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Psoriasis Risk Factors and Triggers
Author(s)
Erica B. Lee, BS
Kevin K. Wu, BA
Michael P. Lee, BS
Tina Bhutani, MD
Jashin J. Wu, MD

Psoriasis is a chronic autoimmune skin disease affecting approximately 6.7 million adults in the United States.1 Although its pathogenesis is not yet clear, risk factors and triggers provide insight into potential pathways by which psoriasis can occur. There is notable overlap between risk factors and triggers of psoriasis; perceived risk factors might, in fact, be triggers causing manifestation of disease in predisposed persons. In this review, we summarize the key factors contributing to onset and exacerbation of psoriasis. When learning to manage this chronic disease, it also may be helpful to educate patients about how these elements may affect the course of psoriasis.

Genetics

The pathogenesis of psoriasis has a strong genetic component, with approximately 70% and 20% concordance rates in monozygotic and dizygotic twins, respectively.2 Moreover, studies have shown a positive family history in approximately 35% of patients.3,4 Family-based studies have found a 50% risk of developing psoriasis in patients with 2 affected parents.5 However, the genetics of psoriasis are complex and are attributed to many different genes. Thus far, genes involving antigen presentation, T-cell receptor development and polarization, and the nuclear factor κβ (NF-κβ) pathway have been identified.6

HLA-Cw6
The most well-studied gene implicated in psoriasis is HLA-Cw6, which encodes a major histocompatibility complex class I allele supporting psoriasis as a T cell–mediated reaction to an autoantigen.6 Two potential antigens for HLA-Cw6 recently have been identified: LL-37, a cathelicidin-related antimicrobial peptide, and the A disintegrin and metalloproteinase with thrombospondin motifs-like protein 5 (ADAMTSL5), found on melanocytes and keratinocytes.7 The percentage of psoriasis patients with HLA-Cw6 ranges from 10.5% to 77.2%, with higher frequency in white individuals than in Asians.7

HLA-Cw6 manifests as specific features in psoriasis, including onset of disease before 21 years of age.8 It also is more strongly associated with guttate-type psoriasis, greater body surface area involvement, and higher incidence of Köbner phenomenon. Patients with positive HLA-Cw6 also reported worsening of psoriasis during and after throat infection.9

Caspase Recruitment Domain Family Member 14
Another gene mutation implicated in psoriasis pathogenesis is caspase recruitment domain family member 14, CARD14 (formerly PSORS2), a gene encoding a scaffolding protein important in the activation of NF-κβ.10,11 Missense CARD14 mutations cause upregulation of NF-κβ through formation of a complex with adapter protein B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1),12 which, in turn, causes increased transcription of cytokines IL-8, C-C motif chemokine ligand 20 (CCL-20), and IL-36 gamma in the keratinocyte.13 Mutations in CARD14 alone lead to psoriasiform skin in mice through amplified activation of the IL-23/IL-17 axis.14,15 Patients with a mutation in a CARD14 variant (p.Arg820Trp) have demonstrated better response to tumor necrosis factor (TNF) inhibitors.16

Further characterization of the genetic pathogenesis of psoriasis might lead to better targeted therapies, including the possibility of MALT1 inhibitors as a treatment option.12

 

 

Infection

Streptococcus
The association between streptococcal infection and psoriasis was first documented more than 100 years ago, specifically the onset of acute guttate psoriasis.17,18 Although classically described following throat infection, psoriasis also occurs following streptococcal vulvovaginitis and perianal streptococcal infection.19,20

This type of psoriasis is typically self-limited but can recur with subsequent streptococcal infections or initiate a more chronic plaque psoriasis. Patients have a 1 in 3 risk of developing chronic psoriasis within 10 years of a single episode of acute guttate psoriasis.21 Moreover, in many patients with existing plaque psoriasis, throat infection exacerbates psoriatic symptoms.22 The mechanism of exacerbation is likely due to cross-reactivity between streptococcal M surface antigen and human keratinocytes and might also be influenced by inherited abnormalities in immune response.23-26 Therefore, tonsillectomy has been studied as a possible treatment of psoriasis but is likely helpful only in patients with exacerbations of disease that are closely associated with recurrent tonsillitis.27

Human Immunodeficiency Virus
The prevalence of psoriasis in human immunodeficiency virus (HIV) patients is similar to or greater than the general population.28 Human immunodeficiency virus infection causes new onset of psoriasis and exacerbation of existing psoriasis; severity often is correlated with worsening immune function.28,29

The clinical subtypes of psoriasis that occur most frequently with HIV include guttate, inverse, and erythrodermic, though patients may present with any subtype.28 The mechanism is puzzling because HIV is primarily mediated by helper T cell 2 (TH2) cytokines, whereas psoriasis is mainly driven by helper T cell 1 (TH1) cytokines.30 Furthermore, despite increased severity with lower CD4+ counts, treatments further lowering T-cell counts paradoxically improve symptoms.31 Current literature suggests that expansion of CD8+ memory T cells might be the primary mechanism in the exacerbation of psoriasis in HIV-mediated immunosuppression.30

Treatment of HIV-associated psoriasis presents challenges because many therapeutics cause further immunosuppression. The National Psoriasis Foundation recommends topical preparations as first-line agents for mild to moderate psoriasis.32 For moderate to severe psoriasis, retroviral agents may be effective as first-line monotherapy or when supplemented by phototherapy with UVB or psoralen plus UVA. Retinoids can be used as second-line agents.32 For cases of severe refractory psoriasis, cyclosporine, methotrexate, TNF inhibitors, or hydroxyurea can be considered. There also is evidence that apremilast is effective without risk for worsening immune function.33

Other Infections
Other bacteria associated with triggering or exacerbating psoriasis include Staphylococcus aureus and Helicobacter pylori.34,35 Fungi, such as species of the genera Malassezia and Candida, and other viruses, including papillomaviruses and retroviruses, also have been implicated.34

 

 

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

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.

