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Role of the Nervous System in Psoriasis

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References

1. Amanat M, Salehi M, Rezaei N. Neurological and psychiatric disorders in psoriasis. Rev Neurosci. 2018;29:805-813.

2. Eberle FC, Brück J, Holstein J, et al. Recent advances in understanding psoriasis [published April 28, 2016]. F1000Res. doi:10.12688/f1000research.7927.1.

3. Lee EB, Reynolds KA, Pithadia DJ, et al. Clearance of psoriasis after ischemic stroke. Cutis. 2019;103:74-76.

4. Zhu TH, Nakamura M, Farahnik B, et al. The role of the nervous system in the pathophysiology of psoriasis: a review of cases of psoriasis remission or improvement following denervation injury. Am J Clin Dermatol. 2016;17:257-263.

5. Raychaudhuri SP, Farber EM. Neuroimmunologic aspects of psoriasis. Cutis. 2000;66:357-362.

6. Kwon CW, Fried RG, Nousari Y, et al. Psoriasis: psychosomatic, somatopsychic, or both? Clin Dermatol. 2018;36:698-703.

7. Lotti T, D’Erme AM, Hercogová J. The role of neuropeptides in the control of regional immunity. Clin Dermatol. 2014;32:633-645.

8. Hall JM, Cruser D, Podawiltz A, et al. Psychological stress and the cutaneous immune response: roles of the HPA axis and the sympathetic nervous system in atopic dermatitis and psoriasis [published online August 30, 2012]. Dermatol Res Pract. 2012;2012:403908.

9. Raychaudhuri SK, Raychaudhuri SP. NGF and its receptor system: a new dimension in the pathogenesis of psoriasis and psoriatic arthritis. Ann N Y Acad Sci. 2009;1173:470-477.

10. Glaser R, Kiecolt-Glaser JK. Stress-induced immune dysfunction: implications for health. Nat Rev Immunol. 2005;5:243-251.

11. Levi-Montalcini R, Skaper SD, Dal Toso R, et al. Nerve growth factor: from neurotrophin to neurokine. Trends Neurosci. 1996;19:514-520.

12. Harvima IT, Viinamäki H, Naukkarinen A, et al. Association of cutaneous mast cells and sensory nerves with psychic stress in psoriasis. Psychother Psychosom. 1993;60:168-176.

13. He Y, Ding G, Wang X, et al. Calcitonin gene‐related peptide in Langerhans cells in psoriatic plaque lesions. Chin Med J (Engl). 2000;113:747-751.

14. Chu DQ, Choy M, Foster P, et al. A comparative study of the ability of calcitonin gene‐related peptide and adrenomedullin13–52 to modulate microvascular but not thermal hyperalgesia responses. Br J Pharmacol. 2000;130:1589-1596.

15. Al’Abadie MS, Senior HJ, Bleehen SS, et al. Neuropeptides and general neuronal marker in psoriasis—an immunohistochemical study. Clin Exp Dermatol. 1995;20:384-389.

16. Farber EM, Nickoloff BJ, Recht B, et al. Stress, symmetry, and psoriasis: possible role of neuropeptides. J Am Acad Dermatol. 1986;14(2, pt 1):305-311.

17. Pincelli C, Fantini F, Romualdi P, et al. Substance P is diminished and vasoactive intestinal peptide is augmented in psoriatic lesions and these peptides exert disparate effects on the proliferation of cultured human keratinocytes. J Invest Dermatol. 1992;98:421-427.

18. Raychaudhuri SP, Jiang WY, Farber EM. Psoriatic keratinocytes express high levels of nerve growth factor. Acta Derm Venereol. 1998;78:84-86.

19. Pincelli C. Nerve growth factor and keratinocytes: a role in psoriasis. Eur J Dermatol. 2000;10:85-90.

20. Sagi L, Trau H. The Koebner phenomenon. Clin Dermatol. 2011;29:231-236.

21. Nakamura M, Toyoda M, Morohashi M. Pruritogenic mediators in psoriasis vulgaris: comparative evaluation of itch-associated cutaneous factors. Br J Dermatol. 2003;149:718-730.

22. Stratigos AJ, Katoulis AK, Stavrianeas NG. Spontaneous clearing of psoriasis after stroke. J Am Acad Dermatol. 1998;38(5, pt 1):768-770.

23. Wang TS, Tsai TF. Psoriasis sparing the lower limb with postpoliomyelitis residual paralysis. Br J Dermatol. 2014;171:429-431.

24. Weiner SR, Bassett LW, Reichman RP. Protective effect of poliomyelitis on psoriatic arthritis. Arthritis Rheum. 1985;28:703-706.

25. Ostrowski SM, Belkai A, Loyd CM, et al. Cutaneous denervation of psoriasiform mouse skin improves acanthosis and inflammation in a sensory neuropeptide-dependent manner. J Invest Dermatol. 2011;131:1530-1538.

26. Farber EM, Lanigan SW, Boer J. The role of cutaneous sensory nerves in the maintenance of psoriasis. Int J Dermatol. 1990;29:418-420.

27. Dewing SB. Remission of psoriasis associated with cutaneous nerve section. Arch Dermatol. 1971;104:220-221.

28. Perlman HH. Remission of psoriasis vulgaris from the use of nerve-blocking agents. Arch Dermatol. 1972;105:128-129.

Author and Disclosure Information

From the Dermatology Research and Education Foundation, Irvine, California.

 

Dr. Wu is an investigator for AbbVie, Amgen Inc, Eli Lilly and Company, Janssen Pharmaceuticals, and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira Inc; Dr. Reddy’s Laboratories Ltd; Eli Lilly and Company; Janssen Pharmaceuticals; LEO Pharma; Novartis; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC. He also is a speaker for AbbVie; Celgene Corporation; Novartis; Regeneron Pharmaceuticals, Inc; Sanofi Genzyme; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC.

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Author and Disclosure Information

From the Dermatology Research and Education Foundation, Irvine, California.

 

Dr. Wu is an investigator for AbbVie, Amgen Inc, Eli Lilly and Company, Janssen Pharmaceuticals, and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira Inc; Dr. Reddy’s Laboratories Ltd; Eli Lilly and Company; Janssen Pharmaceuticals; LEO Pharma; Novartis; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC. He also is a speaker for AbbVie; Celgene Corporation; Novartis; Regeneron Pharmaceuticals, Inc; Sanofi Genzyme; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC.

Author and Disclosure Information

From the Dermatology Research and Education Foundation, Irvine, California.

 

Dr. Wu is an investigator for AbbVie, Amgen Inc, Eli Lilly and Company, Janssen Pharmaceuticals, and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira Inc; Dr. Reddy’s Laboratories Ltd; Eli Lilly and Company; Janssen Pharmaceuticals; LEO Pharma; Novartis; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC. He also is a speaker for AbbVie; Celgene Corporation; Novartis; Regeneron Pharmaceuticals, Inc; Sanofi Genzyme; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC.

References

1. Amanat M, Salehi M, Rezaei N. Neurological and psychiatric disorders in psoriasis. Rev Neurosci. 2018;29:805-813.

2. Eberle FC, Brück J, Holstein J, et al. Recent advances in understanding psoriasis [published April 28, 2016]. F1000Res. doi:10.12688/f1000research.7927.1.

3. Lee EB, Reynolds KA, Pithadia DJ, et al. Clearance of psoriasis after ischemic stroke. Cutis. 2019;103:74-76.

4. Zhu TH, Nakamura M, Farahnik B, et al. The role of the nervous system in the pathophysiology of psoriasis: a review of cases of psoriasis remission or improvement following denervation injury. Am J Clin Dermatol. 2016;17:257-263.

5. Raychaudhuri SP, Farber EM. Neuroimmunologic aspects of psoriasis. Cutis. 2000;66:357-362.

6. Kwon CW, Fried RG, Nousari Y, et al. Psoriasis: psychosomatic, somatopsychic, or both? Clin Dermatol. 2018;36:698-703.

7. Lotti T, D’Erme AM, Hercogová J. The role of neuropeptides in the control of regional immunity. Clin Dermatol. 2014;32:633-645.

8. Hall JM, Cruser D, Podawiltz A, et al. Psychological stress and the cutaneous immune response: roles of the HPA axis and the sympathetic nervous system in atopic dermatitis and psoriasis [published online August 30, 2012]. Dermatol Res Pract. 2012;2012:403908.

9. Raychaudhuri SK, Raychaudhuri SP. NGF and its receptor system: a new dimension in the pathogenesis of psoriasis and psoriatic arthritis. Ann N Y Acad Sci. 2009;1173:470-477.

10. Glaser R, Kiecolt-Glaser JK. Stress-induced immune dysfunction: implications for health. Nat Rev Immunol. 2005;5:243-251.

11. Levi-Montalcini R, Skaper SD, Dal Toso R, et al. Nerve growth factor: from neurotrophin to neurokine. Trends Neurosci. 1996;19:514-520.

12. Harvima IT, Viinamäki H, Naukkarinen A, et al. Association of cutaneous mast cells and sensory nerves with psychic stress in psoriasis. Psychother Psychosom. 1993;60:168-176.

13. He Y, Ding G, Wang X, et al. Calcitonin gene‐related peptide in Langerhans cells in psoriatic plaque lesions. Chin Med J (Engl). 2000;113:747-751.

14. Chu DQ, Choy M, Foster P, et al. A comparative study of the ability of calcitonin gene‐related peptide and adrenomedullin13–52 to modulate microvascular but not thermal hyperalgesia responses. Br J Pharmacol. 2000;130:1589-1596.

15. Al’Abadie MS, Senior HJ, Bleehen SS, et al. Neuropeptides and general neuronal marker in psoriasis—an immunohistochemical study. Clin Exp Dermatol. 1995;20:384-389.

16. Farber EM, Nickoloff BJ, Recht B, et al. Stress, symmetry, and psoriasis: possible role of neuropeptides. J Am Acad Dermatol. 1986;14(2, pt 1):305-311.

17. Pincelli C, Fantini F, Romualdi P, et al. Substance P is diminished and vasoactive intestinal peptide is augmented in psoriatic lesions and these peptides exert disparate effects on the proliferation of cultured human keratinocytes. J Invest Dermatol. 1992;98:421-427.

18. Raychaudhuri SP, Jiang WY, Farber EM. Psoriatic keratinocytes express high levels of nerve growth factor. Acta Derm Venereol. 1998;78:84-86.

19. Pincelli C. Nerve growth factor and keratinocytes: a role in psoriasis. Eur J Dermatol. 2000;10:85-90.

20. Sagi L, Trau H. The Koebner phenomenon. Clin Dermatol. 2011;29:231-236.

21. Nakamura M, Toyoda M, Morohashi M. Pruritogenic mediators in psoriasis vulgaris: comparative evaluation of itch-associated cutaneous factors. Br J Dermatol. 2003;149:718-730.

22. Stratigos AJ, Katoulis AK, Stavrianeas NG. Spontaneous clearing of psoriasis after stroke. J Am Acad Dermatol. 1998;38(5, pt 1):768-770.

