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Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease characterized by painful nodules, abscesses, and draining tunnels in areas such as the axillae, groin, and inframammary regions. It typically emerges in early adulthood, with a global prevalence of approximately 1%, though regional variations exist. HS significantly affects patients’ quality of life and imposes considerable socioeconomic burdens. It is frequently associated with metabolic syndrome, inflammatory arthritis, and inflammatory bowel disease, reflecting its underlying systemic inflammatory nature. The pathogenesis of HS involves innate immune mechanisms, including macrophages, neutrophils, interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and granulocyte colony-stimulating factor, alongside adaptive immune responses mediated by T cells (IL-17, interferon [IFN]-γ) and B cells, which contribute to autoantibody formation and tertiary lymphoid structures. Chronic inflammation results in irreversible tissue damage, tunnel formation, and severe scarring. Treatment strategies vary based on disease severity. Early inflammatory stages benefit from pharmacological therapies, while later stages require a combination of medical and surgical interventions, with surgery often necessary for advanced cases. The introduction of targeted biologic therapies, including TNF-α (adalimumab) and IL-17 inhibitors (secukinumab, bimekizumab), has expanded treatment options beyond traditional antibiotic regimens. Effective management focuses on early intervention to prevent irreversible damage, control symptoms such as pain, and address systemic comorbidities. A timely diagnosis, along with a multidisciplinary and personalized approach, is essential for improving patient outcomes and quality of life.

Background. A range of molecular targets is currently available for the treatment of psoriatic arthritis (PsA). Identifying clinical predictors of treatment persistence is critical for optimizing therapeutic strategies, as drug retention is often used as a proxy for long-term efficacy and safety. This study aimed to evaluate predictors of secukinumab (SEC) retention in PsA patients who previously discontinued the anti-TNF agent adalimumab (ADA).   Methods. PsA patients who initiated SEC following ADA discontinuation between 2019 and 2024 were retrospectively analyzed. Clinical data were collected through systematic chart reviews, including demographic characteristics, involved disease domains, prior treatments, and metabolic comorbidities [e.g., increased body mass index (BMI), diabetes]. SEC treatment persistence was assessed over a follow-up period of up to 36 months. Survival analysis was performed using SEC discontinuation as the event, with demographic and clinical variables as predictors.   Results. Among 327 PsA patients treated with SEC during the study period, 67 had previously discontinued ADA – 54 (81%) due to inadequate response and 13 (19%) due to adverse events. Patients’ characteristics are detailed in Table 1. Over a median follow-up of 1.6 years (Interquartile Range (IQR) 0.7–2.4), 26 SEC discontinuations were recorded, corresponding to an incidence rate of 24.8 per 100 patient-years. SEC retention rates at 12, 24, and 36 months were 69.8% (95% Confidence Interval (CI) 59.3–82.2), 61.6% (95% CI 49.7–76.5), and 49.1% (95% CI 36.0–67.0), respectively. The presence of enthesitis (Hazard Ratio (HR) 0.28, 95% CI 0.08–0.96) and concomitant active skin psoriasis (HR 0.21, 95% CI 0.08–0.59) were significantly associated with a lower risk of SEC discontinuation.   Conclusions. Secukinumab showed higher retention rates in PsA patients with enthesitis and active skin psoriasis after ADA discontinuation. No significant associations were found with demographic variables or metabolic comorbidities. These findings may assist clinicians in identifying patients who are more likely to benefit from IL-17 inhibition following anti-TNF therapy failure.

In two placebo-controlled phase 3 trials, secukinumab, an anti–interleukin-17A monoclonal antibody, was effective in patients with ankylosing spondylitis. Adverse events associated with secukinumab included infections and neutropenia. Ankylosing spondylitis is a chronic, immune-mediated disease that is characterized by inflammation and new bone formation in the axial skeleton 1 , 2 and that often results in progressive, irreversible structural damage, disability, deterioration of functioning, and a reduced quality of life. 3 , 4 Therapy with nonsteroidal antiinflammatory drugs (NSAIDs) is often insufficient to control symptoms, and there is no evidence that conventional disease-modifying antirheumatic drugs (DMARDs) are efficacious in axial disease. 5 Anti–tumor necrosis factor (TNF) therapy is currently recommended for patients with persistent disease activity despite conventional treatment. 5 In some patients, however, such therapy fails to achieve adequate disease control or has . . .

