Treatment of Secukinumab-induced Atopic Dermatitis-like Lesions Using Upadacitinib: A Case Report

Dear Editor,

We present a 52-year-old man with a history of psoriasis spanning over a decade presented with typical signs of the condition, as shown in a skin biopsy [Figure 1a and 1b]. His Psoriasis Area and Severity Index (PASI) was 13.2 [Figure 2a and 2b] prior to the commencement of biologic therapy. Previous treatments involving narrow-band ultraviolet B rays (NB-UVB) irradiation, halcinonide solution, and calcipotriol ointment failed to yield significant results. Subsequently, the patient underwent weekly Secukinumab therapy at 300 mg dosage, which led to complete control of his psoriasis (PASI0) within three weeks. However, post the fourth dose of Secukinumab, he noticed a small number of erythematic papules on his hands. Despite discontinuing Secukinumab for two weeks, his atopic dermatitis-like rash continued to progress. Consequently, he was referred to our department for further evaluation. He had a past medical history of allergic rhinitis and seafood allergy but no personal or family history of AD. Clinical examination revealed erythematous papules, excoriation, and serous exudation on his hands, elbow joints, thighs, and calves [Figure 3a]. Laboratory tests indicated elevated serum immunoglobulin E (1143.6 IU/mol).

Figure 1.

(a) Histopathological manifestations of psoriatic lesions in the lower back. Inflammatory cells mainly infiltrating lymphocytes around the superficial dermal vessels. Hyperkeratosis and parakeratosis of the epidermis are observed, along with clubbing hyperplasia of the epidermis, neutrophil infiltration, and regular thickening of the spinous layer. (Haematoxylin–eosin staining was utilized for histopathology, original magnification ×40). (b) Histopathological manifestations of psoriatic lesions in the lower back. Inflammatory cells mainly infiltrating lymphocytes around the superficial dermal vessels. Hyperkeratosis and parakeratosis of the epidermis are observed, along with clubbing hyperplasia of the epidermis, neutrophil infiltration, and regular thickening of the spinous layer. (Haematoxylin–eosin staining was utilized for histopathology, original magnification ×400)

Figure 2.

(a) Clinical features of psoriasis lesions upon initial diagnosis. Large scattered erythema and scales on the waist, buttocks. (b) Clinical features of psoriasis lesions upon initial diagnosis. Scattered erythema and scales on the back of the hand, with clear boundaries

Figure 3.

(a) The occurrence of atopic dermatitis eczema-like lesions was observed subsequent to the receiving four sessions of Secukinumab treatment. (b) Following a one-week course of treatment consisting exclusively of Upadacitinib. B: Following a two-week course of treatment consisting exclusively of Upadacitinib. (c) Following a two-week course of treatment consisting exclusively of Upadacitinib. (d) Following a six-week course of treatment consisting exclusively of Upadacitinib

Diagnosis of an AD-like eruption was made, and the patient’s Secukinumab treatment was discontinued. Given that Upadacitinib, a JAK1 inhibitor, has therapeutic effects on both psoriasis and AD, a daily 15 mg dosage of Upadacitinib was administered after ruling out contraindications and obtaining informed consent from the patient. Following one week of treatment, the AD-like eruption started to subside [Figure 3b]. After two weeks of continuous administration, significant improvement in the AD-like eruption was observed [Figure 3c]. At the end of the six-week treatment period, the AD-like eruption achieved complete remission [Figure 3d]. Additionally, there were no signs of psoriasis recurrence during the three-month follow-up period.

Psoriasis is characterized by the dominance of type 1 helper T (Th1) cells and type 17 helper T (Th17) cells, which release IL-17, while AD stems from a type-2 helper T cells (Th2)-mediated immune response.[1] These Th1 and Th2 pathways are interrelated; suppressing the Th1 response can increase the Th2 response, and vice versa. The development of AD-like lesions after IL-17A antagonist treatment can be attributed to an imbalance in the Th1/Th2 immune response, leading to increased activity in the antagonistic Th2 axis, associated with conditions like AD, allergic rhinitis, and asthma.[2] Burlando et al.[3] first reported an eczematous reaction during IL-17A antagonist treatment in 2018. Subsequent case reports[4] and clinical trials[5] have also reported the development of AD-like eruptions following IL-17A inhibitor therapy.

For mild, localized AD-like lesions, discontinuation of the IL-17A inhibitor may lead to the gradual disappearance of lesions.[3] However, for moderate to severe AD-like lesions, the IL-17A inhibitor should be discontinued, and treatments effective for both psoriasis and AD, such as JAK inhibitors, should be considered.[4] The JAK/STAT pathway plays a crucial role in the pathophysiological process of psoriasis, inducing proliferation and promoting the production of Th17 cells. Emerging evidence suggests the efficacy of JAK inhibitors in treating psoriasis.[6,7] As a highly selective JAK 1 inhibitor, Upadacitinib has received approval for managing AD.[8,9] Thus, in this case, Upadacitinib was used to treat the AD-like eruption.

In this case, the patient primarily presented with psoriasis, with no skin lesions of AD. Following standard Secukinumab treatment, an AD-like eruption appeared, prompting the discontinuation of Secukinumab. However, this change in treatment did not result in any improvement, and the eruption worsened. Considering that Upadacitinib is more effective than Abrocitinib and can reverse AD faster theoretically,[10] oral Upadacitinib was administered after obtaining informed consent. During the follow-up, the patient’s AD-like eruption was effectively controlled with no recurrence of psoriasis. This study demonstrates the rapid and significant efficacy of Upadacitinib in eliminating skin lesions in clinical practice, which offers valuable clinical insights into the potential of Upadacitinib as a therapeutic option for AD-like lesions post-Secukinumab injection. Nonetheless, further studies are necessary to evaluate long-term safety, efficacy, and underlying mechanisms.

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.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.