23. Wang TS, Tsai TF. Psoriasis sparing the lower limb with postpoliomyelitis residual paralysis. Br J Dermatol. 2014;171:429-431.

24. Weiner SR, Bassett LW, Reichman RP. Protective effect of poliomyelitis on psoriatic arthritis. Arthritis Rheum. 1985;28:703-706.

25. Ostrowski SM, Belkai A, Loyd CM, et al. Cutaneous denervation of psoriasiform mouse skin improves acanthosis and inflammation in a sensory neuropeptide-dependent manner. J Invest Dermatol. 2011;131:1530-1538.

26. Farber EM, Lanigan SW, Boer J. The role of cutaneous sensory nerves in the maintenance of psoriasis. Int J Dermatol. 1990;29:418-420.

27. Dewing SB. Remission of psoriasis associated with cutaneous nerve section. Arch Dermatol. 1971;104:220-221.

28. Perlman HH. Remission of psoriasis vulgaris from the use of nerve-blocking agents. Arch Dermatol. 1972;105:128-129.

References

1. Amanat M, Salehi M, Rezaei N. Neurological and psychiatric disorders in psoriasis. Rev Neurosci. 2018;29:805-813.

2. Eberle FC, Brück J, Holstein J, et al. Recent advances in understanding psoriasis [published April 28, 2016]. F1000Res. doi:10.12688/f1000research.7927.1.

3. Lee EB, Reynolds KA, Pithadia DJ, et al. Clearance of psoriasis after ischemic stroke. Cutis. 2019;103:74-76.

4. Zhu TH, Nakamura M, Farahnik B, et al. The role of the nervous system in the pathophysiology of psoriasis: a review of cases of psoriasis remission or improvement following denervation injury. Am J Clin Dermatol. 2016;17:257-263.

5. Raychaudhuri SP, Farber EM. Neuroimmunologic aspects of psoriasis. Cutis. 2000;66:357-362.

6. Kwon CW, Fried RG, Nousari Y, et al. Psoriasis: psychosomatic, somatopsychic, or both? Clin Dermatol. 2018;36:698-703.

7. Lotti T, D’Erme AM, Hercogová J. The role of neuropeptides in the control of regional immunity. Clin Dermatol. 2014;32:633-645.

8. Hall JM, Cruser D, Podawiltz A, et al. Psychological stress and the cutaneous immune response: roles of the HPA axis and the sympathetic nervous system in atopic dermatitis and psoriasis [published online August 30, 2012]. Dermatol Res Pract. 2012;2012:403908.

9. Raychaudhuri SK, Raychaudhuri SP. NGF and its receptor system: a new dimension in the pathogenesis of psoriasis and psoriatic arthritis. Ann N Y Acad Sci. 2009;1173:470-477.

10. Glaser R, Kiecolt-Glaser JK. Stress-induced immune dysfunction: implications for health. Nat Rev Immunol. 2005;5:243-251.

11. Levi-Montalcini R, Skaper SD, Dal Toso R, et al. Nerve growth factor: from neurotrophin to neurokine. Trends Neurosci. 1996;19:514-520.

12. Harvima IT, Viinamäki H, Naukkarinen A, et al. Association of cutaneous mast cells and sensory nerves with psychic stress in psoriasis. Psychother Psychosom. 1993;60:168-176.

13. He Y, Ding G, Wang X, et al. Calcitonin gene‐related peptide in Langerhans cells in psoriatic plaque lesions. Chin Med J (Engl). 2000;113:747-751.

14. Chu DQ, Choy M, Foster P, et al. A comparative study of the ability of calcitonin gene‐related peptide and adrenomedullin13–52 to modulate microvascular but not thermal hyperalgesia responses. Br J Pharmacol. 2000;130:1589-1596.

15. Al’Abadie MS, Senior HJ, Bleehen SS, et al. Neuropeptides and general neuronal marker in psoriasis—an immunohistochemical study. Clin Exp Dermatol. 1995;20:384-389.

16. Farber EM, Nickoloff BJ, Recht B, et al. Stress, symmetry, and psoriasis: possible role of neuropeptides. J Am Acad Dermatol. 1986;14(2, pt 1):305-311.

17. Pincelli C, Fantini F, Romualdi P, et al. Substance P is diminished and vasoactive intestinal peptide is augmented in psoriatic lesions and these peptides exert disparate effects on the proliferation of cultured human keratinocytes. J Invest Dermatol. 1992;98:421-427.

18. Raychaudhuri SP, Jiang WY, Farber EM. Psoriatic keratinocytes express high levels of nerve growth factor. Acta Derm Venereol. 1998;78:84-86.

19. Pincelli C. Nerve growth factor and keratinocytes: a role in psoriasis. Eur J Dermatol. 2000;10:85-90.

20. Sagi L, Trau H. The Koebner phenomenon. Clin Dermatol. 2011;29:231-236.

21. Nakamura M, Toyoda M, Morohashi M. Pruritogenic mediators in psoriasis vulgaris: comparative evaluation of itch-associated cutaneous factors. Br J Dermatol. 2003;149:718-730.

22. Stratigos AJ, Katoulis AK, Stavrianeas NG. Spontaneous clearing of psoriasis after stroke. J Am Acad Dermatol. 1998;38(5, pt 1):768-770.

23. Wang TS, Tsai TF. Psoriasis sparing the lower limb with postpoliomyelitis residual paralysis. Br J Dermatol. 2014;171:429-431.

24. Weiner SR, Bassett LW, Reichman RP. Protective effect of poliomyelitis on psoriatic arthritis. Arthritis Rheum. 1985;28:703-706.

25. Ostrowski SM, Belkai A, Loyd CM, et al. Cutaneous denervation of psoriasiform mouse skin improves acanthosis and inflammation in a sensory neuropeptide-dependent manner. J Invest Dermatol. 2011;131:1530-1538.

26. Farber EM, Lanigan SW, Boer J. The role of cutaneous sensory nerves in the maintenance of psoriasis. Int J Dermatol. 1990;29:418-420.

27. Dewing SB. Remission of psoriasis associated with cutaneous nerve section. Arch Dermatol. 1971;104:220-221.

28. Perlman HH. Remission of psoriasis vulgaris from the use of nerve-blocking agents. Arch Dermatol. 1972;105:128-129.

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Did You Know? Psoriasis and metabolic syndrome

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Psoriasis Journal Scan: August 2019

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Verrucous psoriasis: A rare variant of psoriasis masquerading as verrucous carcinoma.

Garvie K, McGinley Simpson M, Logemann N, Lackey J. JAAD Case Rep. 2019 Aug 5;5(8):723-725.

Verrucous psoriasis is a rare variant of psoriasis characterized by hyperkeratotic, papillomatous plaques that clinically resemble verrucous carcinoma in lesion appearance and distribution. It is amenable to medical treatments. Conversely, verrucous carcinoma, a rare subtype of well-differentiated squamous cell carcinoma, is treated with surgical excision. Histologically, they may be difficult to differentiate. This case report presents a patient with verrucous psoriasis of the heal that was initially diagnosed as verrucous carcinoma and excised.


 

Re-Categorization of Psoriasis Severity: Delphi Consensus from the International Psoriasis Council.

Strober B, Ryan C, van de Kerkhof P, et al. J Am Acad Dermatol. 2019 Aug 16.

This consensus statement on the classification of psoriasis severity preferentially ranked seven severity definitions. This most preferred statement rejects the mild, moderate and severe categories in favor of a dichotomous definition: Psoriasis patients should be classified as either candidates for topical therapy or candidates for systemic therapy; the latter are patients who meet at least one of the following criteria: 1) BSA > 10%, 2) Disease involving special areas, 3) Failure of topical therapy.


 

Gluten intake and risk of psoriasis, psoriatic arthritis and atopic dermatitis among US women.

Drucker AM, Qureshi AA, Thompson JM, Li T, Cho E. J Am Acad Dermatol. 2019 Aug 9.

Associations between gluten intake and psoriasis, psoriatic arthritis and atopic dermatitis are poorly understood. Gluten content of participants' diet was calculated every four years using food frequency questionnaires. Disease outcomes were assessed by self-report and subsequently validated.


 

Psoriasis and Mortality in the US: Data from the National Health and Nutrition Examination Survey.

Semenov YR, Herbosa CM, Rogers AT, et al. J Am Acad Dermatol. 2019 Aug 12.

In this retrospective population-based cohort study of adults and adolescents > 10 years (n=13,031) who participated in National Health and Nutrition Examination Surveys (2003-2006; 2009-2010), psoriasis was present in 2.7% of the study population. Over an average 52.3 months median follow-up, psoriasis was significantly associated with increased mortality risk. This relationship is partially mediated by an increased prevalence of cardiovascular, infectious, and neoplastic disorders seen among psoriatics.


 

Ostraceous Psoriasis Presenting as Koebner Phenomenon in a Tattoo.

Reinhart J, Willett M, Gibbs N. J Drugs Dermatol. 2019 Aug 1;18(8):825-826.

Psoriasis ostracea is defined as having pronounced adherent scales resembling an oyster shell. Many ostraceous cases occur as generalized outbreaks in patients with long-standing history of psoriasis. Rarely does this variant occur as a direct flare from a cutaneous insult. In these situations, when a pre-existing dermatosis appears in response to a traumatic insult to skin, the process is referred to as the Koebner phenomenon. In addition to lichen planus and vitiligo, psoriasis is a commonly known condition that can present as a Koebner reaction. In this atypical case, the authors present a 21-year-old male with remarkable ostraceous psoriatic lesions precipitated by an upper arm tattoo, demonstrating the Koebner phenomenon.

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Verrucous psoriasis: A rare variant of psoriasis masquerading as verrucous carcinoma.

Garvie K, McGinley Simpson M, Logemann N, Lackey J. JAAD Case Rep. 2019 Aug 5;5(8):723-725.

Verrucous psoriasis is a rare variant of psoriasis characterized by hyperkeratotic, papillomatous plaques that clinically resemble verrucous carcinoma in lesion appearance and distribution. It is amenable to medical treatments. Conversely, verrucous carcinoma, a rare subtype of well-differentiated squamous cell carcinoma, is treated with surgical excision. Histologically, they may be difficult to differentiate. This case report presents a patient with verrucous psoriasis of the heal that was initially diagnosed as verrucous carcinoma and excised.


 

Re-Categorization of Psoriasis Severity: Delphi Consensus from the International Psoriasis Council.

Strober B, Ryan C, van de Kerkhof P, et al. J Am Acad Dermatol. 2019 Aug 16.

This consensus statement on the classification of psoriasis severity preferentially ranked seven severity definitions. This most preferred statement rejects the mild, moderate and severe categories in favor of a dichotomous definition: Psoriasis patients should be classified as either candidates for topical therapy or candidates for systemic therapy; the latter are patients who meet at least one of the following criteria: 1) BSA > 10%, 2) Disease involving special areas, 3) Failure of topical therapy.


 

Gluten intake and risk of psoriasis, psoriatic arthritis and atopic dermatitis among US women.

Drucker AM, Qureshi AA, Thompson JM, Li T, Cho E. J Am Acad Dermatol. 2019 Aug 9.

