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More than just a skin condition


appearance related. Indeed, psoriasis rarely causes a severe physical disability, but it frequently disfigures the patients. Therefore, in order to assess the full burden of psoriasis on QoL, it is important to consider its physical, psychological, social and occupational impact.21


The


physical impact includes symptoms and functional limitations. Functional limitations refer to observable, objective limitations of the patient, such as inability to use the hands or ambulate due to the presence of a painful skin condition or the presence of joint stiffness. Psychological impact refers to the impact of skin disease on self-esteem and body image, as well as depression, anxiety, anger and embarrassment. Social impact refers to the impact on sexual relationships or relationship with friends and family members. Finally, occupational impact refers to the impairment on the types of occupation the patient can engage in, including promotion or rejections in the workplace. The level of QoL impairment in psoriasis has been shown to be comparable to that of some severe medical conditions such as cardiovascular diseases, diabetes and hypertension.22


Personalised management The association between psoriasis and cardiovascular and metabolic disorders has important clinical and therapeutic implications. A comprehensive screening of patients with psoriasis should include a careful assessment of the global cardiovascular risk, such as the measurement of pulse and blood pressure, determination of BMI and the measurement of fasting blood lipids and glucose. The choice of systemic treatment for psoriasis is influenced by the


concomitance of metabolic comorbidities, because methotrexate (MTX), cyclosporine, acitretin and biologics may negatively impact on these associated disorders. Methotrexate should be prescribed with caution in the case of overweight/obese patients, high alcohol consumption, diabetes mellitus or viral hepatitis, due to the increased risk of developing liver toxicity.23


Cyclosporine


can induce or worsen arterial hypertension, alter glucose tolerance and/or interfere with fatty acid metabolism favouring dyslipidaemia.24


Hypertriglyceridaemia and 4


On the other hand, the treatment with methotrexate and/or TNF-α blockers


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hypercholesterolaemia, as well as body weight increase, have also occasionally been reported in patients treated with anti-TNF-α agents.25


might reduce the cardiovascular risk. In a large Danish cohort study, it was found that the rate of cardiovascular events was lower in the group of patients treated with biologics (n=693) and MTX (n=799) than in those treated with cyclosporine, acitretin or phototherapy (n=908).26 Finally, patients with moderate-to-severe psoriasis are candidates for cardiovascular risk reduction. Non-pharmacological intervention, such as a low-calorie diet, should be recommended to obese patients. Indeed, we found that a moderate weight loss (that is, 5–10% of body weight) increases the responsiveness of obese patients with moderate-to-severe chronic plaque psoriasis to sub-optimal-dosed cyclosporine.27


An understanding of the


patient in the context of comorbidities is of paramount importance to ensure treatment is tailored to meet their individual needs and to enhance their overall wellbeing. l


References 1. Parisi R, Griffiths CEM, Ashcroft DM. Systematic review of the incidence and prevalence of psoriasis. B J Dermatol 2011;165:5–9.


2. Elder JT et al. Molecular dissection of psoriasis: integrating genetics and biology. J Invest Dermatol 2010;130:1213–26.


3. Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med 2009;361:496–509.


4. Albanesi C et al. Chemerin expression marks early psoriatic skin lesions and correlates with plasmacytoid dendritic cell recruitment. J Exp Med 2009;206:249–58.


5. Ash ZR et al. Psoriasis patients with nail disease have a greater magnitude of underlying systemic subclinical enthesopathy than those with normal nails. Ann Rheum Dis 2012;71:553–6.


6. Gisondi P, Girolomoni G. Impact of TNF-α antagonists on the quality of life in selected skin diseases. G Ital Dermatol Venereol 2013;148:243–8.


7. Kurd SK, Troxel AB, Crits-Christoph P, Gelfand JM. The risk of depression, anxiety, and suicidality in patients with psoriasis: a population-based cohort study. Arch Dermatol 2010;146:891–5.


8. Davidovici BB et al. Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions. J Invest Dermatol 2010;130:1785–96.


9. Buerger C et al. Interleukin-1β interferes with epidermal homeostasis through induction of insulin resistance: implications for psoriasis pathogenesis. J Invest Dermatol 2012;132:2206–14.


10. Gisondi P et al. Serum chemerin is increased in patients with chronic plaque psoriasis and normalizes following treatment with infliximab. Br J Dermatol 2013;168:749–55.


11. Gladman DD et al. Psoriatic arthritis: epidemiology, clinical features, course and outcome. Ann Rheum Dis 2005;64 (Supp. II):14–17.


12. Eder L, Thavaneswaran A, Chandran V, Gladman DD. Tumour necrosis factor α blockers are more effective than methotrexate in the inhibition of radiographic joint damage progression among patients with psoriatic arthritis. Ann Rheum Dis 2013. [Epub ahead of print].


13. Tinazzi I et al. The early psoriatic arthritis screening questionnaire: a simple and fast method for the identification of arthritis in patients with psoriasis. Rheumatology 2012;51:2058–63.


14. Tinazzi I et al. Preliminary evidence that subclinical enthesopathy may predict psoriatic arthritis in patients with psoriasis. J Rheumatol 2011;38:2691–2.


15. Paller AS et al. Association of pediatric psoriasis severity with excess and central adiposity: an international cross-sectional study. JAMA Dermatol 2013;149:166–76.


16. Gisondi P et al. Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case-control study. Br J Dermatol 2007;157:68–73.


17. Armstrong AW, Harskamp CT, Armstrong EJ. Psoriasis and metabolic syndrome: a systematic review and meta-analysis of observational studies. J Am Acad Dermatol 2013;68:654–62.


18. Gisondi P, Targher G, Zoppini G, Girolomoni G. Non-alcoholic fatty liver disease in patients with chronic plaque psoriasis. J Hepatol 2009;51:758–64.


19. Samarasekera EJ et al. Incidence of cardiovascular disease in individuals with psoriasis: A systematic review and meta-analysis. J Invest Dermatol 2013; [Epub ahead of print].


20. Sampogna F et al. Measuring quality of life of patients with different clinical types of psoriasis using the SF-36. Br J Dermatol 2006;154:844–9.


21. DeLong LK, Chen SC. Future directions in dermatology quality of life measures. Dermatol Clin 2012;30:343–7.


22. Rapp SR et al. Psoriasis causes as much disability as other major medical diseases. J Am Acad Dermatol 1999;41:401–7.


23. Rosenberg P et al. Psoriasis patients with diabetes type 2 are at high risk of developing liver fibrosis during methotrexate treatment. J Hepatol 2007;46:1111–8.


24. Gisondi P et al. Metabolic abnormalities associated with initiation of systemic treatment for psoriasis: evidence from the Italian Psocare Registry. J Eur Acad Dermatol Venereol 2013;27:e30–41.


25. Gisondi P, Cotena C, Tessari G, Girolomoni G. Anti-tumour necrosis factor-alpha therapy increases body weight in patients with chronic plaque psoriasis: a retrospective cohort study. J Eur Acad Dermatol Venereol 2008;22:341–4.


26. Ahlehoff O et al. Pharmacological undertreatment of coronary risk factors in patients with psoriasis: observational study of the Danish nationwide registries. PLoS One 2012;7:e36342.


27. Gisondi P et al. Weight loss improves the response of obese patients with moderate-to-severe chronic plaque psoriasis to low-dose cyclosporine therapy: a randomized, controlled, investigator-blinded clinical trial. Am J Clin Nutr 2008;88:1242–7.


PHEM/IMM/0613/0002a


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