exacerbation of existing disease.41,42 Smoking also is thought to increase the risk for psoriasis, perhaps by a similar mechanism. Lee et al43 found a strong positive correlation between the amount or duration of smoking and the incidence of psoriasis.

The relationship between psoriasis and alcohol consumption is less clear than it is between psoriasis and obesity or smoking; greater consumption is found in psoriasis patients, but evidence is insufficient to deem alcohol a risk factor.44

Conclusion

Various factors, including genetics, infection, pharmacotherapeutic, and lifestyle, can all contribute to the induction or exacerbation of psoriasis. These factors can provide clues to the pathogenesis of psoriasis as well as help clinicians better counsel patients about their disease.