References
  1. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
  2. Bowcock AM. The genetics of psoriasis and autoimmunity. Annu Rev Genomics Hum Genet. 2005;6:93-122.
  3. Swanbeck G, Inerot A, Martinsson T, et al. A population genetic study of psoriasis. Br J Dermatol. 1994;131:32-39.
  4. Kimberling W, Dobson RL. The inheritance of psoriasis. J Invest Dermatol. 1973;60:538-540.
  5. Gupta R, Debbaneh MG, Liao W. Genetic epidemiology of psoriasis. Curr Dermatol Rep. 2014;3:61-78.
  6. Harden JL, Krueger JG, Bowcock AM. The immunogenetics of psoriasis: a comprehensive review. J Autoimmun. 2015;64:66-73.
  7. Chen L, Tsai TF. HLA-Cw6 and psoriasis. Br J Dermatol. 2018;178:854-862.
  8. Enerbäck C, Martinsson T, Ineraot A, et al. Evidence that HLA-Cw6 determines early onset of psoriasis, obtained using sequence-specific primers (PCR-SSP). Acta Derm Venereol. 1997;77:273-276.
  9. Gudjónsson JE, Kárason A, Antonsdóttir EH, et al. HLA-Cw6-positive and HLA-Cw6-negative patients with psoriasis vulgaris have distinct clinical features. J Invest Dermatol. 2002;118:362-365.
  10. Tomfohrde J, Silverman A, Barnes R, et al. Gene for familial psoriasis susceptibility mapped to distal end of human chromosome 17q. Science. 1994;264:1141-1145.
  11. Blonska M, Lin X. NF-κB signaling pathways regulated by CARMA family of scaffold proteins. Cell Res. 2011;21:55-70.
  12. Van Nuffel E, Schmitt A, Afonina IS, et al. CARD14-mediated activation of paracaspase MALT1 in keratinocytes: implications for psoriasis. J Invest Dermatol. 2017;137:569-575.
  13. Jordan CT, Cao L, Roberson ED, et al. PSORS2 is due to mutations in CARD14. Am J Hum Genet. 2012;90:784-795.
  14. Wang M, Zhang S, Zheng G, et al. Gain-of-function mutation of Card14 leads to spontaneous psoriasis-like skin inflammation through enhanced keratinocyte response to IL-17A. Immunity. 2018;49:66-79.
  15. Mellet M, Meier B, Mohanan D, et al. CARD14 gain-of-function mutation alone is sufficient to drive IL-23/IL-17-mediated psoriasiform skin inflammation in vivo. J Invest Dermatol. 2018;138:2010-2023.
  16. Coto-Segura P, González-Fernández D, Batalla A, et al. Common and rare CARD14 gene variants affect the antitumour necrosis factor response among patients with psoriasis. Br J Dermatol. 2016;175:134-141.
  17. Winfield JM. Psoriasis as a sequel to acute inflammations of the tonsils: a clinical note. J Cutan Dis. 1916;34:441-443.
  18. Telfer NR, Chalmers RJG, Whale K, et al. The role of streptococcal infection in the initiation of guttate psoriasis. Arch Dermatol. 1992;128:39-42.
  19. Hernandez M, Simms-Cendan J, Zendell K. Guttate psoriasis following streptococcal vulvovaginitis in a five-year-old girl. J Pediatr Adolesc Gynecol. 2015;28:e127-e129.
  20. Herbst RA, Hoch O, Kapp A, et al. Guttate psoriasis triggered by perianal streptococcal dermatitis in a four-year-old boy. J Am Acad Dermatol. 2000;42(5, pt 2):885-887.
  21. Martin BA, Chalmers RJ, Telfer NR. How great is the risk of further psoriasis following a single episode of acute guttate psoriasis? Arch Dermatol. 1996;132:717-718.
  22. Thorleifsdottir RH, Eysteinsdóttir, Olafsson JH, et al. Throat infections are associated with exacerbation in a substantial proportion of patients with chronic plaque psoriasis. Acta Derm Venereol. 2016;96:788-791.
  23. McFadden J, Valdimarsson H, Fry L. Cross-reactivity between streptococcal M surface antigen and human skin. Br J Dermatol. 1991;125:443-447.
  24. Validmarsson H, Thorleifsdottir RH, Sigurdardottir SL, et al. Psoriasis—as an autoimmune disease caused by molecular mimicry. Trends Immunol. 2009;30:494-501.
  25. Muto M, Fujikara Y, Hamamoto Y, et al. Immune response to Streptococcus pyogenes and the susceptibility to psoriasis. Australas J Dermatol. 1996;37(suppl 1):S54-S55.
  26. Weisenseel P, Laumbacher B, Besgen P, et al. Streptococcal infection distinguishes different types of psoriasis. J Med Genet. 2002;39:767-768.
  27. Rachakonda TD, Dhillon JS, Florek AG, et al. Effect of tonsillectomy on psoriasis: a systematic review. J Am Acad Dermatol. 2015;72:261-275.
  28. Mallon E, Bunker CB. HIV-associated psoriasis. AIDS Patient Care STDS. 2000;14:239-246.
  29. Duvic M, Johnson TM, Rapini RP, et al. Acquired immunodeficiency syndrome-associated psoriasis and Reiter’s syndrome. Arch Dermatol. 1987;123:1622-1632.
  30. Fife DJ, Waller JM, Jeffes EW, et al. Unraveling the paradoxes of HIV-associated psoriasis: a review of T-cell subsets and cytokine profiles. Dermatol Online J. 2007;13:4.
  31. Ortonne JP, Lebwohl M, Em Griffiths C; Alefacept Clinical Study Group. Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis. Eur J Dermatol. 2003;13:117-123.
  32. Menon K, Van Voorhees AS, Bebo BF Jr, et al; National Psoriasis Foundation. Psoriasis in patients with HIV infection: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62:291-299.
  33. Reddy SP, Shah VV, Wu JJ. Apremilast for a psoriasis patient with HIV and hepatitis C. J Eur Acad Dermatol Venereol. 2017;31:e481-e482.
  34. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25:606-615.
  35. Sfikakis PP, Iliopoulos A, Elezoglou A, et al. Psoriasis induced by anti-tumor necrosis factor therapy: a paradoxical adverse reaction. Arthritis Rheum. 2005;52:2513-2518.
  36. Yeung CK, Chan HH. Cutaneous adverse effects of lithium: epidemiology and management. Am J Clin Dermatol. 2004;5:3-8.
  37. Hampton PJ, Jans R, Flockhart RJ, et al. Lithium regulates keratinocyte proliferation via glycogen synthase kinase 3 and NFAT 2 (nuclear factor of activated T cells 2). J Cell Physiol. 2012;227:1529-1537.
  38. Brown G, Wang E, Leon A, et al. Tumor necrosis factor-α inhibitor-induced psoriasis: systematic review of clinical features, histopathological findings, and management experience. J Am Acad Dermatol. 2017;76:334-341.
  39. Collamer AN, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: clinical features and possible immunopathogenesis. Semin Arthritis Rheum. 2010;40:233-240.
  40. Collamer AN, Guerrero KT, Henning JS, et al. Psoriatic skin lesions induced by tumor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum. 2008;59:996-1001.
  41. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.
  42. Barrea L, Nappi F, Di Somma C, et al. Environmental risk factors in psoriasis: the point of view of the nutritionist. Int J Environ Res Public Health. 2016;13:743.
  43. Lee EJ, Han KD, Han JH, et al. Smoking and risk of psoriasis: a nationwide cohort study. J Am Acad Dermatol. 2017;77:573-575.
  44. Brenaut E, Horreau C, Pouplard C, et al. Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venereol. 2013;27(suppl 3):30-35.
Article PDF
CT102005018_S.PDF
Author and Disclosure Information

