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| LETTER TO EDITOR |
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| Year : 2020 | Volume
: 6
| Issue : 1 | Page : 43-45 |
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Secukinumab in erythrodermic psoriasis – A promising drug
Anwita Sinha1, Shekhar Neema2, Radhakrishnan Subramanian2, Anchit Raj Singh3
1 Department of Dermatology, Military Hospital Kirkee, Pune, Maharashtra, India
2 Department of Dermatology, Armed Forces Medical College, Pune, Maharashtra, India
3 Department of Medicine, Armed Forces Medical College, Pune, Maharashtra, India
| Date of Submission | 15-Apr-2020 |
| Date of Acceptance | 18-May-2020 |
| Date of Web Publication | 23-Jun-2020 |
Correspondence Address:
Dr. Anwita Sinha
Department of Dermatology, Military Hospital Kirkee, Pune, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijdd.ijdd_23_20
How to cite this article:
Sinha A, Neema S, Subramanian R, Singh AR. Secukinumab in erythrodermic psoriasis – A promising drug. Indian J Drugs Dermatol 2020;6:43-5 |
How to cite this URL:
Sinha A, Neema S, Subramanian R, Singh AR. Secukinumab in erythrodermic psoriasis – A promising drug. Indian J Drugs Dermatol [serial online] 2020 [cited 2023 Dec 9];6:43-5. Available from: https://www.ijdd.in/text.asp?2020/6/1/43/287428 |
Sir,
Erythrodermic psoriasis (EP) is a rare and severe variant of psoriasis, with an estimated prevalence among psoriatic patients ranging from 1%–2.25% and is the most common cause of erythroderma, responsible for ~25% of all cases.[1] It is characterized by diffuse involvement of the body in the form of generalized erythema and scaling involving >80% body surface area (BSA) and is associated with significant morbidity and mortality due to electrolyte abnormalities, impaired thermoregulation, and sepsis. Evidence-based treatment of EP is limited due to its rarity and the lack of controlled studies. Secukinumab is an anti-interleukin (IL)-17A monoclonal antibody, Food and Drug Administration approved for the treatment of moderate-to-severe plaque psoriasis. Recent studies have suggested IL 17A could be the main inflammatory pathway for EP.[2] However, the data for its use in EP is limited.[3],[4] We report one such case of EP, who showed a rapid and sustained response to Secukinumab.
45-year-old male, a known case of psoriasis vulgaris for 4 years, presented with complaints of generalized redness and flaking of the body of 2 weeks duration associated with cold intolerance, burning sensation over body and swelling of both legs. The patient was treated in the past on multiple occasions with methotrexate and alternative medication with little relief. General examination revealed body mass index of 34, blood pressure of 170/110 mm Hg, and bilateral pitting pedal edema. Dermatological examination revealed the involvement of 90% BSA, including scalp in the form of generalized erythema and scaling [Figure 1]a and [Figure 1]b. Psoriasis area and severity index (PASI) was 48, and dermatology quality of life index (DLQI) was 20. The patient was diagnosed as psoriatic erythroderma and was planned for cyclosporine. However, due to uncontrolled hypertension, the patient was worked up for secukinumab. Routine hematological and biochemical parameters were normal, interferon-gamma release assay, hepatitis B, C, and HIV were negative. Secukinumab was administered as weekly induction doses of 300 mg subcutaneous for 5 weeks followed by monthly injections. The patient responded well to secukinumab with the achievement of PASI 50 (PASI 23.4) at 2 weeks and PASI 90 (PASI 3.4) at 4 weeks of treatment [Figure 2]a and [Figure 2]b. DLQI dropped to seven within 3 weeks. At present, the patient is on monthly secukinumab injections 300 mg subcutaneous for the last 6 months and is maintaining remission. | Figure 1:(a and b) Diffuse erythema and scaling over body involving ~ 90% body surface area
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 | Figure 2: (a and b) Psoriasis area and severity index 90 achieved at 4 weeks of treatment with almost complete resolution of erythroderma
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Although EP may be the first manifestation of psoriasis in some patients, it generally occurs in patients who already have long-standing chronic plaque-type psoriasis, triggered by infections, drugs, stress, or treatment interruption.[1] A possible trigger identified in our patient was intake and interruption of alternative medication with the flare of psoriatic plaques progressing to erythroderma. EP presents as dermatological emergency and poses a distinct challenge in management. EP burdens normal physiology, especially in elderly individuals and can rapidly result in complications such as congestive cardiac failure, sepsis, and acute kidney injury. These patients need the early institution of effective therapy and good supportive treatment for the prevention of complications.
