Research letter
Onset of psoriatic arthritis during ustekinumab treatment for psoriasis: a case series of seven patients DOI: 10.1111/bjd.13645 DEAR EDITOR, Psoriasis is an inflammatory skin disease that affects approximately 2–3% of the population.1 Patients with psoriasis are at risk of developing psoriatic arthritis (PsA), an inflammatory arthritis with a recently estimated prevalence of 30% in patients with psoriasis.2 In recent years tumour necrosis factor (TNF)-a inhibitors (TNFIs) have been used to treat both psoriasis and PsA. More recently, ustekinumab, a monoclonal antibody that binds to p40, the shared subunit of interleukin (IL)-12 and IL-23, was approved for psoriasis and PsA. Clinical trials have demonstrated that ustekinumab is a safe and efficacious therapy for both psoriasis3 and PsA.4,5 Clinical trials for PsA of both TNFIs and ustekinumab have demonstrated that in evaluable study populations both PsA and psoriasis improve. Although not described in the literature, it is our observation in clinical practice that patients sometimes have discordant responses of their skin and joint disease, but new onset of PsA appears uncommon during treatment with TNFIs. This is a report of seven patients with well-controlled psoriasis on ustekinumab, but who experienced new-onset PsA or worsening PsA diagnosed by a rheumatologist. The following case is representative of the seven cases included in this series. Information on all of the cases can be found in Table 1. Patient 1 is a 65-year old obese white woman who was first diagnosed with psoriasis in 1982. She had no prior diagnosis of PsA. She had tried and failed multiple therapies for psoriasis, including alefacept, efalizumab and adalimumab. Following an infusion reaction to infliximab in November 2009 she was started on ustekinumab, initially at 45 mg then 90 mg every 12 weeks. Her psoriasis body surface area involvement improved from 40% to clear within 6 months of initiating ustekinumab therapy. In February 2012 she complained of joint pain and swelling in her hands. Examination was remarkable for dactylitis of the second left toe. Radiographs of her hands and feet revealed multiple erosions and pencil-in-cup deformities. Her C-reactive protein level was 28 mg dL 1. The evaluating rheumatologist diagnosed her with erosive PsA and added sulfasalazine. In July 2012 she discontinued ustekinumab and started golimumab due to persistent PsA symptoms. Over the following 272
British Journal of Dermatology (2015) 173, pp272–274
year the patient’s PsA symptoms improved but did not resolve, and her psoriasis worsened to body surface area involvement of 10%, which was controlled with the addition of narrowband ultraviolet B (NB-UVB). The seven patients in our series were evaluated by a rheumatologist for new-onset PsA or exacerbation of previously controlled PsA after starting ustekinumab for psoriasis. Our report demonstrates that in certain patients receiving ustekinumab, the activity of psoriasis and PsA may be discordant. There were several phenotypic similarities between the cases we evaluated. The majority of our patients were women aged over 49 years with long-standing psoriasis. All but one patient had total or near-total clearance of their cutaneous symptoms while on ustekinumab, but all seven patients experienced onset or worsening of joint symptoms during this period. Notably, five of the seven patients developed new-onset PsA, all of whom were female. Five of the seven had exposure to TNFIs prior to initiating ustekinumab, all of whom switched from a TNFI to ustekinumab. Of the seven patients, four developed peripheral-joint synovitis, five developed enthesitis, four developed dactylitis, three had radiographical changes consistent with PsA, and three had elevated inflammatory markers (Table 1). Three other case series have reported similar findings, including marked improvement of cutaneous symptoms while joint symptoms worsened.6–8 While our patients reported a later time to onset of joint symptoms (≥ 8 months), other cases reported a shorter interval (≤ 5 months). The pathogenesis by which ustekinumab could lead to new onset or worsening of PsA in certain patients remains unknown, but may be