Ms. Lee is from the University of Hawaii, John A. Burns School of Medicine, Honolulu. Mr. Wu is from the Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, Connecticut. Mr. Lee is from Eastern Virginia Medical School, Norfolk. Dr. Bhutani is from the Department of Dermatology, University of California San Francisco. Dr. Wu is from the Dermatology Research and Education Foundation, Irvine, California.

Ms. Lee, Mr. Wu, Mr. Lee, and Dr. Bhutani report no conflict of interest. Dr. Wu is an investigator for AbbVie; Amgen Inc; Eli Lilly and Company; Janssen Biotech, Inc; and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira; Dr. Reddy’s Laboratories; Eli Lilly and Company; Janssen Biotech, Inc; LEO Pharma; Novartis; Ortho Dermatologics; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical; and UCB, as well as a speaker for Celgene Corporation, Novartis, Sun Pharmaceutical, and UCB.

Correspondence: Jashin J. Wu, MD (jashinwu@gmail.com).

Issue
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Publications
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Psoriasis Collection
B-Cell Lymphoma ICYMI
Breast Cancer ICYMI
Topics
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Page Number
18-20
Sections
Clinical Review
Clinical Topics & News
Author(s)
Erica B. Lee, BS
Kevin K. Wu, BA
Michael P. Lee, BS
Tina Bhutani, MD
Jashin J. Wu, MD
Author(s)
Erica B. Lee, BS
Kevin K. Wu, BA
Michael P. Lee, BS
Tina Bhutani, MD
Jashin J. Wu, MD
Author and Disclosure Information

Ms. Lee is from the University of Hawaii, John A. Burns School of Medicine, Honolulu. Mr. Wu is from the Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, Connecticut. Mr. Lee is from Eastern Virginia Medical School, Norfolk. Dr. Bhutani is from the Department of Dermatology, University of California San Francisco. Dr. Wu is from the Dermatology Research and Education Foundation, Irvine, California.

Ms. Lee, Mr. Wu, Mr. Lee, and Dr. Bhutani report no conflict of interest. Dr. Wu is an investigator for AbbVie; Amgen Inc; Eli Lilly and Company; Janssen Biotech, Inc; and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira; Dr. Reddy’s Laboratories; Eli Lilly and Company; Janssen Biotech, Inc; LEO Pharma; Novartis; Ortho Dermatologics; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical; and UCB, as well as a speaker for Celgene Corporation, Novartis, Sun Pharmaceutical, and UCB.

Correspondence: Jashin J. Wu, MD (jashinwu@gmail.com).

Author and Disclosure Information

Ms. Lee is from the University of Hawaii, John A. Burns School of Medicine, Honolulu. Mr. Wu is from the Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, Connecticut. Mr. Lee is from Eastern Virginia Medical School, Norfolk. Dr. Bhutani is from the Department of Dermatology, University of California San Francisco. Dr. Wu is from the Dermatology Research and Education Foundation, Irvine, California.

