This symposium took place on 15th September 2017, as part of the 26th European Academy of Dermatology and Venereology (EADV) Congress, in Geneva, Switzerland
Chairperson: Giampiero Girolomoni1
Speakers: Giampiero Girolomoni,1 Naveed Sattar,2 Frank Behrens,3 Krisztina Gecse4
1. Universitá Degli Studi di Verona, Verona, Italy
2. University of Glasgow, Glasgow, UK
3. Goethe University Frankfurt, Frankfurt, Germany
4. Academic Medical Center, University of Amsterdam, Amsterdam-Zuidoost, Netherlands
Disclosure: Prof Girolomoni has received fees for participation on advisory boards from AbbVie, Abiogen, Almirall, Amgen, Avantgarde, Bayer, Biogen, Boehringer Ingelheim, Celgene, Eli-Lilly, Galderma, Genzyme, Janssen, Hospira, Leo Pharma, Menlo Therapeutics, Merck, MSD, Mundipharma, Novartis, Pfizer, Regeneron, Rottapharm, Samsung, Sanofi, Shiseido, and Sun Pharma; and has received fees for consultations from Bioderma, Ducray, Insiderma, Pierre Fabre, Roche, and Sandoz. Prof Sattar is involved in the European League Against Rheumatism (EULAR) guidelines on cardiovascular disease, the European Society of Cardiology (ESC) cardiovascular disease prevention guidelines, and has consulted for Amgen, Sanofi, Roche, and UCB. Dr Behrens has received research support from Abbvie, Pfizer, Roche, Chugai, Prophylix, Bioline, Novartis, Janssen; consultant/speaker fees from Abbvie, Pfizer, Roche, Hugai, UCB, BMS, Celgene, MSD, Novartis, Biotest, Janssen, Genzyme, Lilly, Sandoz, and Hexal; and is an advisory board member for Abbvie, Pfizer, Roche, Chugai, UCB, Celgene, Novartis, Biotest, Janssen, Genzyme, Hexal, Lilly, and Boehringer-Ingelheim. Dr Gecse reports having received consultancy fees and/or speaker’s honoraria from Amgen, AbbVie, Boehringer Ingelheim, Ferring, Hospira, MSD, Pfizer, Sandoz, Takeda, and Tigenix.
Acknowledgements: Writing assistance was provided by Janet Fricker.
Support: The meeting and publication of this article was funded by Sandoz. The views and opinions expressed are those of the authors and not necessarily of Sandoz.
Citation: EMJ. 2017;2:27-35.
Prof Girolomoni provided an overview of psoriasis, considering how patients are frequently affected by other comorbidities. Cost, he explained, can be a constraint for optimal anti-tumour necrosis factor (TNF) treatment, with biosimilars representing an important opportunity for providing more patients with effective therapy. Data from X-ray crystallography studies, neutralisation studies, and clinical trials were presented, demonstrating that biosimilars have comparable efficacy to reference treatments.
Prof Sattar explained how to define the overall cardiovascular disease (CVD) risk score in psoriasis; the standard risk score should be multiplied by 1.5 for patients with young onset or more severe disease. Throughout the presentation he stressed that all CVD risk factors need to be taken into consideration. Just because someone has severe psoriasis does not mean they are necessarily at high risk of CVD, and just because someone has mild psoriasis does not mean they are at low risk. In the second part of his talk, Prof Sattar reviewed evidence suggesting that psoriasis and obesity are interlinked, and discussed benefits of weight loss.
Dr Behrens considered the hypotheses for psoriatic arthritis (PsA) genetic predisposition in patients with psoriasis. He reviewed data suggesting that psoriasis and PsA are different diseases, with psoriasis acting as a trigger for PsA. Dr Behrens went on to discuss predictors of PsA in patients with psoriasis and the importance of individualising treatment to phenotype.
Dr Gecse reviewed the aetiology, disease course, prognostic factors, and characteristics of inflammatory bowel diseases (IBD), such as Crohn’s disease (CD) and ulcerative colitis (UC). She explained how the prevalence of CD and UC is four-times higher in patients with psoriasis versus the general population, with the highest rates occurring in patients with both psoriasis and PsA. She went on to present studies showing how interleukin (IL)-17 inhibitors, which show promising effects in psoriasis, worsened in IBD.
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