due to lack of efficacy at the doses given.6 Supporting this is the observation that, in one phase 3 trial, more patients in groups receiving the higher dose (90 mg) of ustekinumab achieved ACR20 responses (20% improvement in American College of Rheumatology criteria) than those in groups receiving 45-mg injections.5 Alternatively, articular disease may require more frequent ustekinumab dosing than cutaneous disease to achieve meaningful responses in some people. Our observations may support arguments that PsA and psoriasis involve distinct inflammatory pathways. In some patients, TNF-a inhibition may be superior for joint inflammation, and IL-12/23 inhibition may be more effective for skin inflammation.6 Although head-to-head trials of ustekinumab and TNFIs are lacking in PsA, improvements in joint symptoms, as measured with ACR20 responses, suggest © 2014 British Association of Dermatologists
Research letter
273
Table 1 Summary of the cases reported and results
Patient no. /sex/age (years)
Ps duration (years)
PsA diagnosis prior to starting Ust
Prior TNFI
Ps response to TNFI
Ust dose (mg)
Ps response to Ust
Months of Ust before onset or worsening of PsA
Rheumatologist findings for PsA
1/F/65
31
No
Ada, Eta, Inf
Limited
90
Total clearance
28
Dactylitis, radiographs, elevated CRP
2/F/49
42
No
None
NA
45
Total clearance
22
> 40
Yes
Ada, Eta
90
Near-total clearance
4
4/F/69
18
No
Ada, Eta
90
50% clearance
15
5/F/57
7
No
Ada, Eta
45
Total clearance
8
6/M/65
60
Yes
None
Eta effective for PsA but not Ps Ps initially improved on Eta but patient eventually lost efficacy to both Eta and Ada Stopped Eta due to side-effects. Initial clearance on Ada, then Ps worsened NA
Enthesitis, dactylitis, fasciitis Synovitis, enthesitis, dactylitis Enthesitis, dactylitis, radiographs, elevated CRP
90
Total clearance
7/F/55
14
No
Ada, Eta
Failed both Ada and Eta
90
Near-total clearance
3/M/50
Outcome PsA improved but Ps worsened on sulfasalazine and Gol PsA worsened on Eta. Ps and PsA improved on Ada PsA improved after restarting Eta Failed Gol, but Ps and PsA improved on Inf
Synovitis, enthesitis
Refractory PsA on Gol. Ps improved and PsA stable on Inf
12
Enthesitis, synovitis, radiographs, elevated CRP
19
Synovitis
Ps worsened and PsA did not improve on Eta. Ps improved and PsA worsened after restarting Ust Remained on Ust and methotrexate
Ada, adalimumab; CRP, C-reactive protein; Eta; etanercept; F, female; Gol, golimumab; Inf, infliximab; M, male; NA, not applicable; Ps, psoriasis; PsA; psoriatic arthritis; TNFI, tumour necrosis factor-a inhibitor; Ust; ustekinumab.
that TNFIs are superior to ustekinumab. In one trial, 73% of patients taking etanercept achieved ACR20 at week 12 vs. only 13% of the placebo group, yielding an absolute difference of 60% [confidence interval (CI) 40–80, P < 0001].9 This is compared with a trial evaluating ustekinumab, where only 42% of patients taking 90 mg every 4 weeks achieved an ACR20 response at week 24, compared with 14% of the placebo group, with an absolute difference of 28% (CI 14–416, P < 0001).4 Other trials evaluating infliximab10 and adalimumab11 reported similar results. Our own observations corroborate this, as PsA in five of our patients improved after discontinuing ustekinumab and starting a TNFI, but they required additional therapies such as NB-UVB in some cases to manage their psoriasis. It is also possible that ustekinumab may trigger or unmask inflammation in the joints of patients with PsA. TNFIs are reported paradoxically to trigger PsA, as well as psoriasis, particularly in patients given TNFIs for inflammatory bowel dis© 2014 British Association of Dermatologists
ease or rheumatoid arthritis.12 Further research is needed to determine what changes in the cytokine milieu associate with such paradoxical flares of skin and joint disease. There is an emerging body of evidence that well-controlled cutaneous psoriasis, particularly with TNFIs, may reduce systemic inflammation, as evidenced by improved cardiovascular markers.13 However, this case series illustrates that PsA may develop even when cutaneous symptoms are well controlled. Our observations would seem to indicate that reduction in cutaneous psoriasis may not reflect an empirical decrease in musculoskeletal inflammation. In summary, our report lends further support to observations that new onset or worsening of PsA may occur in patients on ustekinumab for psoriasis. This report is limited by its small sample size. Larger epidemiological studies comparing patients with discordant and concordant cutaneous and articular responses to ustekinumab may better define patients at risk for PsA worsening with ustekinumab. Our report also British Journal of Dermatology (2015) 173, pp272–274