Background Secukinumab, an anti–interleukin-17A monoclonal antibody, improved the signs and symptoms of ankylosing spondylitis (AS) in two phase 3 studies (MEASURE 1 and MEASURE 2). Here, we present 52-week results from the MEASURE 3 study assessing the efficacy and safety of secukinumab 300 and 150 mg subcutaneous maintenance dosing, following an intravenous loading regimen. Methods A total of 226 patients were randomized to intravenous secukinumab 10 mg/kg (baseline, weeks 2 and 4) followed by subcutaneous secukinumab 300 mg (IV-300 mg) or 150 mg (IV-150 mg) every 4 weeks, or matched placebo. Patients in the placebo group were re-randomized to subcutaneous secukinumab at a dose of 300 or 150 mg at week 16. The primary endpoint was the Assessment of SpondyloArthritis international Society criteria for 20% improvement (ASAS20) response rate at week 16 in the IV-300 mg or IV-150 mg versus placebo. Other endpoints assessed through week 52 included improvements in ASAS40, ASAS 5/6, Bath Ankylosing Spondylitis Disease Activity Index, and ASAS partial remission responses, as well as the change from baseline in high-sensitivity C-reactive protein levels. Statistical analyses followed a predefined hierarchical hypothesis testing strategy to adjust for multiplicity of testing, with non-responder imputation used for binary variables and mixed-model repeated measures for continuous variables. Results The primary efficacy endpoint was met; the ASAS20 response rate was significantly greater at week 16 in the IV-300 mg (60.5%; P  < 0.01) and IV-150 mg (58.1%; P  < 0.05) groups versus placebo (36.8%). All secondary endpoints were met at week 16, except ASAS partial remission in the IV-150 mg group. Improvements achieved with secukinumab in all clinical endpoints at week 16 were also sustained at week 52. Infections, including candidiasis, were more common with secukinumab than with placebo during the placebo-controlled period. During the entire treatment period, pooled incidence rates of Candida infections and grade 3–4 neutropenia were 1.8% for both of these adverse events in secukinumab-treated patients. Conclusions Secukinumab (300 mg and 150 mg dose groups) provided rapid, significant and sustained improvement through 52 weeks in the signs and symptoms of patients with AS. The safety profile was consistent with previous reports, with no new or unexpected findings. Trial registration ClinicalTrials.gov, NCT02008916 . Registered on 8 December 2013. EUDRACT 2013-001090-24. Registered on 24 October 2013). The study was not retrospectively registered.

Waner Liu,1,* Yuan Chen,2,* Zhimin Lin,3 Jianglin Zhang,1 Chen Li1 1Department of Dermatology, Shenzhen People’s Hospital (The First Affiliated Hospital, Southern University of Science and Technology; The Second Clinical Medical College, Jinan University), Shenzhen, 518020, People’s Republic of China; 2School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People’s Republic of China; 3Capital Medical University Beijing Hospital of Traditional Chinese Medicine, Beijing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Chen Li, Department of Dermatology, Shenzhen People’s Hospital (The First Affiliated Hospital, Southern University of Science and Technology; The Second Clinical Medical College, Jinan University), Shenzhen, 518020, People’s Republic of China, Email casio1981@163.com Jianglin Zhang, Department of Dermatology, Shenzhen People’s Hospital (The First Affiliated Hospital, Southern University of Science and Technology; The Second Clinical Medical College, Jinan University), Shenzhen, 518020, People’s Republic of China, Email zhang.jianglin@szhospital.comAbstract: Palmoplantar pustulosis (PPP) is a chronic inflammatory dermatosis often treated with IL-17 inhibitors like secukinumab. Paradoxical cutaneous reactions to such biologics, though rare, are increasingly recognized. We report a case of a 25-year-old woman with PPP who developed a biopsy-confirmed acute pityriasis lichenoides et varioliformis acuta (PLEVA) eruption following six weeks of secukinumab therapy. Upon switching treatment to tofacitinib, both the PPP and the paradoxical PLEVA showed significant improvement. This case highlights PLEVA as a potential paradoxical reaction to IL-17 inhibition and suggests JAK inhibitors may be an effective alternative in this scenario.Keywords: IL-17, secukinumab, palmoplantar pustulosis, paradoxical reaction, JAK inhibitors, case report