In 2010, the US National Psoriasis Foundation published consensus guidelines advocating the use of cyclosporine or infliximab as first-line therapy in unstable cases, with acitretin and methotrexate reserved for stable cases.[5] At the time of making these guidelines, secukinumab was not available. The importance of Th17 cells in the pathogenesis of EP has recently been investigated. Th17 cells secrete IL-17, IL-22, and interferon, inducing the production of inflammatory chemokines by T-cells, dendritic cells, and neutrophils. Using immunohistochemical analysis, Moy et al. found Th17 to be the most predominant T-cell subset after Th2 in EP lesions.[6] These findings suggest that secukinumab may be considered a therapeutic option for EP.
Carrasquillo et al. conducted a systematic review on the use of biologics in EP. This review had 19 patients treated with secukinumab. Eighty-four percent of treated patients responded to treatment without any significant adverse event, whereas 31% of patients had a relapse. They concluded that secukinumab has a rapid onset of action and provides sustained clearance and should be considered biologic of choice for the management of EP. We used secukinumab because of ease of administration and our familiarity with the drug.[7],[8]
Efficacy assessment in our patient was performed by measuring PASI and DLQI at baseline. In most of the published reports, PASI 90 was achieved at 12–16 weeks.[1],[3],[4] However, our patient achieved PASI 90 at 4 weeks of treatment. Weng et al., in their reported case series, have suggested previous treatment with biologic as a reason for suboptimal treatment response with secukinumab in EP.[4] Our patient being biologic naïve, may account for rapid and sustained response to secukinumab.
We report this case in view of a striking and rapid response to Secukinumab in EP with an excellent safety profile. To validate the same, further investigations are needed to better understand the role of the IL-23/Th17 pathway in EP, and future studies are warranted toward the identification of the optimal dosage and treatment interval of Secukinumab in EP. Nevertheless, Secukinumab, with its ease of administration and safety has the potential to address the unmet needs of patients with EP and comes forth as a promising intervention in the armamentarium of drugs for EP.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Damiani G, Pacifico A, Russo F, Pigatto PDM, Bragazzi NL, Bonifati C, et al. Use of secukinumab in a cohort of erythrodermic psoriatic patients: A pilot study. J Clin Med 2019;8:770.  |
| 2. | Xing X, Liang Y, Sarkar MK, Wolterink L, Swindell WR, Voorhees JJ, et al. IL-17 Responses are the dominant inflammatory signal linking inverse, erythrodermic, and chronic plaque psoriasis. J Invest Dermatol 2016;136:2498-501. |
| 3. | Mateu-Puchades A, Santos-Alarcón S, Martorell-Calatayud A, Pujol-Marco C, Sánchez-Carazo JL. Erythrodermic psoriasis and secukinumab: Our clinical experience. Dermatol Ther 2018;31:e12607. |
| 4. | Weng HJ, Wang TS, Tsai TF. Clinical experience of secukinumab in the treatment of erythrodermic psoriasis: a case series. Br J Dermatol 2018;178:1439-40. |
| 5. | Singh RK, Lee KM, Ucmak D, Brodsky M, Atanelov Z, Farahnik B, et al. Erythrodermic psoriasis: Pathophysiology and current treatment perspectives. Psoriasis (Auckl) 2016;6:93-104. |
| 6. | Moy AP, Murali M, Kroshinsky D, Duncan LM, Nazarian RM. Immunologic overlap of helper T-cell subtypes 17 and 22 in erythrodermic psoriasis and atopic dermatitis. JAMA Dermatol 2015;151:753-60. |
| 7. | Mugheddu C, Atzori L, Lappi A, Pau M, Murgia S, Rongioletti F. Successful Secukinumab treatment of generalized pustular psoriasis and erythrodermic psoriasis. J Eur Acad Dermatol Venereol 2017;31:e420-1. |
| 8. | Carrasquillo OY, Pabón-Cartagena G, Falto-Aizpurua LA, Santiago-Vázquez M, Cancel-Artau KJ, Arias-Berrios G, et al. Treatment of erythrodermic psoriasis with biologics: A systematic review. [Published online ahead of print, 2020 Apr 02]. J Am Acad Dermatol 2020;S0190-9622(20)30496-5. |
[Figure 1], [Figure 2]
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