274 Research letter
highlights the need for regularly querying patients about joint symptoms, with referral to a rheumatologist for formal evaluation if PsA is suspected. School of Medicine, 3Division of Rheumatology and 4Department of Dermatology, University of Utah, 30N 1900 East, Salt Lake City, UT 84132, U.S.A. 2 University of California, Davis, Department of Dermatology, Sacramento, CA, U.S.A. Correspondence: Kristina Callis Duffin. E-mail: [email protected] 1
B.B. JONES1 J.W. MILLSOP2 J.A. WALSH3 G.G. KRUEGER4 K. CALLIS DUFFIN4
References 1 Sch€ on MP, Boehncke WH. Psoriasis. N Engl J Med 2005; 352:1899– 912. 2 Mease PJ, Gladman DD, Papp KA et al. Prevalence of rheumatologist-diagnosed psoriatic arthritis in patients with psoriasis in European/North American dermatology clinics. J Am Acad Dermatol 2013; 69:729–35. 3 Kimball AB, Gordon KB, Fakharzadeh S et al. Long-term efficacy of ustekinumab in patients with moderate-to-severe psoriasis: results from the PHOENIX 1 trial through up to 3 years. Br J Dermatol 2012; 166:861–72. 4 Gottlieb A, Menter A, Mendelsohn A et al. Ustekinumab, a human interleukin 12/23 monoclonal antibody, for psoriatic arthritis: randomized, double-blind, placebo-controlled, crossover trial. Lancet 2009; 373:633–40. 5 McInnes IB, Kavanaugh A, Gottlieb AB et al. Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial. Lancet 2013; 382:780–9. 6 Stevenson ML, Markowitz O. Selection of therapies in patients with psoriasis and psoriatic arthritis. Psoriasis Forum 2011; 17:144–7.
British Journal of Dermatology (2015) 173, pp272–274
7 de Souza A, Ali-Shaw T, Reddy SM et al. Inflammatory arthritis following ustekinumab treatment for psoriasis: a report of two cases. Br J Dermatol 2013; 168:210–12. 8 Stamell EF, Kutner A, Viola K, Cohen SR. Ustekinumab associated with flares of psoriatic arthritis. JAMA Dermatol 2013; 149:1410– 13. 9 Mease PJ, Goffe BS, Metz J et al. Etanercept in the treatment of psoriatic arthritis and psoriasis: a randomized trial. Lancet 2000; 356:385–90. 10 Kavanaugh A, Krueger GG, Beutler A et al. Infliximab maintains a high degree of clinical response in patients with active psoriatic arthritis through 1 year of treatment: results from the IMPACT 2 trial. Ann Rheum Dis 2007; 66:498–505. 11 Mease PJ, Ory P, Sharp JT et al. Adalimumab for long-term treatment of psoriatic arthritis: 2-year data from the Adalimumab Effectiveness in Psoriatic Arthritis Trial (ADEPT). Ann Rheum Dis 2009; 68:702–9. 12 de Gannes GC, Ghoreishi M, Pope J et al. Psoriasis and pustular dermatitis triggered by TNF-a inhibitors in patients with rheumatologic conditions. Arch Dermatol 2007; 143:223–31. 13 J okai H, Szakonyi J, Kontar O et al. Impact of effective tumor necrosis factor-alfa inhibitor treatment on arterial intima-media thickness in psoriasis: results of a pilot study. J Am Acad Dermatol 2013; 69:523–9. Funding sources: None. Conflicts of interest: K.C.D. has served on the scientific and marketing advisory boards of Amgen; served as a consultant to Amgen, Janssen, Pfizer and Eli Lilly receiving honoraria; received payments for lectures from AbbVie, Amgen and Janssen; and served as an investigator for AbbVie, Amgen, Janssen, Pfizer, Eli Lilly and Vascular Biologics Limited. G.G.K. has received fees as a consultant or advisory board member for AbbVie, Amgen, ApoPharma, Astellas, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Idera, Isis, Janssen, L’Oreal, Novartis, Pfizer, UCB and Vascular Biologics Limited. G.G.K. has also received partial stipend support for a clinical research fellowship from AbbVie, Amgen and Centocor/Janssen, and in the last 12 months has received lecture fees from Abbott, Amgen and Janssen.