Ms. Lee, Mr. Wu, Mr. Lee, and Dr. Bhutani report no conflict of interest. Dr. Wu is an investigator for AbbVie; Amgen Inc; Eli Lilly and Company; Janssen Biotech, Inc; and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira; Dr. Reddy’s Laboratories; Eli Lilly and Company; Janssen Biotech, Inc; LEO Pharma; Novartis; Ortho Dermatologics; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical; and UCB, as well as a speaker for Celgene Corporation, Novartis, Sun Pharmaceutical, and UCB.

Correspondence: Jashin J. Wu, MD (jashinwu@gmail.com).

Article PDF
CT102005018_S.PDF
Article PDF
CT102005018_S.PDF

Psoriasis is a chronic autoimmune skin disease affecting approximately 6.7 million adults in the United States.1 Although its pathogenesis is not yet clear, risk factors and triggers provide insight into potential pathways by which psoriasis can occur. There is notable overlap between risk factors and triggers of psoriasis; perceived risk factors might, in fact, be triggers causing manifestation of disease in predisposed persons. In this review, we summarize the key factors contributing to onset and exacerbation of psoriasis. When learning to manage this chronic disease, it also may be helpful to educate patients about how these elements may affect the course of psoriasis.

Genetics

The pathogenesis of psoriasis has a strong genetic component, with approximately 70% and 20% concordance rates in monozygotic and dizygotic twins, respectively.2 Moreover, studies have shown a positive family history in approximately 35% of patients.3,4 Family-based studies have found a 50% risk of developing psoriasis in patients with 2 affected parents.5 However, the genetics of psoriasis are complex and are attributed to many different genes. Thus far, genes involving antigen presentation, T-cell receptor development and polarization, and the nuclear factor κβ (NF-κβ) pathway have been identified.6

HLA-Cw6
The most well-studied gene implicated in psoriasis is HLA-Cw6, which encodes a major histocompatibility complex class I allele supporting psoriasis as a T cell–mediated reaction to an autoantigen.6 Two potential antigens for HLA-Cw6 recently have been identified: LL-37, a cathelicidin-related antimicrobial peptide, and the A disintegrin and metalloproteinase with thrombospondin motifs-like protein 5 (ADAMTSL5), found on melanocytes and keratinocytes.7 The percentage of psoriasis patients with HLA-Cw6 ranges from 10.5% to 77.2%, with higher frequency in white individuals than in Asians.7

HLA-Cw6 manifests as specific features in psoriasis, including onset of disease before 21 years of age.8 It also is more strongly associated with guttate-type psoriasis, greater body surface area involvement, and higher incidence of Köbner phenomenon. Patients with positive HLA-Cw6 also reported worsening of psoriasis during and after throat infection.9

Caspase Recruitment Domain Family Member 14
Another gene mutation implicated in psoriasis pathogenesis is caspase recruitment domain family member 14, CARD14 (formerly PSORS2), a gene encoding a scaffolding protein important in the activation of NF-κβ.10,11 Missense CARD14 mutations cause upregulation of NF-κβ through formation of a complex with adapter protein B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1),12 which, in turn, causes increased transcription of cytokines IL-8, C-C motif chemokine ligand 20 (CCL-20), and IL-36 gamma in the keratinocyte.13 Mutations in CARD14 alone lead to psoriasiform skin in mice through amplified activation of the IL-23/IL-17 axis.14,15 Patients with a mutation in a CARD14 variant (p.Arg820Trp) have demonstrated better response to tumor necrosis factor (TNF) inhibitors.16

Further characterization of the genetic pathogenesis of psoriasis might lead to better targeted therapies, including the possibility of MALT1 inhibitors as a treatment option.12

 

 

Infection

Streptococcus
The association between streptococcal infection and psoriasis was first documented more than 100 years ago, specifically the onset of acute guttate psoriasis.17,18 Although classically described following throat infection, psoriasis also occurs following streptococcal vulvovaginitis and perianal streptococcal infection.19,20

This type of psoriasis is typically self-limited but can recur with subsequent streptococcal infections or initiate a more chronic plaque psoriasis. Patients have a 1 in 3 risk of developing chronic psoriasis within 10 years of a single episode of acute guttate psoriasis.21 Moreover, in many patients with existing plaque psoriasis, throat infection exacerbates psoriatic symptoms.22 The mechanism of exacerbation is likely due to cross-reactivity between streptococcal M surface antigen and human keratinocytes and might also be influenced by inherited abnormalities in immune response.23-26 Therefore, tonsillectomy has been studied as a possible treatment of psoriasis but is likely helpful only in patients with exacerbations of disease that are closely associated with recurrent tonsillitis.27

Human Immunodeficiency Virus
The prevalence of psoriasis in human immunodeficiency virus (HIV) patients is similar to or greater than the general population.28 Human immunodeficiency virus infection causes new onset of psoriasis and exacerbation of existing psoriasis; severity often is correlated with worsening immune function.28,29

The clinical subtypes of psoriasis that occur most frequently with HIV include guttate, inverse, and erythrodermic, though patients may present with any subtype.28 The mechanism is puzzling because HIV is primarily mediated by helper T cell 2 (TH2) cytokines, whereas psoriasis is mainly driven by helper T cell 1 (TH1) cytokines.30 Furthermore, despite increased severity with lower CD4+ counts, treatments further lowering T-cell counts paradoxically improve symptoms.31 Current literature suggests that expansion of CD8+ memory T cells might be the primary mechanism in the exacerbation of psoriasis in HIV-mediated immunosuppression.30