Associations between gluten intake and psoriasis, psoriatic arthritis and atopic dermatitis are poorly understood. Gluten content of participants' diet was calculated every four years using food frequency questionnaires. Disease outcomes were assessed by self-report and subsequently validated.


 

Psoriasis and Mortality in the US: Data from the National Health and Nutrition Examination Survey.

Semenov YR, Herbosa CM, Rogers AT, et al. J Am Acad Dermatol. 2019 Aug 12.

In this retrospective population-based cohort study of adults and adolescents > 10 years (n=13,031) who participated in National Health and Nutrition Examination Surveys (2003-2006; 2009-2010), psoriasis was present in 2.7% of the study population. Over an average 52.3 months median follow-up, psoriasis was significantly associated with increased mortality risk. This relationship is partially mediated by an increased prevalence of cardiovascular, infectious, and neoplastic disorders seen among psoriatics.


 

Ostraceous Psoriasis Presenting as Koebner Phenomenon in a Tattoo.

Reinhart J, Willett M, Gibbs N. J Drugs Dermatol. 2019 Aug 1;18(8):825-826.

Psoriasis ostracea is defined as having pronounced adherent scales resembling an oyster shell. Many ostraceous cases occur as generalized outbreaks in patients with long-standing history of psoriasis. Rarely does this variant occur as a direct flare from a cutaneous insult. In these situations, when a pre-existing dermatosis appears in response to a traumatic insult to skin, the process is referred to as the Koebner phenomenon. In addition to lichen planus and vitiligo, psoriasis is a commonly known condition that can present as a Koebner reaction. In this atypical case, the authors present a 21-year-old male with remarkable ostraceous psoriatic lesions precipitated by an upper arm tattoo, demonstrating the Koebner phenomenon.

Verrucous psoriasis: A rare variant of psoriasis masquerading as verrucous carcinoma.

Garvie K, McGinley Simpson M, Logemann N, Lackey J. JAAD Case Rep. 2019 Aug 5;5(8):723-725.

Verrucous psoriasis is a rare variant of psoriasis characterized by hyperkeratotic, papillomatous plaques that clinically resemble verrucous carcinoma in lesion appearance and distribution. It is amenable to medical treatments. Conversely, verrucous carcinoma, a rare subtype of well-differentiated squamous cell carcinoma, is treated with surgical excision. Histologically, they may be difficult to differentiate. This case report presents a patient with verrucous psoriasis of the heal that was initially diagnosed as verrucous carcinoma and excised.


 

Re-Categorization of Psoriasis Severity: Delphi Consensus from the International Psoriasis Council.

Strober B, Ryan C, van de Kerkhof P, et al. J Am Acad Dermatol. 2019 Aug 16.

This consensus statement on the classification of psoriasis severity preferentially ranked seven severity definitions. This most preferred statement rejects the mild, moderate and severe categories in favor of a dichotomous definition: Psoriasis patients should be classified as either candidates for topical therapy or candidates for systemic therapy; the latter are patients who meet at least one of the following criteria: 1) BSA > 10%, 2) Disease involving special areas, 3) Failure of topical therapy.


 

Gluten intake and risk of psoriasis, psoriatic arthritis and atopic dermatitis among US women.

Drucker AM, Qureshi AA, Thompson JM, Li T, Cho E. J Am Acad Dermatol. 2019 Aug 9.

Associations between gluten intake and psoriasis, psoriatic arthritis and atopic dermatitis are poorly understood. Gluten content of participants' diet was calculated every four years using food frequency questionnaires. Disease outcomes were assessed by self-report and subsequently validated.


 

Psoriasis and Mortality in the US: Data from the National Health and Nutrition Examination Survey.

Semenov YR, Herbosa CM, Rogers AT, et al. J Am Acad Dermatol. 2019 Aug 12.

In this retrospective population-based cohort study of adults and adolescents > 10 years (n=13,031) who participated in National Health and Nutrition Examination Surveys (2003-2006; 2009-2010), psoriasis was present in 2.7% of the study population. Over an average 52.3 months median follow-up, psoriasis was significantly associated with increased mortality risk. This relationship is partially mediated by an increased prevalence of cardiovascular, infectious, and neoplastic disorders seen among psoriatics.


 

Ostraceous Psoriasis Presenting as Koebner Phenomenon in a Tattoo.

Reinhart J, Willett M, Gibbs N. J Drugs Dermatol. 2019 Aug 1;18(8):825-826.

Psoriasis ostracea is defined as having pronounced adherent scales resembling an oyster shell. Many ostraceous cases occur as generalized outbreaks in patients with long-standing history of psoriasis. Rarely does this variant occur as a direct flare from a cutaneous insult. In these situations, when a pre-existing dermatosis appears in response to a traumatic insult to skin, the process is referred to as the Koebner phenomenon. In addition to lichen planus and vitiligo, psoriasis is a commonly known condition that can present as a Koebner reaction. In this atypical case, the authors present a 21-year-old male with remarkable ostraceous psoriatic lesions precipitated by an upper arm tattoo, demonstrating the Koebner phenomenon.

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Considerations for Psoriasis in Pregnancy

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References

1. Trivedi MK, Vaughn AR, Murase JE. Pustular psoriasis of pregnancy: current perspectives. Int J Womens Health. 2018;10:109-115.

2. Kondo RN, Araújo FM, Pereira AM, et al. Pustular psoriasis of pregnancy (impetigo herpetiformis)—case report. An Bras Dermatol. 2013;88(6 suppl 1):186-189.

3. Oumeish OY, Farraj SE, Bataineh AS. Some aspects of impetigo herpetiformis. Arch Dermatol. 1982;118:103-105.

4. Flynn A, Burke N, Byrne B, et al. Two case reports of generalized pustular psoriasis of pregnancy: different outcomes. Obstet Med. 2016;9:55-59.

5. Shaw CJ, Wu P, Sriemevan A. First trimester impetigo herpetiformis in multiparous female successfully treated with oral cyclosporine. BMJ Case Rep. 2011;2011:bcr0220113915.

6. Pitch M, Somers K, Scott G, et al. A case of pustular psoriasis of pregnancy with positive maternal-fetal outcomes. Cutis. 2018;101:278-280.

7. Namazi N, Dadkhahfar S. Impetigo herpetiformis: review of pathogenesis, complication, and treatment [published April 4, 2018]. Dermatol Res Pract. 2018;2018:5801280. doi:10.1155/2018/5801280. eCollection 2018.

8. Lehrhoff S, Pomeranz MK. Specific dermatoses of pregnancy and their treatment. Dermatol Ther. 2013;26:274-284.

9. Ulubay M, Keskin U, Fidan U, et al. Case report of a rare dermatosis in pregnancy: impetigo herpetiformis. J Obstet Gynaecol Res. 2015;41:301-303.

10. Robinson A, Van Voorhees AS, Hsu S, et al. Treatment of pustular psoriasis: from the Medical Board of the National Psoriasis Foundation. J Am Acad Dermatol. 2012;67:279-288.

11. Hazarika D. Generalized pustular psoriasis of pregnancy successfully treated with cyclosporine. Indian J Dermatol Venereol Leprol. 2009;75:638.

12. Puig L, Barco D, Alomar A. Treatment of psoriasis with anti-TNF drugs during pregnancy: case report and review of the literature. Dermatology. 2010;220:71-76.

13. Bozdag K, Ozturk S, Ermete M. A case of recurrent impetigo herpetiformis treated with systemic corticosteroids and narrow¬band UVB [published online January 20, 2012]. Cutan Ocul Toxicol. 2012;31:67-69.

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From the Department of Dermatology, University of Rochester, New York.

The author reports no conflict of interest.

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From the Department of Dermatology, University of Rochester, New York.

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The author reports no conflict of interest.

References

1. Trivedi MK, Vaughn AR, Murase JE. Pustular psoriasis of pregnancy: current perspectives. Int J Womens Health. 2018;10:109-115.

2. Kondo RN, Araújo FM, Pereira AM, et al. Pustular psoriasis of pregnancy (impetigo herpetiformis)—case report. An Bras Dermatol. 2013;88(6 suppl 1):186-189.

3. Oumeish OY, Farraj SE, Bataineh AS. Some aspects of impetigo herpetiformis. Arch Dermatol. 1982;118:103-105.

4. Flynn A, Burke N, Byrne B, et al. Two case reports of generalized pustular psoriasis of pregnancy: different outcomes. Obstet Med. 2016;9:55-59.

5. Shaw CJ, Wu P, Sriemevan A. First trimester impetigo herpetiformis in multiparous female successfully treated with oral cyclosporine. BMJ Case Rep. 2011;2011:bcr0220113915.

6. Pitch M, Somers K, Scott G, et al. A case of pustular psoriasis of pregnancy with positive maternal-fetal outcomes. Cutis. 2018;101:278-280.

7. Namazi N, Dadkhahfar S. Impetigo herpetiformis: review of pathogenesis, complication, and treatment [published April 4, 2018]. Dermatol Res Pract. 2018;2018:5801280. doi:10.1155/2018/5801280. eCollection 2018.

8. Lehrhoff S, Pomeranz MK. Specific dermatoses of pregnancy and their treatment. Dermatol Ther. 2013;26:274-284.

9. Ulubay M, Keskin U, Fidan U, et al. Case report of a rare dermatosis in pregnancy: impetigo herpetiformis. J Obstet Gynaecol Res. 2015;41:301-303.

10. Robinson A, Van Voorhees AS, Hsu S, et al. Treatment of pustular psoriasis: from the Medical Board of the National Psoriasis Foundation. J Am Acad Dermatol. 2012;67:279-288.

11. Hazarika D. Generalized pustular psoriasis of pregnancy successfully treated with cyclosporine. Indian J Dermatol Venereol Leprol. 2009;75:638.

12. Puig L, Barco D, Alomar A. Treatment of psoriasis with anti-TNF drugs during pregnancy: case report and review of the literature. Dermatology. 2010;220:71-76.

13. Bozdag K, Ozturk S, Ermete M. A case of recurrent impetigo herpetiformis treated with systemic corticosteroids and narrow¬band UVB [published online January 20, 2012]. Cutan Ocul Toxicol. 2012;31:67-69.

References

1. Trivedi MK, Vaughn AR, Murase JE. Pustular psoriasis of pregnancy: current perspectives. Int J Womens Health. 2018;10:109-115.

2. Kondo RN, Araújo FM, Pereira AM, et al. Pustular psoriasis of pregnancy (impetigo herpetiformis)—case report. An Bras Dermatol. 2013;88(6 suppl 1):186-189.

3. Oumeish OY, Farraj SE, Bataineh AS. Some aspects of impetigo herpetiformis. Arch Dermatol. 1982;118:103-105.

4. Flynn A, Burke N, Byrne B, et al. Two case reports of generalized pustular psoriasis of pregnancy: different outcomes. Obstet Med. 2016;9:55-59.

5. Shaw CJ, Wu P, Sriemevan A. First trimester impetigo herpetiformis in multiparous female successfully treated with oral cyclosporine. BMJ Case Rep. 2011;2011:bcr0220113915.