© 2014 British Association of Dermatologists
Onset of psoriatic arthritis during ustekinumab treatment for psoriasis: a case series of seven patients DOI: 10.1111/bjd.13645 DEAR EDITOR, Psoriasis is an inflammatory skin disease that affects approximately 2–3% of the population.1 Patients with psoriasis are at risk of developing psoriatic arthritis (PsA), an inflammatory arthritis with a recently estimated prevalence of 30% in patients with psoriasis.2 In recent years tumour necrosis factor (TNF)-a inhibitors (TNFIs) have been used to treat both psoriasis and PsA. More recently, ustekinumab, a monoclonal antibody that binds to p40, the shared subunit of interleukin (IL)-12 and IL-23, was approved for psoriasis and PsA. Clinical trials have demonstrated that ustekinumab is a safe and efficacious therapy for both psoriasis3 and PsA.4,5 Clinical trials for PsA of both TNFIs and ustekinumab have demonstrated that in evaluable study populations both PsA and psoriasis improve. Although not described in the literature, it is our observation in clinical practice that patients sometimes have discordant responses of their skin and joint disease, but new onset of PsA appears uncommon during treatment with TNFIs. This is a report of seven patients with well-controlled psoriasis on ustekinumab, but who experienced new-onset PsA or worsening PsA diagnosed by a rheumatologist. The following case is representative of the seven cases included in this series. Information on all of the cases can be found in Table 1. Patient 1 is a 65-year old obese white woman who was first diagnosed with psoriasis in 1982. She had no prior diagnosis of PsA. She had tried and failed multiple therapies for psoriasis, including alefacept, efalizumab and adalimumab. Following an infusion reaction to infliximab in November 2009 she was started on ustekinumab, initially at 45 mg then 90 mg every 12 weeks. Her psoriasis body surface area involvement improved from 40% to clear within 6 months of initiating ustekinumab therapy. In February 2012 she complained of joint pain and swelling in her hands. Examination was remarkable for dactylitis of the second left toe. Radiographs of her hands and feet revealed multiple erosions and pencil-in-cup deformities. Her C-reactive protein level was 28 mg dL 1. The evaluating rheumatologist diagnosed her with erosive PsA and added sulfasalazine. In July 2012 she discontinued ustekinumab and started golimumab due to persistent PsA symptoms. Over the following 272
British Journal of Dermatology (2015) 173, pp272–274
year the patient’s PsA symptoms improved but did not resolve, and her psoriasis worsened to body surface area involvement of 10%, which was controlled with the addition of narrowband ultraviolet B (NB-UVB). The seven patients in our series were evaluated by a rheumatologist for new-onset PsA or exacerbation of previously controlled PsA after starting ustekinumab for psoriasis. Our report demonstrates that in certain patients receiving ustekinumab, the activity of psoriasis and PsA may be discordant. There were several phenotypic similarities between the cases we evaluated. The majority of our patients were women aged over 49 years with long-standing psoriasis. All but one patient had total or near-total clearance of their cutaneous symptoms while on ustekinumab, but all seven patients experienced onset or worsening of joint symptoms during this period. Notably, five of the seven patients developed new-onset PsA, all of whom were female. Five of the seven had exposure to TNFIs prior to initiating ustekinumab, all of whom switched from a TNFI to ustekinumab. Of the seven patients, four developed peripheral-joint synovitis, five developed enthesitis, four developed dactylitis, three had radiographical changes consistent with PsA, and three had elevated inflammatory markers (Table 1). Three other case series have reported similar findings, including marked improvement of cutaneous symptoms while joint symptoms worsened.6–8 While our patients reported a later time to onset of joint symptoms (≥ 8 months), other cases reported a shorter interval (≤ 5 months). The pathogenesis by which ustekinumab could lead to new onset or worsening of PsA in certain patients remains unknown, but