Treatment of HIV-associated psoriasis presents challenges because many therapeutics cause further immunosuppression. The National Psoriasis Foundation recommends topical preparations as first-line agents for mild to moderate psoriasis.32 For moderate to severe psoriasis, retroviral agents may be effective as first-line monotherapy or when supplemented by phototherapy with UVB or psoralen plus UVA. Retinoids can be used as second-line agents.32 For cases of severe refractory psoriasis, cyclosporine, methotrexate, TNF inhibitors, or hydroxyurea can be considered. There also is evidence that apremilast is effective without risk for worsening immune function.33

Other Infections
Other bacteria associated with triggering or exacerbating psoriasis include Staphylococcus aureus and Helicobacter pylori.34,35 Fungi, such as species of the genera Malassezia and Candida, and other viruses, including papillomaviruses and retroviruses, also have been implicated.34

 

 

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

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.

Psoriasis is a chronic autoimmune skin disease affecting approximately 6.7 million adults in the United States.1 Although its pathogenesis is not yet clear, risk factors and triggers provide insight into potential pathways by which psoriasis can occur. There is notable overlap between risk factors and triggers of psoriasis; perceived risk factors might, in fact, be triggers causing manifestation of disease in predisposed persons. In this review, we summarize the key factors contributing to onset and exacerbation of psoriasis. When learning to manage this chronic disease, it also may be helpful to educate patients about how these elements may affect the course of psoriasis.

Genetics

The pathogenesis of psoriasis has a strong genetic component, with approximately 70% and 20% concordance rates in monozygotic and dizygotic twins, respectively.2 Moreover, studies have shown a positive family history in approximately 35% of patients.3,4 Family-based studies have found a 50% risk of developing psoriasis in patients with 2 affected parents.5 However, the genetics of psoriasis are complex and are attributed to many different genes. Thus far, genes involving antigen presentation, T-cell receptor development and polarization, and the nuclear factor κβ (NF-κβ) pathway have been identified.6

HLA-Cw6
The most well-studied gene implicated in psoriasis is HLA-Cw6, which encodes a major histocompatibility complex class I allele supporting psoriasis as a T cell–mediated reaction to an autoantigen.6 Two potential antigens for HLA-Cw6 recently have been identified: LL-37, a cathelicidin-related antimicrobial peptide, and the A disintegrin and metalloproteinase with thrombospondin motifs-like protein 5 (ADAMTSL5), found on melanocytes and keratinocytes.7 The percentage of psoriasis patients with HLA-Cw6 ranges from 10.5% to 77.2%, with higher frequency in white individuals than in Asians.7

HLA-Cw6 manifests as specific features in psoriasis, including onset of disease before 21 years of age.8 It also is more strongly associated with guttate-type psoriasis, greater body surface area involvement, and higher incidence of Köbner phenomenon. Patients with positive HLA-Cw6 also reported worsening of psoriasis during and after throat infection.9

Caspase Recruitment Domain Family Member 14
Another gene mutation implicated in psoriasis pathogenesis is caspase recruitment domain family member 14, CARD14 (formerly PSORS2), a gene encoding a scaffolding protein important in the activation of NF-κβ.10,11 Missense CARD14 mutations cause upregulation of NF-κβ through formation of a complex with adapter protein B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1),12 which, in turn, causes increased transcription of cytokines IL-8, C-C motif chemokine ligand 20 (CCL-20), and IL-36 gamma in the keratinocyte.13 Mutations in CARD14 alone lead to psoriasiform skin in mice through amplified activation of the IL-23/IL-17 axis.14,15 Patients with a mutation in a CARD14 variant (p.Arg820Trp) have demonstrated better response to tumor necrosis factor (TNF) inhibitors.16

Further characterization of the genetic pathogenesis of psoriasis might lead to better targeted therapies, including the possibility of MALT1 inhibitors as a treatment option.12

 

 

Infection

Streptococcus
The association between streptococcal infection and psoriasis was first documented more than 100 years ago, specifically the onset of acute guttate psoriasis.17,18 Although classically described following throat infection, psoriasis also occurs following streptococcal vulvovaginitis and perianal streptococcal infection.19,20

This type of psoriasis is typically self-limited but can recur with subsequent streptococcal infections or initiate a more chronic plaque psoriasis. Patients have a 1 in 3 risk of developing chronic psoriasis within 10 years of a single episode of acute guttate psoriasis.21 Moreover, in many patients with existing plaque psoriasis, throat infection exacerbates psoriatic symptoms.22 The mechanism of exacerbation is likely due to cross-reactivity between streptococcal M surface antigen and human keratinocytes and might also be influenced by inherited abnormalities in immune response.23-26 Therefore, tonsillectomy has been studied as a possible treatment of psoriasis but is likely helpful only in patients with exacerbations of disease that are closely associated with recurrent tonsillitis.27

Human Immunodeficiency Virus
The prevalence of psoriasis in human immunodeficiency virus (HIV) patients is similar to or greater than the general population.28 Human immunodeficiency virus infection causes new onset of psoriasis and exacerbation of existing psoriasis; severity often is correlated with worsening immune function.28,29

The clinical subtypes of psoriasis that occur most frequently with HIV include guttate, inverse, and erythrodermic, though patients may present with any subtype.28 The mechanism is puzzling because HIV is primarily mediated by helper T cell 2 (TH2) cytokines, whereas psoriasis is mainly driven by helper T cell 1 (TH1) cytokines.30 Furthermore, despite increased severity with lower CD4+ counts, treatments further lowering T-cell counts paradoxically improve symptoms.31 Current literature suggests that expansion of CD8+ memory T cells might be the primary mechanism in the exacerbation of psoriasis in HIV-mediated immunosuppression.30