6. Pitch M, Somers K, Scott G, et al. A case of pustular psoriasis of pregnancy with positive maternal-fetal outcomes. Cutis. 2018;101:278-280.

7. Namazi N, Dadkhahfar S. Impetigo herpetiformis: review of pathogenesis, complication, and treatment [published April 4, 2018]. Dermatol Res Pract. 2018;2018:5801280. doi:10.1155/2018/5801280. eCollection 2018.

8. Lehrhoff S, Pomeranz MK. Specific dermatoses of pregnancy and their treatment. Dermatol Ther. 2013;26:274-284.

9. Ulubay M, Keskin U, Fidan U, et al. Case report of a rare dermatosis in pregnancy: impetigo herpetiformis. J Obstet Gynaecol Res. 2015;41:301-303.

10. Robinson A, Van Voorhees AS, Hsu S, et al. Treatment of pustular psoriasis: from the Medical Board of the National Psoriasis Foundation. J Am Acad Dermatol. 2012;67:279-288.

11. Hazarika D. Generalized pustular psoriasis of pregnancy successfully treated with cyclosporine. Indian J Dermatol Venereol Leprol. 2009;75:638.

12. Puig L, Barco D, Alomar A. Treatment of psoriasis with anti-TNF drugs during pregnancy: case report and review of the literature. Dermatology. 2010;220:71-76.

13. Bozdag K, Ozturk S, Ermete M. A case of recurrent impetigo herpetiformis treated with systemic corticosteroids and narrow¬band UVB [published online January 20, 2012]. Cutan Ocul Toxicol. 2012;31:67-69.

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Did You Know? Psoriasis and cardiovascular disease

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Psoriasis Journal Scan: July 2019

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Facial involvement and the severity of psoriasis.

Passos AN, de A Rêgo VRP, Duarte GV, Santos E Miranda RC, de O Rocha B, de F S P de Oliveira M. Int J Dermatol. 2019 Jul 26.

The aim of this cross-sectional study is to compare the severity of psoriasis, measured by the Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI), in patients with and without facial lesions.


 

Genital Psoriasis: Impact on Quality of Life and Treatment Options.

Kelly A, Ryan C. Am J Clin Dermatol. 2019 Jul 16

Psoriasis involving the genital skin occurs in up to two-thirds of psoriasis patients but is often overlooked by physicians. Furthermore, psoriasis objective and subjective severity indexes for common plaque psoriasis often neglect the impact this small area of psoriasis can have on a patient. It can have a significant impact on patients' psychosocial function due to intrusive physical symptoms such as genital itch and pain, and a detrimental impact on sexual health and impaired relationships.


 

Lifestyle changes for treating psoriasis.

Ko SH, Chi CC, Yeh ML, Wang SH, Tsai YS, Hsu MY. Cochrane Database Syst Rev. 2019 Jul 16

The objective of this review is to assess the effects of lifestyle changes for psoriasis, including weight reduction, alcohol abstinence, smoking cessation, dietary modification, exercise, and other lifestyle change interventions. Dietary intervention may reduce the severity of psoriasis (low-quality evidence) and probably improves quality of life and reduces BMI (moderate-quality evidence) in obese people when compared with usual care, while combined dietary intervention and exercise programme probably improves psoriasis severity and BMI when compared with information only (moderate-quality evidence).


 

The Incidence Rates and Risk Factors of Parkinson's Disease in Patients with Psoriasis: A Nationwide Population-based Cohort Study.

Lee JH, Han K, Gee HY. J Am Acad Dermatol. 2019 Jul 11.

This was a nationwide population-based cohort study to determine the incidence rates and risk factors of Parkinson's disease in patients with psoriasis. The psoriasis group showed a significantly increased risk of developing Parkinson's disease. The risk of Parkinson's disease was significantly high among the psoriasis patients who were not receiving systemic therapy and was low among the psoriasis patients on systemic therapy.


 

Psoriasis-associated itch: etiology, assessment, impact, and management.

Pithadia DJ, Reynolds KA, Lee EB, Wu JJ. J Dermatolog Treat. 2019 Jul 5:1-9.

Pruritus, a very broad, subjective, and complex symptom, troubles the majority of patients with psoriasis. However, the subjective and multidimensional nature of the symptom renders it challenging for patients to appropriately communicate their experiences with itch to providers. This review explores current perspectives regarding the underlying mechanisms, assessment tools, burden, and treatment modalities for psoriatic pruritus. It emphasizes the significance of incorporating a standardized, thorough, and verified metric that incorporates severity, distribution, and character of pruritus as well as its effects on various aspects of quality of life. It also underscores the importance of continued research to fully understand the pathogenesis of psoriatic itch for establishment of novel, targeted therapeutics.

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Facial involvement and the severity of psoriasis.

Passos AN, de A Rêgo VRP, Duarte GV, Santos E Miranda RC, de O Rocha B, de F S P de Oliveira M. Int J Dermatol. 2019 Jul 26.

The aim of this cross-sectional study is to compare the severity of psoriasis, measured by the Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI), in patients with and without facial lesions.


 

Genital Psoriasis: Impact on Quality of Life and Treatment Options.

Kelly A, Ryan C. Am J Clin Dermatol. 2019 Jul 16

Psoriasis involving the genital skin occurs in up to two-thirds of psoriasis patients but is often overlooked by physicians. Furthermore, psoriasis objective and subjective severity indexes for common plaque psoriasis often neglect the impact this small area of psoriasis can have on a patient. It can have a significant impact on patients' psychosocial function due to intrusive physical symptoms such as genital itch and pain, and a detrimental impact on sexual health and impaired relationships.


 

Lifestyle changes for treating psoriasis.

Ko SH, Chi CC, Yeh ML, Wang SH, Tsai YS, Hsu MY. Cochrane Database Syst Rev. 2019 Jul 16

The objective of this review is to assess the effects of lifestyle changes for psoriasis, including weight reduction, alcohol abstinence, smoking cessation, dietary modification, exercise, and other lifestyle change interventions. Dietary intervention may reduce the severity of psoriasis (low-quality evidence) and probably improves quality of life and reduces BMI (moderate-quality evidence) in obese people when compared with usual care, while combined dietary intervention and exercise programme probably improves psoriasis severity and BMI when compared with information only (moderate-quality evidence).


 

The Incidence Rates and Risk Factors of Parkinson's Disease in Patients with Psoriasis: A Nationwide Population-based Cohort Study.

Lee JH, Han K, Gee HY. J Am Acad Dermatol. 2019 Jul 11.

This was a nationwide population-based cohort study to determine the incidence rates and risk factors of Parkinson's disease in patients with psoriasis. The psoriasis group showed a significantly increased risk of developing Parkinson's disease. The risk of Parkinson's disease was significantly high among the psoriasis patients who were not receiving systemic therapy and was low among the psoriasis patients on systemic therapy.


 

Psoriasis-associated itch: etiology, assessment, impact, and management.

Pithadia DJ, Reynolds KA, Lee EB, Wu JJ. J Dermatolog Treat. 2019 Jul 5:1-9.

Pruritus, a very broad, subjective, and complex symptom, troubles the majority of patients with psoriasis. However, the subjective and multidimensional nature of the symptom renders it challenging for patients to appropriately communicate their experiences with itch to providers. This review explores current perspectives regarding the underlying mechanisms, assessment tools, burden, and treatment modalities for psoriatic pruritus. It emphasizes the significance of incorporating a standardized, thorough, and verified metric that incorporates severity, distribution, and character of pruritus as well as its effects on various aspects of quality of life. It also underscores the importance of continued research to fully understand the pathogenesis of psoriatic itch for establishment of novel, targeted therapeutics.

Facial involvement and the severity of psoriasis.

Passos AN, de A Rêgo VRP, Duarte GV, Santos E Miranda RC, de O Rocha B, de F S P de Oliveira M. Int J Dermatol. 2019 Jul 26.

The aim of this cross-sectional study is to compare the severity of psoriasis, measured by the Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI), in patients with and without facial lesions.


 

Genital Psoriasis: Impact on Quality of Life and Treatment Options.

Kelly A, Ryan C. Am J Clin Dermatol. 2019 Jul 16

Psoriasis involving the genital skin occurs in up to two-thirds of psoriasis patients but is often overlooked by physicians. Furthermore, psoriasis objective and subjective severity indexes for common plaque psoriasis often neglect the impact this small area of psoriasis can have on a patient. It can have a significant impact on patients' psychosocial function due to intrusive physical symptoms such as genital itch and pain, and a detrimental impact on sexual health and impaired relationships.


 

Lifestyle changes for treating psoriasis.

Ko SH, Chi CC, Yeh ML, Wang SH, Tsai YS, Hsu MY. Cochrane Database Syst Rev. 2019 Jul 16

The objective of this review is to assess the effects of lifestyle changes for psoriasis, including weight reduction, alcohol abstinence, smoking cessation, dietary modification, exercise, and other lifestyle change interventions. Dietary intervention may reduce the severity of psoriasis (low-quality evidence) and probably improves quality of life and reduces BMI (moderate-quality evidence) in obese people when compared with usual care, while combined dietary intervention and exercise programme probably improves psoriasis severity and BMI when compared with information only (moderate-quality evidence).


 

The Incidence Rates and Risk Factors of Parkinson's Disease in Patients with Psoriasis: A Nationwide Population-based Cohort Study.

Lee JH, Han K, Gee HY. J Am Acad Dermatol. 2019 Jul 11.

This was a nationwide population-based cohort study to determine the incidence rates and risk factors of Parkinson's disease in patients with psoriasis. The psoriasis group showed a significantly increased risk of developing Parkinson's disease. The risk of Parkinson's disease was significantly high among the psoriasis patients who were not receiving systemic therapy and was low among the psoriasis patients on systemic therapy.


 

Psoriasis-associated itch: etiology, assessment, impact, and management.

Pithadia DJ, Reynolds KA, Lee EB, Wu JJ. J Dermatolog Treat. 2019 Jul 5:1-9.

Pruritus, a very broad, subjective, and complex symptom, troubles the majority of patients with psoriasis. However, the subjective and multidimensional nature of the symptom renders it challenging for patients to appropriately communicate their experiences with itch to providers. This review explores current perspectives regarding the underlying mechanisms, assessment tools, burden, and treatment modalities for psoriatic pruritus. It emphasizes the significance of incorporating a standardized, thorough, and verified metric that incorporates severity, distribution, and character of pruritus as well as its effects on various aspects of quality of life. It also underscores the importance of continued research to fully understand the pathogenesis of psoriatic itch for establishment of novel, targeted therapeutics.

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Impact of Psoriasis Treatment on Comorbidities

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References

1. Elmets CA, Leonardi CL, Davis DMR, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities. J Am Acad Dermatol. 2019;80:1073-1113.

2. Davidovici BB, Sattar N, Prinz J, et al. Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions. J Invest Dermatol. 2010;130:1785-1796.

3. Oliveira Mde F, Rocha Bde O, Duarte GV. Psoriasis: classical and emerging comorbidities. An Bras Dermatol. 2015;90:9-20.

4. Shah K, Mellars L, Changolkar A, Feldman SR. Real-world burden of comorbidities in US patients with psoriasis. J Am Acad Dermatol. 2017;77:287-292.

