Adalimumab and secukinumab are the only FDA-approved biologic drugs to treat hidradenitis suppurativa, limiting options for patients, especially those who experience loss of response.
Adalimumab and secukinumab are the only FDA-approved biologic drugs to treat hidradenitis suppurativa, limiting options for patients, especially those who experience loss of response. | Image Credit: Lea - stock.adobe.com
Hidradenitis suppurativa (HS) can be managed with either adalimumab or secukinumab, both valuable treatment options, but ongoing research is crucial to identify the best biologic therapies for individual patients while optimizing long-term outcomes, according to a review published in the Journal of the American Academy of Dermatology.1
HS, a chronic inflammatory dermatologic disease, can be defined by inflamed, painful lesions that frequent the armpits, groin, buttocks, and breasts.2 Sometimes referred to as acne inversa, painful nodules develop under the skin and usually rupture.3 This causes abscesses that drain fluid and pus, leaving prominent scarring on the skin when healed.
Adalimumab (Humira),, a tumor necrosis factor (TNF)-α inhibitor, was approved by the FDA in 2015 to treat HS.1 Prior to its approval, patients with HS relied on surgery to remove the skin affected by the disease along with antibiotics.
Secukinumab (Cosentyx), an interleukin-17A (IL-17A) biologic inhibitor, received FDA approval in 2023, almost 10 years after adalimumab.1 Results from the phase 3 SUNSHINE (NCT03713619) and SUNRISE (NCT03713632) trials led to the drug’s approval.4 Both adalimumab and secukinumab are biologic drugs or biologics, a class of medications manufactured from a natural resource, often composed of an antibody to a specific human target.1
The authors discussed approved treatments, biologic management, and outlined the evolving biologic pipeline throughout the review. Adalimumab and secukinumab are approved for patients with moderate to severe HS, defined as a minimum of 3 to 5 abscesses and nodules.
Progressive scarring, draining tunnels, and severe or frequent flareups require urgent evaluation to prevent further developments. Treatment methods are based on the patient’s age, comorbidity status, immunosuppression risks, speed of onset, and other factors.
In cases of HS that stop responding to TNF-α inhibitors, physicians may increase the dosage of FDA-approved drugs or look to alternative medications approved for other indications. Off-label TNF-α inhibitor dosing or usage typically consists of 80 mg adalimumab administered weekly or infusion of infliximab or its biosimilars.
Golimumab and certolizumab have not been studied extensively for treatment of HS but have been options when other TNF-α inhibitors are limited. However, significant research has been completed on IL-17 inhibitors like lutikizumab, izokibep, and sonelokimab. Additional research is needed to determine which patients have the most robust responses to each biologic target, the authors noted.
Loss of response to biologic therapies, particularly TNF-α inhibitors, is common in patients with HS. Biologic management strategies often rely on therapeutic drug monitoring to identify the underlying cause of treatment failure. Possible reasons for response loss include changes in disease mechanisms, drug sequestration within inflammatory sites, or the development of antidrug antibodies (ADAs).
“Therapeutic drug monitoring is commercially available for use in patients treated with adalimumab and biosimilars, infliximab and biosimilars, and ustekinumab,” the study authors wrote, noting that physicians assess biologic drug levels and ADA levels to determine the etiology of treatment failure. Importantly, patients who develop ADAs to one biologic medication may have an increased risk of developing ADAs to other medications within the same class.
References
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