Treatment of HIV-associated psoriasis presents challenges because many therapeutics cause further immunosuppression. The National Psoriasis Foundation recommends topical preparations as first-line agents for mild to moderate psoriasis.32 For moderate to severe psoriasis, retroviral agents may be effective as first-line monotherapy or when supplemented by phototherapy with UVB or psoralen plus UVA. Retinoids can be used as second-line agents.32 For cases of severe refractory psoriasis, cyclosporine, methotrexate, TNF inhibitors, or hydroxyurea can be considered. There also is evidence that apremilast is effective without risk for worsening immune function.33

Other Infections
Other bacteria associated with triggering or exacerbating psoriasis include Staphylococcus aureus and Helicobacter pylori.34,35 Fungi, such as species of the genera Malassezia and Candida, and other viruses, including papillomaviruses and retroviruses, also have been implicated.34

 

 

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

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.

References
  1. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
  2. Bowcock AM. The genetics of psoriasis and autoimmunity. Annu Rev Genomics Hum Genet. 2005;6:93-122.
  3. Swanbeck G, Inerot A, Martinsson T, et al. A population genetic study of psoriasis. Br J Dermatol. 1994;131:32-39.
  4. Kimberling W, Dobson RL. The inheritance of psoriasis. J Invest Dermatol. 1973;60:538-540.
  5. Gupta R, Debbaneh MG, Liao W. Genetic epidemiology of psoriasis. Curr Dermatol Rep. 2014;3:61-78.
  6. Harden JL, Krueger JG, Bowcock AM. The immunogenetics of psoriasis: a comprehensive review. J Autoimmun. 2015;64:66-73.
  7. Chen L, Tsai TF. HLA-Cw6 and psoriasis. Br J Dermatol. 2018;178:854-862.
  8. Enerbäck C, Martinsson T, Ineraot A, et al. Evidence that HLA-Cw6 determines early onset of psoriasis, obtained using sequence-specific primers (PCR-SSP). Acta Derm Venereol. 1997;77:273-276.
  9. Gudjónsson JE, Kárason A, Antonsdóttir EH, et al. HLA-Cw6-positive and HLA-Cw6-negative patients with psoriasis vulgaris have distinct clinical features. J Invest Dermatol. 2002;118:362-365.
  10. Tomfohrde J, Silverman A, Barnes R, et al. Gene for familial psoriasis susceptibility mapped to distal end of human chromosome 17q. Science. 1994;264:1141-1145.
  11. Blonska M, Lin X. NF-κB signaling pathways regulated by CARMA family of scaffold proteins. Cell Res. 2011;21:55-70.
  12. Van Nuffel E, Schmitt A, Afonina IS, et al. CARD14-mediated activation of paracaspase MALT1 in keratinocytes: implications for psoriasis. J Invest Dermatol. 2017;137:569-575.
  13. Jordan CT, Cao L, Roberson ED, et al. PSORS2 is due to mutations in CARD14. Am J Hum Genet. 2012;90:784-795.
  14. Wang M, Zhang S, Zheng G, et al. Gain-of-function mutation of Card14 leads to spontaneous psoriasis-like skin inflammation through enhanced keratinocyte response to IL-17A. Immunity. 2018;49:66-79.
  15. Mellet M, Meier B, Mohanan D, et al. CARD14 gain-of-function mutation alone is sufficient to drive IL-23/IL-17-mediated psoriasiform skin inflammation in vivo. J Invest Dermatol. 2018;138:2010-2023.
  16. Coto-Segura P, González-Fernández D, Batalla A, et al. Common and rare CARD14 gene variants affect the antitumour necrosis factor response among patients with psoriasis. Br J Dermatol. 2016;175:134-141.
  17. Winfield JM. Psoriasis as a sequel to acute inflammations of the tonsils: a clinical note. J Cutan Dis. 1916;34:441-443.
  18. Telfer NR, Chalmers RJG, Whale K, et al. The role of streptococcal infection in the initiation of guttate psoriasis. Arch Dermatol. 1992;128:39-42.
  19. Hernandez M, Simms-Cendan J, Zendell K. Guttate psoriasis following streptococcal vulvovaginitis in a five-year-old girl. J Pediatr Adolesc Gynecol. 2015;28:e127-e129.
  20. Herbst RA, Hoch O, Kapp A, et al. Guttate psoriasis triggered by perianal streptococcal dermatitis in a four-year-old boy. J Am Acad Dermatol. 2000;42(5, pt 2):885-887.
  21. Martin BA, Chalmers RJ, Telfer NR. How great is the risk of further psoriasis following a single episode of acute guttate psoriasis? Arch Dermatol. 1996;132:717-718.
  22. Thorleifsdottir RH, Eysteinsdóttir, Olafsson JH, et al. Throat infections are associated with exacerbation in a substantial proportion of patients with chronic plaque psoriasis. Acta Derm Venereol. 2016;96:788-791.
  23. McFadden J, Valdimarsson H, Fry L. Cross-reactivity between streptococcal M surface antigen and human skin. Br J Dermatol. 1991;125:443-447.
  24. Validmarsson H, Thorleifsdottir RH, Sigurdardottir SL, et al. Psoriasis—as an autoimmune disease caused by molecular mimicry. Trends Immunol. 2009;30:494-501.
  25. Muto M, Fujikara Y, Hamamoto Y, et al. Immune response to Streptococcus pyogenes and the susceptibility to psoriasis. Australas J Dermatol. 1996;37(suppl 1):S54-S55.
