Why Hidradenitis Suppurativa Abscesses Are Developing Into Keloids
Keloid formation is a recognized complication of hidradenitis suppurativa, occurring as part of the chronic inflammatory and scarring process that characterizes this disease—particularly in patients with darker skin types or genetic predisposition to abnormal wound healing.
Understanding Keloid Formation in HS
Keloids and hypertrophic scarring are well-documented cutaneous complications of hidradenitis suppurativa, arising from the repeated cycles of profound inflammation, tissue destruction, and aberrant wound healing that define this condition 1, 2.
Chronic inflammation drives pathologic scarring. The massive immune cell infiltration—including neutrophils, macrophages, plasma cells, and lymphocytes—combined with high levels of proinflammatory cytokines (IL-1β, TNF-α, IL-17) creates a wound-healing environment that favors excessive collagen deposition and keloid formation 3.
Repeated episodes of rupture and repair. HS lesions undergo cycles of follicular plugging, rupture, abscess formation, and healing. Each cycle deposits more scar tissue, and in susceptible individuals this process becomes dysregulated, leading to keloid development rather than normal scar maturation 2, 3.
Back location increases keloid risk. The back is a high-tension anatomic site where mechanical stress on healing wounds promotes keloid formation. Patients with HS affecting the back often develop distinctive hypertrophic rope-like bridged scars, raised plaques with multiple openings, and "worm-eaten scars"—all manifestations of pathologic scarring 4.
Why This Patient May Be Different
Individual genetic susceptibility. Approximately 42% of HS patients have a positive family history, and some carry mutations in γ-secretase complex genes that may also influence wound-healing pathways 3, 5. Your patient may have inherited a predisposition to keloid formation that is being triggered by the chronic inflammation of HS.
Skin phototype matters. Keloid formation is significantly more common in individuals of African descent, who also have higher HS prevalence 6, 5. If your patient has darker skin, this substantially increases keloid risk.
Disease severity and chronicity. Patients with Hurley Stage II or III disease—characterized by recurrent abscesses, sinus tracts, and extensive scarring—are at highest risk for keloid complications because of the repeated inflammatory insults 7, 2.
Clinical Implications and Management
Keloids represent advanced disease. The presence of keloids indicates that this patient has moved beyond simple inflammatory nodules into a phase of chronic tissue destruction and pathologic repair 1, 2.
Aggressive medical therapy is essential. For moderate-to-severe disease with keloid formation, initiate clindamycin 300 mg twice daily plus rifampicin 300–600 mg daily for 10–12 weeks to control active inflammation 7, 8. If no response after 12 weeks, escalate to adalimumab (160 mg week 0,80 mg week 2, then 40 mg weekly) 7, 6.
Surgical excision may be required. Established keloids and hypertrophic scars in HS often require radical surgical excision with wide margins to prevent recurrence, achieving non-recurrence rates of approximately 81% 7, 1. Combining adalimumab with surgery produces better outcomes than either modality alone 7.
Intralesional steroids for active lesions. For inflamed nodules that are at risk of progressing to keloids, inject triamcinolone 10 mg/mL (0.2–2.0 mL per lesion) to rapidly reduce inflammation and potentially prevent keloid formation 7, 8.
Critical Pitfalls to Avoid
Do not perform simple incision and drainage. This approach worsens scarring and increases keloid risk without addressing the underlying HS pathology 8.
Do not delay biologic therapy. Waiting too long to escalate treatment allows continued inflammation and progressive keloid formation. If antibiotics fail after 12 weeks, move immediately to adalimumab 7, 6.
Do not ignore comorbidity screening. Screen for depression, anxiety, and cardiovascular risk factors, as these are highly prevalent in HS patients and significantly impact quality of life 7, 6.
Why Other HS Patients May Not Develop Keloids
Most HS patients do not develop keloids because they lack the genetic predisposition to pathologic scarring, have milder disease (Hurley Stage I) with less tissue destruction, receive earlier and more aggressive treatment that limits chronic inflammation, or have lighter skin phototypes with lower baseline keloid risk 6, 4, 5. Your patient's keloid formation reflects a convergence of genetic susceptibility, disease severity, anatomic location (back), and possibly delayed or inadequate treatment.