Yanjie Wei,1,* Peilian Zhang,2,* Jintao Chuan,1 Jianzhou Ye,2 Tao Liu3 1Department of Dermatology, The First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming, People’s Republic of China; 2Department of Dermatology, Yunnan Provincial Hospital of Traditional Chinese Medicine, Kunming, Yunnan, People’s Republic of China; 3Department of Pathology, Yunnan Provincial Hospital of Traditional Chinese Medicine, Kunming, Yunnan, People’s Republic of China*These authors contributed equally to this workCorrespondence: Peilian Zhang, Department of Dermatology, Yunnan Provincial Hospital of Traditional Chinese Medicine, Kunming, People’s Republic of China, Email mzczpl1968@163.comPurpose: This report presents a rare paradoxical reaction manifesting as Behçet’s-like features, which developed three months following the initiation of secukinumab therapy for psoriasis.Patients and Methods: A 38-year-old female with a 30-year history of plaque psoriasis achieved significant remission of psoriatic lesions following seven doses of secukinumab (cumulative dose: 2100 mg). However, she subsequently developed systemic adverse events, including pharyngodynia, painful tonsillar and genital ulcers, folliculitis-like papules on the trunk and extremities, and erythema nodosum-like lesions on the extensor surfaces of both lower limbs. Laboratory tests, including bacterial, viral, and fungal cultures, excluded infectious etiologies. Histopathological examination of a skin biopsy demonstrated superficial and deep perivascular and interstitial inflammation with dense infiltration of lymphocytes, neutrophils, and eosinophils. Consequently, a diagnosis of secukinumab-induced Behçet’s-like syndrome was established, as the patient did not fully meet the International Criteria for Behçet’s Disease (ICBD). Secukinumab was immediately discontinued, and the patient was initiated on thalidomide (50 mg, three times daily) and colchicine (0.5 mg, twice daily).Results: Two weeks after treatment initiation, oral and genital ulcers resolved. Folliculitis-like papules and erythema nodosum-like lesions regressed significantly, leaving only residual post-inflammatory hyperpigmentation. The patient was subsequently switched to ustekinumab maintenance therapy at a standard dosage. Psoriasis remained well-controlled, with no recurrence of Behçet’s-like manifestations during a 4-year follow-up period.Conclusion: This report underscores the critical need for vigilant patient monitoring during anti-IL-17 therapy to detect such uncommon yet clinically significant paradoxical reactions. Furthermore, precise characterization of the onset timing of such adverse events is crucial, as it enables clinicians to implement timely preventive measures, mitigate risks, and rapidly identify emerging adverse reactions.Keywords: secukinumab, psoriasis, Behçet’s disease, adverse reaction, paradoxical reaction

Purpose: Secukinumab was approved for the treatment of psoriasis, psoriatic arthritis, and ankylosing spondylitis. However, the long-term safety of secukinumab in large sample population was unknown. The current study was to evaluate the secukinumab-assocaited adverse events (AEs) through data mining of the US Food and Drug Administration Adverse Event Reporting System (FAERS). Methods: Reports in the FAERS from the first quarter of 2015 (FDA approval of secukinumab) to the third quarter of 2021 were collected and analyzed. Disproportionality analyses, including the reporting odds ratio (ROR), the proportional reporting ratio (PRR), the Bayesian confidence propagation neural network (BCPNN), and the multi-item gamma Poisson shrinker (MGPS) algorithms, were employed in data mining to quantify the signals of secukinumab-related AEs. Results: A total of 89,228 reports of secukinumab as the “primary suspected (PS)” and 254,886 AEs induced by secukinumab were identified. Secukinumab-induced AE occurrence targeted 27 system organ classes (SOCs). A total of 257 signals of secukinumab-induced AEs in 19 SOCs were detected after conforming to the four algorithms simultaneously. Common significant signals of infections, respiratory disorders, skin and subcutaneous tissue disorders, immune system disorders, and ear and labyrinth disorders have emerged. Unexpected significant AEs such as injection site pain, vessel puncture site haemorrhage, arthralgia, hypokinesia, Bell’s palsy, parotid gland enlargement, and stress might also occur. The median onset time of secukinumab-associated AEs was 56 days (interquartile range [IQR] 5–214 days), and most of the onsets occurred within the first 1, 2, 3, and 4 months after initiation of secukinumab. Conclusion: Our study found potential new AE signals and provided a broader understanding of secukinumab’s safety profiles, supporting its rational use in chronic systemic inflammatory diseases.

In two trials in patients with moderate-to-severe plaque psoriasis, the anti–interleukin-17A monoclonal antibody secukinumab was more effective than placebo and etanercept. Infectious complications occurred more often with secukinumab than with placebo. Psoriasis is a chronic, immune-mediated inflammatory skin disease that is associated with substantial impairment of physical and psychological quality of life. 1 , 2 Our understanding of the pathogenesis of psoriasis was advanced by the discovery of the class of type 17 helper T (Th17) cells, which regulates innate and adaptive immunity. The proinflammatory cytokine interleukin-17A is the primary effector of Th17 cells, but it is also produced by other cell types in psoriatic lesions, including γδ T cells, neutrophils, and possibly mast cells. 3 – 7 Interleukin-17A stimulates keratinocytes to secrete chemokines and other proinflammatory mediators that recruit additional inflammatory cells, including neutrophils, . . .