  26. Weisenseel P, Laumbacher B, Besgen P, et al. Streptococcal infection distinguishes different types of psoriasis. J Med Genet. 2002;39:767-768.
  27. Rachakonda TD, Dhillon JS, Florek AG, et al. Effect of tonsillectomy on psoriasis: a systematic review. J Am Acad Dermatol. 2015;72:261-275.
  28. Mallon E, Bunker CB. HIV-associated psoriasis. AIDS Patient Care STDS. 2000;14:239-246.
  29. Duvic M, Johnson TM, Rapini RP, et al. Acquired immunodeficiency syndrome-associated psoriasis and Reiter’s syndrome. Arch Dermatol. 1987;123:1622-1632.
  30. Fife DJ, Waller JM, Jeffes EW, et al. Unraveling the paradoxes of HIV-associated psoriasis: a review of T-cell subsets and cytokine profiles. Dermatol Online J. 2007;13:4.
  31. Ortonne JP, Lebwohl M, Em Griffiths C; Alefacept Clinical Study Group. Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis. Eur J Dermatol. 2003;13:117-123.
  32. Menon K, Van Voorhees AS, Bebo BF Jr, et al; National Psoriasis Foundation. Psoriasis in patients with HIV infection: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62:291-299.
  33. Reddy SP, Shah VV, Wu JJ. Apremilast for a psoriasis patient with HIV and hepatitis C. J Eur Acad Dermatol Venereol. 2017;31:e481-e482.
  34. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25:606-615.
  35. Sfikakis PP, Iliopoulos A, Elezoglou A, et al. Psoriasis induced by anti-tumor necrosis factor therapy: a paradoxical adverse reaction. Arthritis Rheum. 2005;52:2513-2518.
  36. Yeung CK, Chan HH. Cutaneous adverse effects of lithium: epidemiology and management. Am J Clin Dermatol. 2004;5:3-8.
  37. Hampton PJ, Jans R, Flockhart RJ, et al. Lithium regulates keratinocyte proliferation via glycogen synthase kinase 3 and NFAT 2 (nuclear factor of activated T cells 2). J Cell Physiol. 2012;227:1529-1537.
  38. Brown G, Wang E, Leon A, et al. Tumor necrosis factor-α inhibitor-induced psoriasis: systematic review of clinical features, histopathological findings, and management experience. J Am Acad Dermatol. 2017;76:334-341.
  39. Collamer AN, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: clinical features and possible immunopathogenesis. Semin Arthritis Rheum. 2010;40:233-240.
  40. Collamer AN, Guerrero KT, Henning JS, et al. Psoriatic skin lesions induced by tumor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum. 2008;59:996-1001.
  41. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.
  42. Barrea L, Nappi F, Di Somma C, et al. Environmental risk factors in psoriasis: the point of view of the nutritionist. Int J Environ Res Public Health. 2016;13:743.
  43. Lee EJ, Han KD, Han JH, et al. Smoking and risk of psoriasis: a nationwide cohort study. J Am Acad Dermatol. 2017;77:573-575.
  44. Brenaut E, Horreau C, Pouplard C, et al. Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venereol. 2013;27(suppl 3):30-35.
References
  1. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
  2. Bowcock AM. The genetics of psoriasis and autoimmunity. Annu Rev Genomics Hum Genet. 2005;6:93-122.
  3. Swanbeck G, Inerot A, Martinsson T, et al. A population genetic study of psoriasis. Br J Dermatol. 1994;131:32-39.
  4. Kimberling W, Dobson RL. The inheritance of psoriasis. J Invest Dermatol. 1973;60:538-540.
  5. Gupta R, Debbaneh MG, Liao W. Genetic epidemiology of psoriasis. Curr Dermatol Rep. 2014;3:61-78.
  6. Harden JL, Krueger JG, Bowcock AM. The immunogenetics of psoriasis: a comprehensive review. J Autoimmun. 2015;64:66-73.
  7. Chen L, Tsai TF. HLA-Cw6 and psoriasis. Br J Dermatol. 2018;178:854-862.
  8. Enerbäck C, Martinsson T, Ineraot A, et al. Evidence that HLA-Cw6 determines early onset of psoriasis, obtained using sequence-specific primers (PCR-SSP). Acta Derm Venereol. 1997;77:273-276.
  9. Gudjónsson JE, Kárason A, Antonsdóttir EH, et al. HLA-Cw6-positive and HLA-Cw6-negative patients with psoriasis vulgaris have distinct clinical features. J Invest Dermatol. 2002;118:362-365.
  10. Tomfohrde J, Silverman A, Barnes R, et al. Gene for familial psoriasis susceptibility mapped to distal end of human chromosome 17q. Science. 1994;264:1141-1145.
  11. Blonska M, Lin X. NF-κB signaling pathways regulated by CARMA family of scaffold proteins. Cell Res. 2011;21:55-70.
  12. Van Nuffel E, Schmitt A, Afonina IS, et al. CARD14-mediated activation of paracaspase MALT1 in keratinocytes: implications for psoriasis. J Invest Dermatol. 2017;137:569-575.
  13. Jordan CT, Cao L, Roberson ED, et al. PSORS2 is due to mutations in CARD14. Am J Hum Genet. 2012;90:784-795.
  14. Wang M, Zhang S, Zheng G, et al. Gain-of-function mutation of Card14 leads to spontaneous psoriasis-like skin inflammation through enhanced keratinocyte response to IL-17A. Immunity. 2018;49:66-79.
  15. Mellet M, Meier B, Mohanan D, et al. CARD14 gain-of-function mutation alone is sufficient to drive IL-23/IL-17-mediated psoriasiform skin inflammation in vivo. J Invest Dermatol. 2018;138:2010-2023.