5. Hu SC, Lan CE. Psoriasis and cardiovascular comorbidities: focusing on severe vascular events, cardiovascular risk factors and implications for treatment [published online October 21, 2017]. Int J Mol Sci. doi:10.3390/ijms18102211.

6. Hugh J, Van Voorhees AS, Nijhawan RI, et al. From the Medical Board of The National Psoriasis Foundation: the risk of cardiovascular disease in individuals with psoriasis and the potential impact of current therapies. J Am Acad Dermatol. 2014;70:168-177.

7. Churton S, Brown L, Shin TM, et al. Does treatment of psoriasis reduce the risk of cardiovascular disease? Drugs. 2014;74:169-182.

8. Prodanovich S, Ma F, Taylor J, et al. Methotrexate reduces incidence of vascular diseases in veterans with psoriasis or rheumatoid arthritis. J Am Acad Dermatol. 2005;52:262-226.

9. Gulliver WP, Young HM, Bachelez H, et al. Psoriasis patients treated with biologics and methotrexate have a reduced rate of myocardial infarction: a collaborative analysis using international cohorts. J Cutan Med Surg. 2016;20:550-554.

10. Ahlehoff O, Skov L, Gislason G, et al. Cardiovascular disease event rates in patients with severe psoriasis treated with systemic anti-inflammatory drugs: a Danish real-world cohort study. J Intern Med. 2013;273:197-204.

11. Wu JJ, Poon KY, Channual JC, et al. Association between tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. Arch Dermatol. 2012;148:1244-1250.

12. Wu JJ, Poon KY. Association of ethnicity, tumor necrosis factor inhibitor therapy, and myocardial infarction risk in patients with psoriasis. J Am Acad Dermatol. 2013;69:167-168.

13. Wu JJ, Poon KY, Bebchuk JD. Association between the type and length of tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. J Drugs Dermatol. 2013;12:899-903.

14. Wu JJ, Poon KY, Bebchuk JD. Tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis, psoriatic arthritis, or both. J Drugs Dermatol. 2014;13:932-934.

15. Famenini S, Sako EY, Wu JJ. Effect of treating psoriasis on cardiovascular co-morbidities: focus on TNF inhibitors. Am J Clin Dermatol. 2014;15:45-50.

16. Nguyen T, Wu JJ. Relationship between tumor necrosis factor-alpha inhibitors and cardiovascular disease in psoriasis: a review. Perm J. 2014;18:49-54.

17. Shaaban D, Al-Mutairi N. The effect of tumour necrosis factor inhibitor therapy on the incidence of myocardial infarction in patients with psoriasis: a retrospective study [published online November 17, 2017]. J Dermatol Treat. doi:10.1080/09546634.2016.1254145. 

18. Wu D, Hou SY, Zhao S, et al. Efficacy and safety of interleukin-17 antagonists in patients with plaque psoriasis: A meta-analysis from phase 3 randomized controlled trials. J Eur Acad Dermatol Venereol. 2017;31:992-100.

19. Yang ZS, Lin NN, Li L, et al. The effect of TNF inhibitors on cardiovascular events in psoriasis and psoriatic arthritis: an updated meta-analysis. Clin Rev Allergy Immunol. 2016;51:240-247.

20. Heredi E, Vegh J, Pogacsas L, et al. Subclinical cardiovascular disease and it’s improvement after long-term TNF-alpha inhibitor therapy in severe psoriatic patients. J Eur Acad Dermatol Venereol. 2016;30:1531-1536.

21. Pina T, Corrales A, Lopez-Mejias R, et al. Anti-tumor necrosis factor-alpha therapy improves endothelial function and arterial stiffness in patients with moderate to severe psoriasis: a 6-month prospective study. J Dermatol. 2016;43:1267-1272.

22. Piaserico S, Osto E, Famoso G, et al. Treatment with tumor necrosis factor inhibitors restores coronary microvascular function in young patients with severe psoriasis. Atherosclerosis. 2016;251:25-30.

23. Van de Kerkhof PC, Griffiths CE, Reich K, et al. Secukinumab long-term safety experience: a pooled analysis of 10 phase II and III clinical studies in patients with moderate to severe plaque psoriasis. J Am Acad Dermatol. 2016;75:83-98.

24. Wu JJ, Guerin A, Sundaram M, et al. Cardiovascular event risk assessment in psoriasis patients treated with tumor necrosis factor-alpha inhibitors versus methotrexate. J Am Acad Dermatol. 2017;76:81-90.

25. Torres T, Raposo I, Selores M. IL-17 blockade in psoriasis: friend or foe in cardiovascular risk? Am J Clin Dermatol. 2016;17:107-112.

26. Deeks ED. Apremilast: a review in psoriasis and psoriatic arthritis. Drugs. 2015;75:1393-1403.

27. Crowley J, Thaci D, Joly P, et al. Long-term safety and tolerability of apremilast in patients with psoriasis: pooled safety analysis for >/= 156 weeks from 2 phase 3, randomized, controlled trials (ESTEEM 1 and 2). J Am Acad Dermatol. 2017;77:310-317.

28. Kavanaugh A, Mease PJ, Gomez-Reino JJ, et al. Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor. Ann Rheum Dis. 2014;73:1020-1026.

29. Daudén E, Griffiths CE, Ortonne JP, et al. Improvements in patient-reported outcomes in moderate-to-severe psoriasis patients receiving continuous or paused etanercept treatment over 54 weeks: the CRYSTEL study. J Eur Acad Dermatol Venereol. 2009;23:1374-1382.

30. Menter A, Augustin M, Signorovitch J, et al. The effect of adalimumab on reducing depression symptoms in patients with moderate to severe psoriasis: a randomized clinical trial. J Am Acad Dermatol. 2010;62:812-818.

31. Tyring S, Gottlieb A, Papp K, et al. Etanercept and clinical outcomes, fatigue, and depression in psoriasis: double-blind placebo-controlled randomised phase III trial. Lancet. 2006;367:29-35.

32. Strober B, Gooderham M, de Jong EMGJ, et al. Depressive symptoms, depression, and the effect of biologic therapy among patients in Psoriasis Longitudinal Assessment and Registry (PSOLAR). J Am Acad Dermatol. 2018;78:70-80.

33. Egeberg A, Khalid U, Gislason GH, et al. Association of psoriatic disease with uveitis: a Danish nationwide cohort study. JAMA Dermatol. 2015;151:1200-1205.

34. Huynh N, Cervantes-Castaneda RA, Bhat P, et al. Biologic response modifier therapy for psoriatic ocular inflammatory disease. Ocul Immunol Inflamm. 2008;16:89-93.

35. Pulusani S, McMurray SL, Jensen K, et al. Psoriasis treatment in patients with sickle cell disease Cutis. 2019;103:93-94.

36. Nnodim J, Meludu SC, Dioka CE, et al. Cytokine expression in homozygous sickle cell anaemia. JKIMSU. 2015;4:34-37.

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References

1. Elmets CA, Leonardi CL, Davis DMR, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities. J Am Acad Dermatol. 2019;80:1073-1113.

2. Davidovici BB, Sattar N, Prinz J, et al. Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions. J Invest Dermatol. 2010;130:1785-1796.

3. Oliveira Mde F, Rocha Bde O, Duarte GV. Psoriasis: classical and emerging comorbidities. An Bras Dermatol. 2015;90:9-20.

4. Shah K, Mellars L, Changolkar A, Feldman SR. Real-world burden of comorbidities in US patients with psoriasis. J Am Acad Dermatol. 2017;77:287-292.

5. Hu SC, Lan CE. Psoriasis and cardiovascular comorbidities: focusing on severe vascular events, cardiovascular risk factors and implications for treatment [published online October 21, 2017]. Int J Mol Sci. doi:10.3390/ijms18102211.

6. Hugh J, Van Voorhees AS, Nijhawan RI, et al. From the Medical Board of The National Psoriasis Foundation: the risk of cardiovascular disease in individuals with psoriasis and the potential impact of current therapies. J Am Acad Dermatol. 2014;70:168-177.

7. Churton S, Brown L, Shin TM, et al. Does treatment of psoriasis reduce the risk of cardiovascular disease? Drugs. 2014;74:169-182.

8. Prodanovich S, Ma F, Taylor J, et al. Methotrexate reduces incidence of vascular diseases in veterans with psoriasis or rheumatoid arthritis. J Am Acad Dermatol. 2005;52:262-226.

9. Gulliver WP, Young HM, Bachelez H, et al. Psoriasis patients treated with biologics and methotrexate have a reduced rate of myocardial infarction: a collaborative analysis using international cohorts. J Cutan Med Surg. 2016;20:550-554.

10. Ahlehoff O, Skov L, Gislason G, et al. Cardiovascular disease event rates in patients with severe psoriasis treated with systemic anti-inflammatory drugs: a Danish real-world cohort study. J Intern Med. 2013;273:197-204.

11. Wu JJ, Poon KY, Channual JC, et al. Association between tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. Arch Dermatol. 2012;148:1244-1250.

12. Wu JJ, Poon KY. Association of ethnicity, tumor necrosis factor inhibitor therapy, and myocardial infarction risk in patients with psoriasis. J Am Acad Dermatol. 2013;69:167-168.

13. Wu JJ, Poon KY, Bebchuk JD. Association between the type and length of tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. J Drugs Dermatol. 2013;12:899-903.

14. Wu JJ, Poon KY, Bebchuk JD. Tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis, psoriatic arthritis, or both. J Drugs Dermatol. 2014;13:932-934.

15. Famenini S, Sako EY, Wu JJ. Effect of treating psoriasis on cardiovascular co-morbidities: focus on TNF inhibitors. Am J Clin Dermatol. 2014;15:45-50.

16. Nguyen T, Wu JJ. Relationship between tumor necrosis factor-alpha inhibitors and cardiovascular disease in psoriasis: a review. Perm J. 2014;18:49-54.

17. Shaaban D, Al-Mutairi N. The effect of tumour necrosis factor inhibitor therapy on the incidence of myocardial infarction in patients with psoriasis: a retrospective study [published online November 17, 2017]. J Dermatol Treat. doi:10.1080/09546634.2016.1254145. 

18. Wu D, Hou SY, Zhao S, et al. Efficacy and safety of interleukin-17 antagonists in patients with plaque psoriasis: A meta-analysis from phase 3 randomized controlled trials. J Eur Acad Dermatol Venereol. 2017;31:992-100.

19. Yang ZS, Lin NN, Li L, et al. The effect of TNF inhibitors on cardiovascular events in psoriasis and psoriatic arthritis: an updated meta-analysis. Clin Rev Allergy Immunol. 2016;51:240-247.

20. Heredi E, Vegh J, Pogacsas L, et al. Subclinical cardiovascular disease and it’s improvement after long-term TNF-alpha inhibitor therapy in severe psoriatic patients. J Eur Acad Dermatol Venereol. 2016;30:1531-1536.

21. Pina T, Corrales A, Lopez-Mejias R, et al. Anti-tumor necrosis factor-alpha therapy improves endothelial function and arterial stiffness in patients with moderate to severe psoriasis: a 6-month prospective study. J Dermatol. 2016;43:1267-1272.