may be due to lack of efficacy at the doses given.6 Supporting this is the observation that, in one phase 3 trial, more patients in groups receiving the higher dose (90 mg) of ustekinumab achieved ACR20 responses (20% improvement in American College of Rheumatology criteria) than those in groups receiving 45-mg injections.5 Alternatively, articular disease may require more frequent ustekinumab dosing than cutaneous disease to achieve meaningful responses in some people. Our observations may support arguments that PsA and psoriasis involve distinct inflammatory pathways. In some patients, TNF-a inhibition may be superior for joint inflammation, and IL-12/23 inhibition may be more effective for skin inflammation.6 Although head-to-head trials of ustekinumab and TNFIs are lacking in PsA, improvements in joint symptoms, as measured with ACR20 responses, suggest © 2014 British Association of Dermatologists
Research letter
273
Table 1 Summary of the cases reported and results
Patient no. /sex/age (years)
Ps duration (years)
PsA diagnosis prior to starting Ust
Prior TNFI
Ps response to TNFI
Ust dose (mg)
Ps response to Ust
Months of Ust before onset or worsening of PsA
Rheumatologist findings for PsA
1/F/65
31
No
Ada, Eta, Inf
Limited
90
Total clearance
28
Dactylitis, radiographs, elevated CRP
2/F/49
42
No
None
NA
45
Total clearance
22
> 40
Yes
Ada, Eta
90
Near-total clearance
4
4/F/69
18
No
Ada, Eta
90
50% clearance
15
5/F/57
7
No
Ada, Eta
45
Total clearance
8
6/M/65
60
Yes
None
Eta effective for PsA but not Ps Ps initially improved on Eta but patient eventually lost efficacy to both Eta and Ada Stopped Eta due to side-effects. Initial clearance on Ada, then Ps worsened NA
Enthesitis, dactylitis, fasciitis Synovitis, enthesitis, dactylitis Enthesitis, dactylitis, radiographs, elevated CRP
90
Total clearance
7/F/55
14
No
Ada, Eta
Failed both Ada and Eta
90
Near-total clearance
3/M/50
Outcome PsA improved but Ps worsened on sulfasalazine and Gol PsA worsened on Eta. Ps and PsA improved on Ada PsA improved after restarting Eta Failed Gol, but Ps and PsA improved on Inf
Synovitis, enthesitis
Refractory PsA on Gol. Ps improved and PsA stable on Inf
12
Enthesitis, synovitis, radiographs, elevated CRP
19
Synovitis
Ps worsened and PsA did not improve on Eta. Ps improved and PsA worsened after restarting Ust Remained on Ust and methotrexate
Ada, adalimumab; CRP, C-reactive protein; Eta; etanercept; F, female; Gol, golimumab; Inf, infliximab; M, male; NA, not applicable; Ps, psoriasis; PsA; psoriatic arthritis; TNFI, tumour necrosis factor-a inhibitor; Ust; ustekinumab.
that TNFIs are superior to ustekinumab. In one trial, 73% of patients taking etanercept achieved ACR20 at week 12 vs. only 13% of the placebo group, yielding an absolute difference of 60% [confidence interval (CI) 40–80, P < 0001].9 This is compared with a trial evaluating ustekinumab, where only 42% of patients taking 90 mg every 4 weeks achieved an ACR20 response at week 24, compared with 14% of the placebo group, with an absolute difference of 28% (CI 14–416, P < 0001).4 Other trials evaluating infliximab10 and adalimumab11 reported similar results. Our own observations corroborate this, as PsA in five of our patients improved after discontinuing ustekinumab and starting a TNFI, but they required additional therapies such as NB-UVB in some cases to manage their psoriasis. It is also possible that ustekinumab may trigger or unmask inflammation in the joints of patients with PsA. TNFIs are reported paradoxically to trigger PsA, as well as psoriasis, particularly in patients given TNFIs for inflammatory bowel dis© 2014 British Association of Dermatologists
ease or rheumatoid arthritis.12 Further research is needed to determine what changes in the cytokine milieu associate with such paradoxical flares of skin and joint disease. There is an emerging body of evidence that well-controlled cutaneous psoriasis, particularly with TNFIs, may reduce systemic inflammation, as evidenced by improved cardiovascular markers.13 However, this case series illustrates that PsA may develop even when cutaneous symptoms are well controlled. Our observations would seem to indicate that reduction in cutaneous psoriasis may not reflect an empirical decrease in musculoskeletal inflammation. In summary, our report lends further support to observations that new onset or worsening of PsA may occur in patients on ustekinumab for psoriasis. This report is limited by its small sample size. Larger epidemiological studies comparing patients with discordant and concordant cutaneous and articular responses to ustekinumab may better define patients at risk for PsA worsening with ustekinumab. Our report also British Journal of Dermatology (2015) 173, pp272–274
