INTRODUCTION
Hidradenitis suppurativa (HS) is an inflammatory skin disease characterized by deep suppurative nodules and abscesses generally in areas containing apocrine glands. Previously thought to be caused by dysregulated processes affecting the sweat glands, HS is now thought to be due to follicular occlusion, hyperkeratosis, and inflammation in the pilosebaceous unit.1-3 The Hurley Staging system is used to categorize disease severity into mild, moderate, or severe (Hurley Stages I-III).2,6 Patients suffering from HS experience poor quality of life due to unsightly scars, leaking abscesses, and frustration with the need to try numerous treatments for a chance at experiencing remission.4
The pathophysiology of HS is due to hyperkeratinization of hair follicles followed by follicular rupture and subsequent inflammation leading to the formation of sinus tracts, abscesses, and fistulas.1,5 In HS lesions, there is an elevation of numerous cytokines and chemokines with those most elevated being TNF-α, IFN-γ, IL-1β, IL-17, and IL-23. These have proven to be effective targets for therapy.7-8
Treatment goals for moderate to severe HS is disease control/remission and prevention of flares. The only current FDA-approved drug for HS is adalimumab.3,10 Treatment regimens offered to patients with HS are based on clinical experience and include a variety of topical agents, intralesional treatments, antibiotics (topical or systemic), anti-diabetic agents (eg metformin), retinoids, immunosuppressants, surgery, anti-inflammatory drugs, and biologics. Some biologics for HS include adalimumab (anti-TNF-α monoclonal antibody), infliximab (chimeric anti-TNF-α monoclonal antibody given via infusions), anakinra (IL-1 receptor antagonist), ustekinumab (anti-IL-12/23 monoclonal antibody), guselkumab (anti-IL-23 monoclonal antibody) and secukinumab (anti-IL-17A monoclonal antibody).7,11 Secukinumab has been an effective treatment in several cases of moderate-severe HS.12-14 In this case report, we discuss a promising novel dosing regimen of secukinumab and possible benefits of IL-17A inhibition in treatment of HS.
The pathophysiology of HS is due to hyperkeratinization of hair follicles followed by follicular rupture and subsequent inflammation leading to the formation of sinus tracts, abscesses, and fistulas.1,5 In HS lesions, there is an elevation of numerous cytokines and chemokines with those most elevated being TNF-α, IFN-γ, IL-1β, IL-17, and IL-23. These have proven to be effective targets for therapy.7-8
Treatment goals for moderate to severe HS is disease control/remission and prevention of flares. The only current FDA-approved drug for HS is adalimumab.3,10 Treatment regimens offered to patients with HS are based on clinical experience and include a variety of topical agents, intralesional treatments, antibiotics (topical or systemic), anti-diabetic agents (eg metformin), retinoids, immunosuppressants, surgery, anti-inflammatory drugs, and biologics. Some biologics for HS include adalimumab (anti-TNF-α monoclonal antibody), infliximab (chimeric anti-TNF-α monoclonal antibody given via infusions), anakinra (IL-1 receptor antagonist), ustekinumab (anti-IL-12/23 monoclonal antibody), guselkumab (anti-IL-23 monoclonal antibody) and secukinumab (anti-IL-17A monoclonal antibody).7,11 Secukinumab has been an effective treatment in several cases of moderate-severe HS.12-14 In this case report, we discuss a promising novel dosing regimen of secukinumab and possible benefits of IL-17A inhibition in treatment of HS.
CASE
Patient is a 36-year-old man with extensive and treatment-resistant Hurley Stage 3 disease. On presentation, he had multiple deep nodules and abscesses with fistulous tracts in the neck, groin, and underarms with extensive scarring. He subsequently developed abscesses on his neck, scalp, groin, axillae, inguinal folds, chest, back, buttocks, abdomen, thighs, pubic region, and waistline (Figure 1). Throughout the course of his disease, he was treated with numerous topical and systemic medications including doxycycline, minocycline, clindamycin (topical and oral), rifampin, trimethoprim/sulfamethoxazole, amoxicillin, methotrexate, prednisone, and metformin. He