  16. Coto-Segura P, González-Fernández D, Batalla A, et al. Common and rare CARD14 gene variants affect the antitumour necrosis factor response among patients with psoriasis. Br J Dermatol. 2016;175:134-141.
  17. Winfield JM. Psoriasis as a sequel to acute inflammations of the tonsils: a clinical note. J Cutan Dis. 1916;34:441-443.
  18. Telfer NR, Chalmers RJG, Whale K, et al. The role of streptococcal infection in the initiation of guttate psoriasis. Arch Dermatol. 1992;128:39-42.
  19. Hernandez M, Simms-Cendan J, Zendell K. Guttate psoriasis following streptococcal vulvovaginitis in a five-year-old girl. J Pediatr Adolesc Gynecol. 2015;28:e127-e129.
  20. Herbst RA, Hoch O, Kapp A, et al. Guttate psoriasis triggered by perianal streptococcal dermatitis in a four-year-old boy. J Am Acad Dermatol. 2000;42(5, pt 2):885-887.
  21. Martin BA, Chalmers RJ, Telfer NR. How great is the risk of further psoriasis following a single episode of acute guttate psoriasis? Arch Dermatol. 1996;132:717-718.
  22. Thorleifsdottir RH, Eysteinsdóttir, Olafsson JH, et al. Throat infections are associated with exacerbation in a substantial proportion of patients with chronic plaque psoriasis. Acta Derm Venereol. 2016;96:788-791.
  23. McFadden J, Valdimarsson H, Fry L. Cross-reactivity between streptococcal M surface antigen and human skin. Br J Dermatol. 1991;125:443-447.
  24. Validmarsson H, Thorleifsdottir RH, Sigurdardottir SL, et al. Psoriasis—as an autoimmune disease caused by molecular mimicry. Trends Immunol. 2009;30:494-501.
  25. Muto M, Fujikara Y, Hamamoto Y, et al. Immune response to Streptococcus pyogenes and the susceptibility to psoriasis. Australas J Dermatol. 1996;37(suppl 1):S54-S55.
  26. Weisenseel P, Laumbacher B, Besgen P, et al. Streptococcal infection distinguishes different types of psoriasis. J Med Genet. 2002;39:767-768.
  27. Rachakonda TD, Dhillon JS, Florek AG, et al. Effect of tonsillectomy on psoriasis: a systematic review. J Am Acad Dermatol. 2015;72:261-275.
  28. Mallon E, Bunker CB. HIV-associated psoriasis. AIDS Patient Care STDS. 2000;14:239-246.
  29. Duvic M, Johnson TM, Rapini RP, et al. Acquired immunodeficiency syndrome-associated psoriasis and Reiter’s syndrome. Arch Dermatol. 1987;123:1622-1632.
  30. Fife DJ, Waller JM, Jeffes EW, et al. Unraveling the paradoxes of HIV-associated psoriasis: a review of T-cell subsets and cytokine profiles. Dermatol Online J. 2007;13:4.
  31. Ortonne JP, Lebwohl M, Em Griffiths C; Alefacept Clinical Study Group. Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis. Eur J Dermatol. 2003;13:117-123.
  32. Menon K, Van Voorhees AS, Bebo BF Jr, et al; National Psoriasis Foundation. Psoriasis in patients with HIV infection: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62:291-299.
  33. Reddy SP, Shah VV, Wu JJ. Apremilast for a psoriasis patient with HIV and hepatitis C. J Eur Acad Dermatol Venereol. 2017;31:e481-e482.
  34. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol. 2007;25:606-615.
  35. Sfikakis PP, Iliopoulos A, Elezoglou A, et al. Psoriasis induced by anti-tumor necrosis factor therapy: a paradoxical adverse reaction. Arthritis Rheum. 2005;52:2513-2518.
  36. Yeung CK, Chan HH. Cutaneous adverse effects of lithium: epidemiology and management. Am J Clin Dermatol. 2004;5:3-8.
  37. Hampton PJ, Jans R, Flockhart RJ, et al. Lithium regulates keratinocyte proliferation via glycogen synthase kinase 3 and NFAT 2 (nuclear factor of activated T cells 2). J Cell Physiol. 2012;227:1529-1537.
  38. Brown G, Wang E, Leon A, et al. Tumor necrosis factor-α inhibitor-induced psoriasis: systematic review of clinical features, histopathological findings, and management experience. J Am Acad Dermatol. 2017;76:334-341.
  39. Collamer AN, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: clinical features and possible immunopathogenesis. Semin Arthritis Rheum. 2010;40:233-240.
  40. Collamer AN, Guerrero KT, Henning JS, et al. Psoriatic skin lesions induced by tumor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum. 2008;59:996-1001.
  41. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.
  42. Barrea L, Nappi F, Di Somma C, et al. Environmental risk factors in psoriasis: the point of view of the nutritionist. Int J Environ Res Public Health. 2016;13:743.
  43. Lee EJ, Han KD, Han JH, et al. Smoking and risk of psoriasis: a nationwide cohort study. J Am Acad Dermatol. 2017;77:573-575.
  44. Brenaut E, Horreau C, Pouplard C, et al. Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venereol. 2013;27(suppl 3):30-35.
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Cutis - 102(5S)
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Cutis - 102(5S)
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Psoriasis Risk Factors and Triggers
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Cutis. 2018 November;102(5S):18-20
Inside the Article

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.
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