22. Piaserico S, Osto E, Famoso G, et al. Treatment with tumor necrosis factor inhibitors restores coronary microvascular function in young patients with severe psoriasis. Atherosclerosis. 2016;251:25-30.

23. Van de Kerkhof PC, Griffiths CE, Reich K, et al. Secukinumab long-term safety experience: a pooled analysis of 10 phase II and III clinical studies in patients with moderate to severe plaque psoriasis. J Am Acad Dermatol. 2016;75:83-98.

24. Wu JJ, Guerin A, Sundaram M, et al. Cardiovascular event risk assessment in psoriasis patients treated with tumor necrosis factor-alpha inhibitors versus methotrexate. J Am Acad Dermatol. 2017;76:81-90.

25. Torres T, Raposo I, Selores M. IL-17 blockade in psoriasis: friend or foe in cardiovascular risk? Am J Clin Dermatol. 2016;17:107-112.

26. Deeks ED. Apremilast: a review in psoriasis and psoriatic arthritis. Drugs. 2015;75:1393-1403.

27. Crowley J, Thaci D, Joly P, et al. Long-term safety and tolerability of apremilast in patients with psoriasis: pooled safety analysis for >/= 156 weeks from 2 phase 3, randomized, controlled trials (ESTEEM 1 and 2). J Am Acad Dermatol. 2017;77:310-317.

28. Kavanaugh A, Mease PJ, Gomez-Reino JJ, et al. Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor. Ann Rheum Dis. 2014;73:1020-1026.

29. Daudén E, Griffiths CE, Ortonne JP, et al. Improvements in patient-reported outcomes in moderate-to-severe psoriasis patients receiving continuous or paused etanercept treatment over 54 weeks: the CRYSTEL study. J Eur Acad Dermatol Venereol. 2009;23:1374-1382.

30. Menter A, Augustin M, Signorovitch J, et al. The effect of adalimumab on reducing depression symptoms in patients with moderate to severe psoriasis: a randomized clinical trial. J Am Acad Dermatol. 2010;62:812-818.

31. Tyring S, Gottlieb A, Papp K, et al. Etanercept and clinical outcomes, fatigue, and depression in psoriasis: double-blind placebo-controlled randomised phase III trial. Lancet. 2006;367:29-35.

32. Strober B, Gooderham M, de Jong EMGJ, et al. Depressive symptoms, depression, and the effect of biologic therapy among patients in Psoriasis Longitudinal Assessment and Registry (PSOLAR). J Am Acad Dermatol. 2018;78:70-80.

33. Egeberg A, Khalid U, Gislason GH, et al. Association of psoriatic disease with uveitis: a Danish nationwide cohort study. JAMA Dermatol. 2015;151:1200-1205.

34. Huynh N, Cervantes-Castaneda RA, Bhat P, et al. Biologic response modifier therapy for psoriatic ocular inflammatory disease. Ocul Immunol Inflamm. 2008;16:89-93.

35. Pulusani S, McMurray SL, Jensen K, et al. Psoriasis treatment in patients with sickle cell disease Cutis. 2019;103:93-94.

36. Nnodim J, Meludu SC, Dioka CE, et al. Cytokine expression in homozygous sickle cell anaemia. JKIMSU. 2015;4:34-37.

References

1. Elmets CA, Leonardi CL, Davis DMR, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities. J Am Acad Dermatol. 2019;80:1073-1113.

2. Davidovici BB, Sattar N, Prinz J, et al. Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions. J Invest Dermatol. 2010;130:1785-1796.

3. Oliveira Mde F, Rocha Bde O, Duarte GV. Psoriasis: classical and emerging comorbidities. An Bras Dermatol. 2015;90:9-20.

4. Shah K, Mellars L, Changolkar A, Feldman SR. Real-world burden of comorbidities in US patients with psoriasis. J Am Acad Dermatol. 2017;77:287-292.

5. Hu SC, Lan CE. Psoriasis and cardiovascular comorbidities: focusing on severe vascular events, cardiovascular risk factors and implications for treatment [published online October 21, 2017]. Int J Mol Sci. doi:10.3390/ijms18102211.

6. Hugh J, Van Voorhees AS, Nijhawan RI, et al. From the Medical Board of The National Psoriasis Foundation: the risk of cardiovascular disease in individuals with psoriasis and the potential impact of current therapies. J Am Acad Dermatol. 2014;70:168-177.

7. Churton S, Brown L, Shin TM, et al. Does treatment of psoriasis reduce the risk of cardiovascular disease? Drugs. 2014;74:169-182.

8. Prodanovich S, Ma F, Taylor J, et al. Methotrexate reduces incidence of vascular diseases in veterans with psoriasis or rheumatoid arthritis. J Am Acad Dermatol. 2005;52:262-226.

9. Gulliver WP, Young HM, Bachelez H, et al. Psoriasis patients treated with biologics and methotrexate have a reduced rate of myocardial infarction: a collaborative analysis using international cohorts. J Cutan Med Surg. 2016;20:550-554.

10. Ahlehoff O, Skov L, Gislason G, et al. Cardiovascular disease event rates in patients with severe psoriasis treated with systemic anti-inflammatory drugs: a Danish real-world cohort study. J Intern Med. 2013;273:197-204.

11. Wu JJ, Poon KY, Channual JC, et al. Association between tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. Arch Dermatol. 2012;148:1244-1250.

12. Wu JJ, Poon KY. Association of ethnicity, tumor necrosis factor inhibitor therapy, and myocardial infarction risk in patients with psoriasis. J Am Acad Dermatol. 2013;69:167-168.

13. Wu JJ, Poon KY, Bebchuk JD. Association between the type and length of tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. J Drugs Dermatol. 2013;12:899-903.

14. Wu JJ, Poon KY, Bebchuk JD. Tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis, psoriatic arthritis, or both. J Drugs Dermatol. 2014;13:932-934.

15. Famenini S, Sako EY, Wu JJ. Effect of treating psoriasis on cardiovascular co-morbidities: focus on TNF inhibitors. Am J Clin Dermatol. 2014;15:45-50.

16. Nguyen T, Wu JJ. Relationship between tumor necrosis factor-alpha inhibitors and cardiovascular disease in psoriasis: a review. Perm J. 2014;18:49-54.

17. Shaaban D, Al-Mutairi N. The effect of tumour necrosis factor inhibitor therapy on the incidence of myocardial infarction in patients with psoriasis: a retrospective study [published online November 17, 2017]. J Dermatol Treat. doi:10.1080/09546634.2016.1254145. 

18. Wu D, Hou SY, Zhao S, et al. Efficacy and safety of interleukin-17 antagonists in patients with plaque psoriasis: A meta-analysis from phase 3 randomized controlled trials. J Eur Acad Dermatol Venereol. 2017;31:992-100.

19. Yang ZS, Lin NN, Li L, et al. The effect of TNF inhibitors on cardiovascular events in psoriasis and psoriatic arthritis: an updated meta-analysis. Clin Rev Allergy Immunol. 2016;51:240-247.

20. Heredi E, Vegh J, Pogacsas L, et al. Subclinical cardiovascular disease and it’s improvement after long-term TNF-alpha inhibitor therapy in severe psoriatic patients. J Eur Acad Dermatol Venereol. 2016;30:1531-1536.

21. Pina T, Corrales A, Lopez-Mejias R, et al. Anti-tumor necrosis factor-alpha therapy improves endothelial function and arterial stiffness in patients with moderate to severe psoriasis: a 6-month prospective study. J Dermatol. 2016;43:1267-1272.

22. Piaserico S, Osto E, Famoso G, et al. Treatment with tumor necrosis factor inhibitors restores coronary microvascular function in young patients with severe psoriasis. Atherosclerosis. 2016;251:25-30.

23. Van de Kerkhof PC, Griffiths CE, Reich K, et al. Secukinumab long-term safety experience: a pooled analysis of 10 phase II and III clinical studies in patients with moderate to severe plaque psoriasis. J Am Acad Dermatol. 2016;75:83-98.

24. Wu JJ, Guerin A, Sundaram M, et al. Cardiovascular event risk assessment in psoriasis patients treated with tumor necrosis factor-alpha inhibitors versus methotrexate. J Am Acad Dermatol. 2017;76:81-90.

25. Torres T, Raposo I, Selores M. IL-17 blockade in psoriasis: friend or foe in cardiovascular risk? Am J Clin Dermatol. 2016;17:107-112.

26. Deeks ED. Apremilast: a review in psoriasis and psoriatic arthritis. Drugs. 2015;75:1393-1403.

27. Crowley J, Thaci D, Joly P, et al. Long-term safety and tolerability of apremilast in patients with psoriasis: pooled safety analysis for >/= 156 weeks from 2 phase 3, randomized, controlled trials (ESTEEM 1 and 2). J Am Acad Dermatol. 2017;77:310-317.

28. Kavanaugh A, Mease PJ, Gomez-Reino JJ, et al. Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor. Ann Rheum Dis. 2014;73:1020-1026.

29. Daudén E, Griffiths CE, Ortonne JP, et al. Improvements in patient-reported outcomes in moderate-to-severe psoriasis patients receiving continuous or paused etanercept treatment over 54 weeks: the CRYSTEL study. J Eur Acad Dermatol Venereol. 2009;23:1374-1382.

30. Menter A, Augustin M, Signorovitch J, et al. The effect of adalimumab on reducing depression symptoms in patients with moderate to severe psoriasis: a randomized clinical trial. J Am Acad Dermatol. 2010;62:812-818.

31. Tyring S, Gottlieb A, Papp K, et al. Etanercept and clinical outcomes, fatigue, and depression in psoriasis: double-blind placebo-controlled randomised phase III trial. Lancet. 2006;367:29-35.

32. Strober B, Gooderham M, de Jong EMGJ, et al. Depressive symptoms, depression, and the effect of biologic therapy among patients in Psoriasis Longitudinal Assessment and Registry (PSOLAR). J Am Acad Dermatol. 2018;78:70-80.

33. Egeberg A, Khalid U, Gislason GH, et al. Association of psoriatic disease with uveitis: a Danish nationwide cohort study. JAMA Dermatol. 2015;151:1200-1205.

34. Huynh N, Cervantes-Castaneda RA, Bhat P, et al. Biologic response modifier therapy for psoriatic ocular inflammatory disease. Ocul Immunol Inflamm. 2008;16:89-93.

35. Pulusani S, McMurray SL, Jensen K, et al. Psoriasis treatment in patients with sickle cell disease Cutis. 2019;103:93-94.

36. Nnodim J, Meludu SC, Dioka CE, et al. Cytokine expression in homozygous sickle cell anaemia. JKIMSU. 2015;4:34-37.

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In psoriasis, risankizumab outperforms adalimumab

IL-23 inhibitor expands psoriasis arsenal
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In a phase 3, active comparator controlled trial, treatment with risankizumab led to better skin clearance than treatment with adalimumab in patients with moderate-to-severe plaque psoriasis. Results of the IMMvent trial were published online ahead of print July 4 in the Lancet.

