Certolizumab pegol for hidradenitis suppurativa: Case report and literature review

Holm, Jesper Grønlund; Jørgensen, Astrid‐Helene Ravn; Yao, Yiqiu; Thomsen, Simon Francis

doi:10.1111/dth.14494

Cited by 21 publications

(27 citation statements)

References 9 publications

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“…118,119 Real-life data provided in a retrospective, multicenter cohort study showed ADA efficacy/safety and an inverse correlation between therapeutic delay and clinical response, supporting early ADA use and providing evidence for a 'window of opportunity' in HS treatment. 120 Real-life data provided in a retrospective cross-sectional study Tampouratzi et al, 133 Holm et al, 134 Esme et al, 135 Wohlmuth- 165 Sharon et al, 166 Santos-Pérez et al, 167 Eisen, 168 Scholl et al, 169 Takeda et al, 170 Cline and Pichardo, 171 Montero-Vilchez et al, 172 Valenzuela Case reports and case series (n = 19) 100 mg sc at weeks 0, 4, and then every 8 weeks 100 mg sc at weeks 0, 4, and then every 4 weeks…”

Section: Surgerymentioning

confidence: 99%

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New perspectives on the treatment of hidradenitis suppurativa

Amat-Samaranch

Agut-Busquet

Vilarrasa

et al. 2021

Therapeutic Advances in Chronic Disease

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Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease characterized by the presence of painful nodules, abscesses, chronically draining fistulas, and scarring in apocrine gland-bearing areas of the body. The exact pathogenesis of HS is not yet well understood, but there is a consensus in considering HS a multifactorial disease with a genetic predisposition, an inflammatory dysregulation, and an influence of environmental modifying factors. Therapeutic approach of HS is challenging due to the wide clinical manifestations of the disease and the complex pathogenesis. This review describes evidence for effectiveness of current and emerging HS therapies. Topical therapy, systemic treatments, biological agents, surgery, and light therapy have been used for HS with variable results. Adalimumab is the only US Food and Drug Administration (FDA) approved biologic agent for moderate-to-severe HS, but new therapeutic options are being studied, targeting different specific cytokines involved in HS pathogenesis. Comparing treatment outcomes between therapies is difficult due to the lack of randomized controlled trials. Treatment strategy should be selected in concordance to disease severity and requires combination of treatments in most cases.

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Section: Surgerymentioning

confidence: 99%

“…A retrospective study on off-label use of TNF-inhibitors reported no efficacy of low-dose CZP (200 mg every 2 weeks) in two patients. 132 Several case reports purport successful results of CZP 400 mg sc every 2 weeks 133–136 in patients with moderate to HS refractory to other biologics.…”

Section: Treatmentmentioning

confidence: 99%

New perspectives on the treatment of hidradenitis suppurativa

Amat-Samaranch

Agut-Busquet

Vilarrasa

et al. 2021

Therapeutic Advances in Chronic Disease

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“…However, drugs which are being tested for HS are very numerous and further include also complement 5a (C5a) and C5a receptor blocking agents (avacopan and IFX-1), janus kinase (JAK), signalling inhibitors (tofacitnib and upadacitinib), anti-CD40 (iscalimab), and anti-iIL23 agents (guselkumab and risankizumab) [117,130]. Furthermore, case reports or case series also show good results for other drugs, such as certolizumab pegol (anti-TNF-α) [131][132][133], tildrakizumab (anti-IL23) [134], ixekizumab (anti-IL17) [135], and brodalumab (anti-IL17 receptor) [136]. In this crowded future treatment scenario, it should be emphasized that HS is a complicated disease that involves both pathological and environmental factors.…”

Section: Future Treatments and Personalized Therapiesmentioning

confidence: 99%

Hidradenitis Suppurativa: Where We Are and Where We Are Going

Scala

Cacciapuoti

Garzorz‐Stark

et al. 2021

Cells

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Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease primarily affecting apocrine gland-rich areas of the body. It is a multifactorial disease in which genetic and environmental factors play a key role. The primary defect in HS pathophysiology involves follicular occlusion of the folliculopilosebaceous unit, followed by follicular rupture and immune responses. Innate pro-inflammatory cytokines (e.g., IL-1β, and TNF-α); mediators of activated T helper (Th)1 and Th17 cells (e.g., IFN-γ, and IL-17); and effector mechanisms of neutrophilic granulocytes, macrophages, and plasma cells are involved. On the other hand, HS lesions contain anti-inflammatory mediators (e.g., IL-10) and show limited activity of Th22 cells. The inflammatory vicious circle finally results in pain, purulence, tissue destruction, and scarring. HS pathogenesis is still enigmatic, and a valid animal model for HS is currently not available. All these aspects represent a challenge for the development of therapeutic approaches, which are urgently needed for this debilitating disease. Available treatments are limited, mostly off-label, and surgical interventions are often required to achieve remission. In this paper, we provide an overview of the current knowledge surrounding HS, including the diagnosis, pathogenesis, treatments, and existing translational studies.

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“…Certolizumab pegol is a pegylated antigen-binding fragment (Fab) of a recombinant humanized monoclonal antibody targeting TNF-α [ 200 ]. In two case reports (involving two male patients), certolizumab pegol appeared to be effective in treating recalcitrant (both patients had previously failed biological therapies) HS [ 201 , 202 ]. A case report of a female patient with concomitant psoriasis, psoriatic arthritis, and HS successfully treated with certolizumab pegol was recently described [ 203 ].…”

Section: (New Medical) Therapeutical Approaches In Hsmentioning

confidence: 99%

“…A case report of a female patient with concomitant psoriasis, psoriatic arthritis, and HS successfully treated with certolizumab pegol was recently described [ 203 ]. In all these case reports, the initial dose was 400 mg, followed by 400 mg every other week (only 1 male patient increased to 200 mg every week) [ 201 , 202 , 203 ]. In the literature, a successful treatment with certolizumab pegol of a pregnant patient with HS was reported [ 204 ].…”

Section: (New Medical) Therapeutical Approaches In Hsmentioning

confidence: 99%

Insights into the Pathogenesis of HS and Therapeutical Approaches

et al. 2021

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Hidradenitis suppurativa (HS) is a debilitating, chronic, (auto)inflammatory disease primarily affecting apocrine gland-rich areas of the body. Although pathogenic mechanisms responsible for HS have not yet been fully elucidated, it is a multifactorial process whose main target is the terminal follicle. The role of the inflammatory process (and consequently of cytokine milieu) and of several other factors (genetics, lifestyle, hormonal status, microbiome, innate and adaptive immune systems) involved in HS pathogenesis has been investigated (and often defined) over the years with a view to transferring research results from bench to bedside and describing a unique and universally accepted pathogenetic model. This review will update readers on recent advances in our understanding of HS pathogenesis and novel (potential) medical therapies for patients with moderate-to-severe HS.

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Certolizumab pegol for hidradenitis suppurativa: Case report and literature review

Cited by 21 publications

References 9 publications

New perspectives on the treatment of hidradenitis suppurativa

New perspectives on the treatment of hidradenitis suppurativa

Hidradenitis Suppurativa: Where We Are and Where We Are Going

Insights into the Pathogenesis of HS and Therapeutical Approaches

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