274 Research letter
highlights the need for regularly querying patients about joint symptoms, with referral to a rheumatologist for formal evaluation if PsA is suspected. School of Medicine, 3Division of Rheumatology and 4Department of Dermatology, University of Utah, 30N 1900 East, Salt Lake City, UT 84132, U.S.A. 2 University of California, Davis, Department of Dermatology, Sacramento, CA, U.S.A. Correspondence: Kristina Callis Duffin. E-mail: [email protected] 1
B.B. JONES1 J.W. MILLSOP2 J.A. WALSH3 G.G. KRUEGER4 K. CALLIS DUFFIN4
References 1 Sch€ on MP, Boehncke WH. Psoriasis. N Engl J Med 2005; 352:1899– 912. 2 Mease PJ, Gladman DD, Papp KA et al. Prevalence of rheumatologist-diagnosed psoriatic arthritis in patients with psoriasis in European/North American dermatology clinics. J Am Acad Dermatol 2013; 69:729–35. 3 Kimball AB, Gordon KB, Fakharzadeh S et al. Long-term efficacy of ustekinumab in patients with moderate-to-severe psoriasis: results from the PHOENIX 1 trial through up to 3 years. Br J Dermatol 2012; 166:861–72. 4 Gottlieb A, Menter A, Mendelsohn A et al. Ustekinumab, a human interleukin 12/23 monoclonal antibody, for psoriatic arthritis: randomized, double-blind, placebo-controlled, crossover trial. Lancet 2009; 373:633–40. 5 McInnes IB, Kavanaugh A, Gottlieb AB et al. Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial. Lancet 2013; 382:780–9. 6 Stevenson ML, Markowitz O. Selection of therapies in patients with psoriasis and psoriatic arthritis. Psoriasis Forum 2011; 17:144–7.
British Journal of Dermatology (2015) 173, pp272–274
7 de Souza A, Ali-Shaw T, Reddy SM et al. Inflammatory arthritis following ustekinumab treatment for psoriasis: a report of two cases. Br J Dermatol 2013; 168:210–12. 8 Stamell EF, Kutner A, Viola K, Cohen SR. Ustekinumab associated with flares of psoriatic arthritis. JAMA Dermatol 2013; 149:1410– 13. 9 Mease PJ, Goffe BS, Metz J et al. Etanercept in the treatment of psoriatic arthritis and psoriasis: a randomized trial. Lancet 2000; 356:385–90. 10 Kavanaugh A, Krueger GG, Beutler A et al. Infliximab maintains a high degree of clinical response in patients with active psoriatic arthritis through 1 year of treatment: results from the IMPACT 2 trial. Ann Rheum Dis 2007; 66:498–505. 11 Mease PJ, Ory P, Sharp JT et al. Adalimumab for long-term treatment of psoriatic arthritis: 2-year data from the Adalimumab Effectiveness in Psoriatic Arthritis Trial (ADEPT). Ann Rheum Dis 2009; 68:702–9. 12 de Gannes GC, Ghoreishi M, Pope J et al. Psoriasis and pustular dermatitis triggered by TNF-a inhibitors in patients with rheumatologic conditions. Arch Dermatol 2007; 143:223–31. 13 J okai H, Szakonyi J, Kontar O et al. Impact of effective tumor necrosis factor-alfa inhibitor treatment on arterial intima-media thickness in psoriasis: results of a pilot study. J Am Acad Dermatol 2013; 69:523–9. Funding sources: None. Conflicts of interest: K.C.D. has served on the scientific and marketing advisory boards of Amgen; served as a consultant to Amgen, Janssen, Pfizer and Eli Lilly receiving honoraria; received payments for lectures from AbbVie, Amgen and Janssen; and served as an investigator for AbbVie, Amgen, Janssen, Pfizer, Eli Lilly and Vascular Biologics Limited. G.G.K. has received fees as a consultant or advisory board member for AbbVie, Amgen, ApoPharma, Astellas, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Idera, Isis, Janssen, L’Oreal, Novartis, Pfizer, UCB and Vascular Biologics Limited. G.G.K. has also received partial stipend support for a clinical research fellowship from AbbVie, Amgen and Centocor/Janssen, and in the last 12 months has received lecture fees from Abbott, Amgen and Janssen.
© 2014 British Association of Dermatologists