Risankizumab targets the p19 subunit of the cytokine IL-23. Selectivity for p19 has the potential to be safer than some other approaches that target the p40 subunit, because p19 is specific to IL-23, and many immune defense processes can function without IL-23. The p40 subunit is shared with IL-12, and blocking it can therefore lead to off-target effects.

Risankizumab was previously shown to have superior safety and efficacy over ustekinumab, which inhibits a subunit shared by IL-23 and IL-12 (Gordon KB et al. Lancet. 2018;392[10148]:650-61). Adalimumab is a TNF-alpha inhibitor that is frequently used to treat psoriasis, and which became available in biosimilar form in Europe in 2018.

The researchers randomized 605 adult patients from 66 sites in 11 countries to receive either risankizumab or adalimumab. The first phase (Part A) of the trial lasted up to 16 weeks, and tested the general superiority of risankizumab over adalimumab. The second phase (Part B), from week 16 to 44, evaluated the efficacy of risankizumab in participants who experienced an intermediate response, defined as Psoriasis Area and Severity Index (PASI) score of 50-90.

At the start of Part B, subjects initially receiving adalimumab who had at least a 90% improvement in PASI stayed on adalimumab (PASI 90), while those who had less than 50% improvement in PASI were switched to risankizumab. The remaining intermediate responders (PASI 50-90) were re-randomized to continue adalimumab or switch to risankizumab. All subjects initially randomized to risankizumab continued risankizumab during part B.

At the end of Part A, 72% of the risankizumab group achieved PASI 90, compared with 47% in the adalimumab group (p < 0.0001). A total of 84% in the risankizumab group had a static Physician’s Global Assessment (sPGA) score of 0 or 1 at the end of Part A, compared with 60% in the adalimumab group (p < 0.0001).

During Part B, among intermediate adalimumab responders, 66% of those switched to risankizumab achieved PASI 90, compared with 21% of continued on adalimumab (p < 0.0001).

In Part A, 56% of patients taking risankizumab experienced an adverse event, as did 57% of those taking adalimumab. Among adalimumab intermediate responders, 75% of those who switched to risankizumab during Part B had an adverse event, compared with 66% of those who continued adalimumab.

SOURCE: Reich K, et al. Lancet 2019, July 4 .

Body

Until recently, TNF-alpha inhibitors have been the most commonly prescribed biologic agents for psoriasis. They are more targeted than small molecules like cyclosporine or methotrexate, but still are associated with immune side effects like infection and malignancy. Drugs that specifically target IL-23 home in on the pathogenicity of psoriasis, and they are not associated with infection and malignancy. The results of this study offer evidence that IL-23 inhibitors represent another effective and convenient option for the treatment of psoriasis. Physicians can select from IL-23 inhibitors, IL-17 inhibitors, and TNF-alpha inhibitors to determine the optimal treatment for patients based on patient weight, childbearing status, age, and comorbid conditions.

Mark Lebwohl, MD, is in the department of dermatology at Icahn School of Medicine at Mount Sinai, New York.

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Until recently, TNF-alpha inhibitors have been the most commonly prescribed biologic agents for psoriasis. They are more targeted than small molecules like cyclosporine or methotrexate, but still are associated with immune side effects like infection and malignancy. Drugs that specifically target IL-23 home in on the pathogenicity of psoriasis, and they are not associated with infection and malignancy. The results of this study offer evidence that IL-23 inhibitors represent another effective and convenient option for the treatment of psoriasis. Physicians can select from IL-23 inhibitors, IL-17 inhibitors, and TNF-alpha inhibitors to determine the optimal treatment for patients based on patient weight, childbearing status, age, and comorbid conditions.

Mark Lebwohl, MD, is in the department of dermatology at Icahn School of Medicine at Mount Sinai, New York.

Body

Until recently, TNF-alpha inhibitors have been the most commonly prescribed biologic agents for psoriasis. They are more targeted than small molecules like cyclosporine or methotrexate, but still are associated with immune side effects like infection and malignancy. Drugs that specifically target IL-23 home in on the pathogenicity of psoriasis, and they are not associated with infection and malignancy. The results of this study offer evidence that IL-23 inhibitors represent another effective and convenient option for the treatment of psoriasis. Physicians can select from IL-23 inhibitors, IL-17 inhibitors, and TNF-alpha inhibitors to determine the optimal treatment for patients based on patient weight, childbearing status, age, and comorbid conditions.

Mark Lebwohl, MD, is in the department of dermatology at Icahn School of Medicine at Mount Sinai, New York.

Title
IL-23 inhibitor expands psoriasis arsenal
IL-23 inhibitor expands psoriasis arsenal

In a phase 3, active comparator controlled trial, treatment with risankizumab led to better skin clearance than treatment with adalimumab in patients with moderate-to-severe plaque psoriasis. Results of the IMMvent trial were published online ahead of print July 4 in the Lancet.

Risankizumab targets the p19 subunit of the cytokine IL-23. Selectivity for p19 has the potential to be safer than some other approaches that target the p40 subunit, because p19 is specific to IL-23, and many immune defense processes can function without IL-23. The p40 subunit is shared with IL-12, and blocking it can therefore lead to off-target effects.

Risankizumab was previously shown to have superior safety and efficacy over ustekinumab, which inhibits a subunit shared by IL-23 and IL-12 (Gordon KB et al. Lancet. 2018;392[10148]:650-61). Adalimumab is a TNF-alpha inhibitor that is frequently used to treat psoriasis, and which became available in biosimilar form in Europe in 2018.

The researchers randomized 605 adult patients from 66 sites in 11 countries to receive either risankizumab or adalimumab. The first phase (Part A) of the trial lasted up to 16 weeks, and tested the general superiority of risankizumab over adalimumab. The second phase (Part B), from week 16 to 44, evaluated the efficacy of risankizumab in participants who experienced an intermediate response, defined as Psoriasis Area and Severity Index (PASI) score of 50-90.

At the start of Part B, subjects initially receiving adalimumab who had at least a 90% improvement in PASI stayed on adalimumab (PASI 90), while those who had less than 50% improvement in PASI were switched to risankizumab. The remaining intermediate responders (PASI 50-90) were re-randomized to continue adalimumab or switch to risankizumab. All subjects initially randomized to risankizumab continued risankizumab during part B.

At the end of Part A, 72% of the risankizumab group achieved PASI 90, compared with 47% in the adalimumab group (p < 0.0001). A total of 84% in the risankizumab group had a static Physician’s Global Assessment (sPGA) score of 0 or 1 at the end of Part A, compared with 60% in the adalimumab group (p < 0.0001).

During Part B, among intermediate adalimumab responders, 66% of those switched to risankizumab achieved PASI 90, compared with 21% of continued on adalimumab (p < 0.0001).

In Part A, 56% of patients taking risankizumab experienced an adverse event, as did 57% of those taking adalimumab. Among adalimumab intermediate responders, 75% of those who switched to risankizumab during Part B had an adverse event, compared with 66% of those who continued adalimumab.

SOURCE: Reich K, et al. Lancet 2019, July 4 .

In a phase 3, active comparator controlled trial, treatment with risankizumab led to better skin clearance than treatment with adalimumab in patients with moderate-to-severe plaque psoriasis. Results of the IMMvent trial were published online ahead of print July 4 in the Lancet.

Risankizumab targets the p19 subunit of the cytokine IL-23. Selectivity for p19 has the potential to be safer than some other approaches that target the p40 subunit, because p19 is specific to IL-23, and many immune defense processes can function without IL-23. The p40 subunit is shared with IL-12, and blocking it can therefore lead to off-target effects.

Risankizumab was previously shown to have superior safety and efficacy over ustekinumab, which inhibits a subunit shared by IL-23 and IL-12 (Gordon KB et al. Lancet. 2018;392[10148]:650-61). Adalimumab is a TNF-alpha inhibitor that is frequently used to treat psoriasis, and which became available in biosimilar form in Europe in 2018.

The researchers randomized 605 adult patients from 66 sites in 11 countries to receive either risankizumab or adalimumab. The first phase (Part A) of the trial lasted up to 16 weeks, and tested the general superiority of risankizumab over adalimumab. The second phase (Part B), from week 16 to 44, evaluated the efficacy of risankizumab in participants who experienced an intermediate response, defined as Psoriasis Area and Severity Index (PASI) score of 50-90.

At the start of Part B, subjects initially receiving adalimumab who had at least a 90% improvement in PASI stayed on adalimumab (PASI 90), while those who had less than 50% improvement in PASI were switched to risankizumab. The remaining intermediate responders (PASI 50-90) were re-randomized to continue adalimumab or switch to risankizumab. All subjects initially randomized to risankizumab continued risankizumab during part B.

At the end of Part A, 72% of the risankizumab group achieved PASI 90, compared with 47% in the adalimumab group (p < 0.0001). A total of 84% in the risankizumab group had a static Physician’s Global Assessment (sPGA) score of 0 or 1 at the end of Part A, compared with 60% in the adalimumab group (p < 0.0001).

During Part B, among intermediate adalimumab responders, 66% of those switched to risankizumab achieved PASI 90, compared with 21% of continued on adalimumab (p < 0.0001).

In Part A, 56% of patients taking risankizumab experienced an adverse event, as did 57% of those taking adalimumab. Among adalimumab intermediate responders, 75% of those who switched to risankizumab during Part B had an adverse event, compared with 66% of those who continued adalimumab.

SOURCE: Reich K, et al. Lancet 2019, July 4 .

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Psoriasis Treatment in Patients With HIV

