Case report: successful treatment of pustular plantar psoriasis with an interleukin-17A inhibitor, netakimab

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Abstract

Pustular psoriasis (PP) is a chronic immune-mediated skin disease that is difficult to treat. Affecting areas of the skin in the area of the palms and feet (socially significant and subject to constant external influences in everyday life), the disease has a negative impact on the psycho-emotional background of patients, and the difficulties in selecting therapy and its low effectiveness aggravate the patient’s condition. This article discusses the classification, etiology and pathogenesis of pustular psoriasis, aspects of the differential diagnosis of localized forms of pustular psoriasis, and a modern approach to the treatment of this disease. The issue of classification of PP, especially its localized forms, remained controversial for a long time. Currently, it is recommended to follow the classification proposed by ERASPEN, according to which PP is divided into three subtypes: generalized PP, palmoplantar pustulosis (PPP) and persistent Allopo acrodermatitis. The study of the immune-mediated reaction and key links in the pathogenesis of psoriasis opens up new possibilities in the treatment of severe psoriasis, which is difficult to treat with basic anti-inflammatory drugs. Interleukin (IL)-17 is a pro-inflammatory cytokine and is involved in many stages of the immune response, affecting various cell types, including endothelial cells, fibroblasts, chondrocytes, synovial cells, monocytes, and epithelial cells, including keratinocytes. It is known that IL-17 plays a leading role in the cascade of immune-mediated inflammation in the pathogenesis of psoriasis vulgaris. Papers have been published indicating active expression of IL-17A in the skin of the palms and soles of patients with palmoplantar PP, in contrast to IL-12 and IL-23. Standard external therapy, local PUVA therapy, photodynamic therapy with PP are often ineffective, do not lead to stable remission, so systemic therapy is required. Currently, genetically engineered biological therapy is a successful and promising therapy option. Randomized placebo-controlled trials failed to demonstrate a statistically significant efficacy of inhibitors of TNF-α, IL-12, IL-23 in patients with palmoplantar psoriasis, while the IL-17A inhibitor secukinumab showed a positive result of therapy – by the 52nd week of treatment 41 % of patients achieved PPPASI-75. In the article, we will consider the clinical case of a patient with severe PP who received systemic therapy (methotrexate, guselcumablm and netakimab), and were able to evaluate the effectiveness of various drugs in relation to this disease.

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About the authors

Elena V. Svechnikova

Polyclinic № 1 of the Administrative Department of the President of the Russian Federation; Russian Biotechnological University

Author for correspondence.
Email: elene-elene@bk.ru
ORCID iD: 0000-0002-5885-4872

Dr. Sci. (Med.), Professor, Department of Skin and Venereal Diseases; Head of the Department of Dermatovenereology and Cosmetology

Russian Federation, Moscow; Moscow

Svetlana E. Zhufina

Polyclinic № 1 of the Administrative Department of the President of the Russian Federation

Email: elene-elene@bk.ru
ORCID iD: 0000-0001-5694-2847
Russian Federation, Moscow

Alexandra V. Parfenova

Polyclinic № 1 of the Administrative Department of the President of the Russian Federation

Email: elene-elene@bk.ru
ORCID iD: 0009-0008-2287-9438
Russian Federation, Moscow

K. A. Fomin

Polyclinic № 1 of the Administrative Department of the President of the Russian Federation

Email: elene-elene@bk.ru
Russian Federation, Moscow

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Supplementary files

Supplementary Files
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1. JATS XML
2. Fig.1-2. Patient K., 70 years old, clinical picture before treatment

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3. Fig.3-4. Patient K., 70 years old, clinical picture on the background of HIBT with the IL-23 blocker guselkumab

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4. Fig.5. Patient K., 70 years old, clinical picture before the start of treatment with netakimab

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5. Fig.6-7. Patient K., 70 years old, results of the initiation period with netakimab

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6. Fig.8-9. Results of netakimab therapy at week 24 of treatment

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