Dear Editor, Erythrodermic psoriasis (EP) is a rare but severe variant of psoriasis. Evidence‐based treatment of EP is limited due to its rarity and the lack of controlled studies. Secukinumab is an anti‐interleukin‐17A monoclonal antibody approved for the treatment of moderate‐to‐severe plaque psoriasis with superior efficacy over etanercept and ustekinumab.1,2 Since 2015 it has been approved by the Food and Drug Administration in the U.S.A. and it has gained increasing popularity for the treatment of plaque psoriasis. However, there are very few reports showing secukinumab as an option for treating EP.3 Here we present a series of 10 cases in which secukinumab was prescribed for EP (Table 1). The erythrodermic state was defined as psoriasis involvement of > 75% body surface area. Before the initiation of secukinumab, all patients were treated with different combinations of systemic regimens, including ciclosporin, methotrexate, acitretin, phototherapy and various biologics. Discontinuation of systemic treatment was identified as the possible cause of erythrodermic status in some of the patients. All patients were prescribed secukinumab 300 mg (except one with 150 mg, bodyweight 56 kg) once per week for the first 5 weeks and then every 4 weeks, per label. Summary of the 10 cases of erythrodermic psoriasis BSA, body surface area; PASI, Psoriasis Area and Severity Index. aValues are n (%) or mean ± SD; median. bThis value may be overestimated as one of the cases was prescribed topical clobetasol propionate at week 20, resulting in 76·7% reduction in PASI. Summary of the 10 cases of erythrodermic psoriasis BSA, body surface area; PASI, Psoriasis Area and Severity Index. aValues are n (%) or mean ± SD; median. bThis value may be overestimated as one of the cases was prescribed topical clobetasol propionate at week 20, resulting in 76·7% reduction in PASI. Our data indicate that secukinumab showed suboptimal effects for the treatment of EP, compared with plaque psoriasis.1 At week 16, four (40%) and seven patients (70%) were able to achieve ≥ 90% improvement in Psoriasis Area and Severity Index (PASI 90) and PASI 75, respectively. At week 24, the percentages of patients achieving PASI 90 and PASI 75 decreased to 30% and 60% (Table 1). Only two cases showed sustained clearance of psoriasis lesions up to 24 weeks (full data on all patients available on request). Of the three cases who failed to achieve PASI 75, two had a history of biological treatment failure and one had never received any biological agent before. Moreover, in our case series body mass index did not correlate with treatment response at week 16 (R2 = 0·0002, data not shown). Although the PASI 75 and PASI 90 response rates were lower in our series than in the original phase III study,1 they are still superior to the results with ustekinumab from our previous EP case series.4 The results are consistent with the pivotal study showing the superiority of secukinumab over ustekinumab.5 Moreover, issues of disease relapse and compromised treatment efficacy were also documented. It has been reported that the effects of secukinumab treatment on psoriasis peaked at week 16, and a significant proportion of secukinumab‐treated patients started to lose efficacy around week 24–32.1 In our series we also observed flaring of psoriasis after week 16. Two of 10 patients had relapses, defined as having compromised treatment effects below 50% of the maximal improvements in PASI at week 24. Five of the 10 patients (50%) were prescribed a rescue regimen for relapse as early as week 16. These agents include additional secukinumab, methotrexate and topical clobetasol propionate. The early relapse may be responsible for the treatment failure in our series. The lowered treatment responses may be partly explained by the history of prior biological failure in our patients.6 Six of these 10 patients (60%) were resistant to at least one previous biological agent and three of them (30%) were resistant to more than one biological agent. However, in real‐world practice, most patients on secukinumab have previously received biologics.7 Our series might more accurately represent the population receiving secukinumab in the clinic. It suggests that the real treatment effects of biologics may be compromised in comparison with the original studies.1 Furthermore, several factors might also contribute to the poorer responses in EP than in plaque psoriasis. Firstly, the inflammatory burden in EP may be higher, and thus a higher dosage or shorter treatment interval may be required. Secondly, other inflammatory mediators in addition to interleukin‐17 may be also important in EP (e.g. T helper 2 cytokines). Thirdly, hypoalbuminaemia, which is frequently associated with erythrodermic status, may compromise the pharmacodynamics of secukinumab.8 In summary, our study is the largest series reporting the treatment effects of secukinumab in EP. The results indicate that secukinumab may be an option for the treatment of EP. However, its effectiveness is suboptimal in real‐world practice, in which most patients have failed multiple prior therapies, including biologics. Future investigation is warranted towards identification of the optimal dosage and treatment interval, as well as the predictive factors for treatment success. Funding sources: none. Conflicts of interest: none to declare.
No takes yet. Share an insight, caveat, or question.
Weng et al. (2017) studied this question.