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References
  1. Nakamura M, Abrouk M, Farahnik B, et al. Psoriasis treatment in HIV-positive patients: a systematic review of systemic immunosuppressive therapies. Cutis. 2018;101:38, 42, 56.
  2. Patel RV, Weinberg JM. Psoriasis in the patient with human immunodeficiency virus, part 2: review of treatment. Cutis. 2008;82:202-210.
  3. Ceccarelli M, Venanzi Rullo E, Vaccaro M, et al. HIV‐associated psoriasis: epidemiology, pathogenesis, and management [published online January 6, 2019]. Dermatol Ther. 2019;32:e12806. doi:10.1111/dth.12806.
  4. Zarbafian M, Richer V. Treatment of moderate to severe psoriasis with apremilast over 2 years in the context of long-term treated HIV infection: a case report. SAGE Open Med Case Rep. 2019;7:2050313X19845193. doi:10.1177/2050313X19845193. 
  5. Menon K, Van Vorhees AS, Bebo, BF, et al. Psoriasis in patients with HIV infection: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62:291-299. 
  6. Mallon E, Bunker CB. HIV-associated psoriasis. AIDS Patient Care STDS. 2000;14:239-246.
  7. Patel VA, Weinberg JM. Psoriasis in the patient with human immunodeficiency virus, part 1: review of pathogenesis. Cutis. 2008;82:117-122.
  8. Castillo RL, Racaza GZ, Dela Cruz Roa F. Ostraceous and inverse psoriasis with psoriatic arthritis as the presenting features of advanced HIV infection. Singapore Med J. 2014;55:e60-e63.
  9. Duvic M, Crane MM, Conant M, et al. Zidovudine improves psoriasis in human immunodeficiency virus- positive males. Arch Dermatol. 1994;130:447.
  10. Jaffee D, May LP, Sanchez M, et al. Staphylococcal sepsis in HIV antibody seropositive psoriasis patients. J Am Acad Dermatol. 1991;24:970-972.
  11. King LE, Dufresne RG, Lovette GL, et al. Erythroderma: review of 82 cases. South Med J. 1986;79:1210-1215.
  12. Kaminetsky J, Aziz M, Kaushik S. A review of biologics and other treatment modalities in HIV-associated psoriasis. Skin. 2018;2:389-401.
  13. Wolff K. Side effects of psoralen photochemotherapy (PUVA). Br J Dermatol. 1990;122:117-125.
  14. Stern RS, Mills DK, Krell K, et al. HIV-positive patients differ from HIV-negative patients in indications for and type of UV therapy used. J Am Acad Dermatol. 1998;39:48-55.
  15. Oracion RM, Skiest DJ, Keiser PH, et al. HIV-related skin diseases. Prog Dermatol. 1999;33:1-6.
  16. Finkelstein M, Berman B. HIV and AIDS in inpatient dermatology: approach to the consultation. Dermatol Clin. 2000;18:509-520.
  17. Kaushik SB, Lebwohl MG. Psoriasis: which therapy for which patient: focus on special populations and chronic infections. J Am Acad Dermatol. 2019;80:43-53.
  18. Sellam J, Bouvard B, Masson C, et al. Use of infliximab to treat psoriatic arthritis in HIV-positive patients. Joint Bone Spine. 2007;74:197-200.
  19. Reddy SP, Lee E, Wu JJ. Apremilast and phototherapy for treatment of psoriasis in a patient with human immunodeficiency virus. Cutis. 2019;103:E1-E7.
  20. Otezla (apremilast). Summit, NJ: Celgene Corporation; 2017.
  21. Schafer P. Apremilast mechanism of action and application to psoriasis and psoriatic arthritis. Biochem Pharmacol. 2012;83:1583-1590.
Author and Disclosure Information

From the Dermatology Research and Education Foundation, Irvine, California.

Dr. Wu is an investigator for AbbVie, Amgen Inc, Eli Lilly and Company, Janssen Pharmaceuticals, and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira Inc; Dr. Reddy’s Laboratories Ltd; Eli Lilly and Company; Janssen Pharmaceuticals; LEO Pharma; Novartis; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC. He also is a speaker for AbbVie; Celgene Corporation; Novartis; Regeneron Pharmaceuticals, Inc; Sanofi Genzyme; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC.

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Author and Disclosure Information

From the Dermatology Research and Education Foundation, Irvine, California.

Dr. Wu is an investigator for AbbVie, Amgen Inc, Eli Lilly and Company, Janssen Pharmaceuticals, and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira Inc; Dr. Reddy’s Laboratories Ltd; Eli Lilly and Company; Janssen Pharmaceuticals; LEO Pharma; Novartis; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC. He also is a speaker for AbbVie; Celgene Corporation; Novartis; Regeneron Pharmaceuticals, Inc; Sanofi Genzyme; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC.

Author and Disclosure Information

From the Dermatology Research and Education Foundation, Irvine, California.

Dr. Wu is an investigator for AbbVie, Amgen Inc, Eli Lilly and Company, Janssen Pharmaceuticals, and Novartis. He also is a consultant for AbbVie; Almirall; Amgen Inc; Bristol-Myers Squibb; Celgene Corporation; Dermira Inc; Dr. Reddy’s Laboratories Ltd; Eli Lilly and Company; Janssen Pharmaceuticals; LEO Pharma; Novartis; Promius Pharma; Regeneron Pharmaceuticals, Inc; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC. He also is a speaker for AbbVie; Celgene Corporation; Novartis; Regeneron Pharmaceuticals, Inc; Sanofi Genzyme; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals North America LLC.

References
  1. Nakamura M, Abrouk M, Farahnik B, et al. Psoriasis treatment in HIV-positive patients: a systematic review of systemic immunosuppressive therapies. Cutis. 2018;101:38, 42, 56.
  2. Patel RV, Weinberg JM. Psoriasis in the patient with human immunodeficiency virus, part 2: review of treatment. Cutis. 2008;82:202-210.
  3. Ceccarelli M, Venanzi Rullo E, Vaccaro M, et al. HIV‐associated psoriasis: epidemiology, pathogenesis, and management [published online January 6, 2019]. Dermatol Ther. 2019;32:e12806. doi:10.1111/dth.12806.
  4. Zarbafian M, Richer V. Treatment of moderate to severe psoriasis with apremilast over 2 years in the context of long-term treated HIV infection: a case report. SAGE Open Med Case Rep. 2019;7:2050313X19845193. doi:10.1177/2050313X19845193. 
  5. Menon K, Van Vorhees AS, Bebo, BF, et al. Psoriasis in patients with HIV infection: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62:291-299. 
  6. Mallon E, Bunker CB. HIV-associated psoriasis. AIDS Patient Care STDS. 2000;14:239-246.
  7. Patel VA, Weinberg JM. Psoriasis in the patient with human immunodeficiency virus, part 1: review of pathogenesis. Cutis. 2008;82:117-122.
  8. Castillo RL, Racaza GZ, Dela Cruz Roa F. Ostraceous and inverse psoriasis with psoriatic arthritis as the presenting features of advanced HIV infection. Singapore Med J. 2014;55:e60-e63.
  9. Duvic M, Crane MM, Conant M, et al. Zidovudine improves psoriasis in human immunodeficiency virus- positive males. Arch Dermatol. 1994;130:447.
  10. Jaffee D, May LP, Sanchez M, et al. Staphylococcal sepsis in HIV antibody seropositive psoriasis patients. J Am Acad Dermatol. 1991;24:970-972.
  11. King LE, Dufresne RG, Lovette GL, et al. Erythroderma: review of 82 cases. South Med J. 1986;79:1210-1215.
  12. Kaminetsky J, Aziz M, Kaushik S. A review of biologics and other treatment modalities in HIV-associated psoriasis. Skin. 2018;2:389-401.
  13. Wolff K. Side effects of psoralen photochemotherapy (PUVA). Br J Dermatol. 1990;122:117-125.
  14. Stern RS, Mills DK, Krell K, et al. HIV-positive patients differ from HIV-negative patients in indications for and type of UV therapy used. J Am Acad Dermatol. 1998;39:48-55.
  15. Oracion RM, Skiest DJ, Keiser PH, et al. HIV-related skin diseases. Prog Dermatol. 1999;33:1-6.
  16. Finkelstein M, Berman B. HIV and AIDS in inpatient dermatology: approach to the consultation. Dermatol Clin. 2000;18:509-520.
  17. Kaushik SB, Lebwohl MG. Psoriasis: which therapy for which patient: focus on special populations and chronic infections. J Am Acad Dermatol. 2019;80:43-53.
  18. Sellam J, Bouvard B, Masson C, et al. Use of infliximab to treat psoriatic arthritis in HIV-positive patients. Joint Bone Spine. 2007;74:197-200.
  19. Reddy SP, Lee E, Wu JJ. Apremilast and phototherapy for treatment of psoriasis in a patient with human immunodeficiency virus. Cutis. 2019;103:E1-E7.
  20. Otezla (apremilast). Summit, NJ: Celgene Corporation; 2017.
  21. Schafer P. Apremilast mechanism of action and application to psoriasis and psoriatic arthritis. Biochem Pharmacol. 2012;83:1583-1590.
References
  1. Nakamura M, Abrouk M, Farahnik B, et al. Psoriasis treatment in HIV-positive patients: a systematic review of systemic immunosuppressive therapies. Cutis. 2018;101:38, 42, 56.
  2. Patel RV, Weinberg JM. Psoriasis in the patient with human immunodeficiency virus, part 2: review of treatment. Cutis. 2008;82:202-210.
  3. Ceccarelli M, Venanzi Rullo E, Vaccaro M, et al. HIV‐associated psoriasis: epidemiology, pathogenesis, and management [published online January 6, 2019]. Dermatol Ther. 2019;32:e12806. doi:10.1111/dth.12806.
  4. Zarbafian M, Richer V. Treatment of moderate to severe psoriasis with apremilast over 2 years in the context of long-term treated HIV infection: a case report. SAGE Open Med Case Rep. 2019;7:2050313X19845193. doi:10.1177/2050313X19845193. 
  5. Menon K, Van Vorhees AS, Bebo, BF, et al. Psoriasis in patients with HIV infection: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62:291-299. 
  6. Mallon E, Bunker CB. HIV-associated psoriasis. AIDS Patient Care STDS. 2000;14:239-246.
  7. Patel VA, Weinberg JM. Psoriasis in the patient with human immunodeficiency virus, part 1: review of pathogenesis. Cutis. 2008;82:117-122.
  8. Castillo RL, Racaza GZ, Dela Cruz Roa F. Ostraceous and inverse psoriasis with psoriatic arthritis as the presenting features of advanced HIV infection. Singapore Med J. 2014;55:e60-e63.
  9. Duvic M, Crane MM, Conant M, et al. Zidovudine improves psoriasis in human immunodeficiency virus- positive males. Arch Dermatol. 1994;130:447.
  10. Jaffee D, May LP, Sanchez M, et al. Staphylococcal sepsis in HIV antibody seropositive psoriasis patients. J Am Acad Dermatol. 1991;24:970-972.
  11. King LE, Dufresne RG, Lovette GL, et al. Erythroderma: review of 82 cases. South Med J. 1986;79:1210-1215.
  12. Kaminetsky J, Aziz M, Kaushik S. A review of biologics and other treatment modalities in HIV-associated psoriasis. Skin. 2018;2:389-401.
  13. Wolff K. Side effects of psoralen photochemotherapy (PUVA). Br J Dermatol. 1990;122:117-125.
  14. Stern RS, Mills DK, Krell K, et al. HIV-positive patients differ from HIV-negative patients in indications for and type of UV therapy used. J Am Acad Dermatol. 1998;39:48-55.
  15. Oracion RM, Skiest DJ, Keiser PH, et al. HIV-related skin diseases. Prog Dermatol. 1999;33:1-6.
  16. Finkelstein M, Berman B. HIV and AIDS in inpatient dermatology: approach to the consultation. Dermatol Clin. 2000;18:509-520.
  17. Kaushik SB, Lebwohl MG. Psoriasis: which therapy for which patient: focus on special populations and chronic infections. J Am Acad Dermatol. 2019;80:43-53.
  18. Sellam J, Bouvard B, Masson C, et al. Use of infliximab to treat psoriatic arthritis in HIV-positive patients. Joint Bone Spine. 2007;74:197-200.
  19. Reddy SP, Lee E, Wu JJ. Apremilast and phototherapy for treatment of psoriasis in a patient with human immunodeficiency virus. Cutis. 2019;103:E1-E7.
  20. Otezla (apremilast). Summit, NJ: Celgene Corporation; 2017.
  21. Schafer P. Apremilast mechanism of action and application to psoriasis and psoriatic arthritis. Biochem Pharmacol. 2012;83:1583-1590.
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