Pustular Psoriasis Appearing Induced by Dupilumab Therapy in a Patient With Atopic Dermatitis

March 2022 | Volume 21 | Issue 3 | Case Reports | 311 | Copyright © March 2022


Published online February 25, 2022

Xinrui Jia BS,a Chanchan Li MS,b Jianbo Wu MD,a Qin Liu MDc

aZhongnan Hospital of Wuhan University, Wuhan, China

Abstract
Dupilumab inhibits T-helper 2 (Th2)-driven inflammation cascade by blocking interleukin-4 (IL-4) and IL-13 signaling, which has been recognized to play a crucial role in the pathogenesis of atopic dermatitis (AD) and shown encouraging efficacy on moderate to severe AD.1 We report an interesting Chinese AD case, which developed into pustular psoriasis after treatment with dupilumab.

INTRODUCTION

Dupilumab inhibits T-helper 2 (Th2)-driven inflammation cascade by blocking interleukin-4 (IL-4) and IL-13 signaling, which has been recognized to play a crucial role in the pathogenesis of atopic dermatitis (AD) and shown encouraging efficacy on moderate to severe AD.1 We report an interesting Chinese AD case, which developed into pustular psoriasis after treatment with dupilumab.

CASE

A 23-year-old Chinese male with a history of allergic rhinitis and AD presented to the clinic with multiple pustules on the lower legs. A clinical diagnosis of AD was made 13 years ago, which had been treated with intermittent courses of traditional Chinese medicine. 1 year ago, new pruritic red papules and small vesicles developed over his limbs, with intense itching that also involved his trunk to a lesser extent (Figure 1 A, B). Dupilumab was initiated 2 months ago. After the first injection (600 mg, subcutaneously, day 0), the skin lesions were remarkably improved, and the itching was much relieved. However, 10 days later, superficial tiny pustules appeared on the original lesions of both lower legs. On day 14, he received the second injection of 300 mg dupilumab, then his pruritus was aggravated again, the lesions became redder, scaly, and pustules on them also continued to increase. The patient was afebrile and not exposed to any other new drugs in the past month. Our clinical differential diagnosis included other types of drug-induced aseptic pustular eruptions, especially acute generalized exanthematous pustulosis. Meanwhile, infectious pustulosis also need to be differentiated, such as impetigo, bacterial folliculitis, and so on. Laboratory evaluation showed that eosinophils were slightly higher (1.64x109/L, 17.2%). Leukocytes (9.51x109/L), and procalcitonin (<0.05 ng/ml) were normal. The pustules were cultured with negative result.

Skin biopsy from the pustular skin of his right calf extremity found parakeratosis, hyperkeratosis, epidermal hyperplasia, dilated capillaries, and lymphocyte infiltrate in the upper dermis. Dense neutrophil infiltration was seen within the stratum corneum and subcorneal zone forming spongiform abscesses, which were characteristic for pustular psoriasis. (Figure 1 C, D).

Based on the above results, pustular psoriasis was finally diagnosed. Dupilumab was discontinued, cyclosporine and topical steroids were prescribed instead. 2 weeks later, most of his pustules subsided, and the scales became thinner than before. The patient’s condition continued to improve in the following month, and he is still under follow-up.

DISCUSSION

Psoriasis and AD are both chronic inflammatory skin diseases considered as two opposite poles of the T-helper cell mediated inflammation. Recent studies have established that psoriasis is primarily a Th17/Th1-driven disease with IL-17, IL-22, and IL-23 increasing. In contrast, AD is mainly mediated by Th2 with IL-4, IL-13, and IL-31 growing, but Th17 and Th22 pathways also