Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition characterized by the formation of painful, deep-seated lumps, nodules, and abscesses. These recurring lesions primarily develop in areas where skin rubs together, such as the armpits, groin, under the breasts, and on the buttocks. The condition often leads to scarring and can significantly impact a person’s quality of life.
Addressing the Contagion Question
Hidradenitis suppurativa is definitively not contagious and cannot be spread from one person to another. It is an internal inflammatory process, not an infectious disease caused by a transmissible pathogen like a virus or bacteria. Consequently, a person cannot contract HS through casual skin-to-skin contact, sexual contact, or sharing towels.
While the lesions can sometimes develop a secondary bacterial infection, the underlying HS itself remains an internal dysfunction of the hair follicle. Understanding this non-infectious nature helps reduce the stigma often associated with the condition.
Understanding Hidradenitis Suppurativa
HS is a chronic disease involving the hair follicles, which become blocked and subsequently inflamed. The initial event is the occlusion of the hair follicle, often with keratin, leading to rupture and a profound immune response within the skin. This results in the formation of painful, boil-like nodules and abscesses beneath the skin’s surface.
Over time, chronic inflammation can lead to the creation of sinus tracts, which are narrow, tunnel-like passages connecting multiple lesions beneath the skin. The severity of the disease is commonly classified using the Hurley staging system, which ranges from mild to severe.
Hurley Staging System
Stage I involves isolated abscesses without tunnels or scarring. Stage II introduces recurrent abscesses with sinus tracts and some scarring. Stage III, the most severe form, presents with widespread, interconnected tracts and extensive scarring across the entire affected area.
Underlying Causes and Risk Factors
HS involves a complex interplay between genetics, the immune system, and environmental influences. The primary physical mechanism is the blockage of the hair follicle, followed by rupture and a destructive immune-mediated inflammatory cascade. This process is distinct from a simple infection and is considered an autoinflammatory condition.
Approximately one-third of people with HS report a family history of the condition, suggesting a genetic predisposition. Hormonal factors also play a part, as the condition often appears after puberty and can fluctuate with menstrual cycles. Lifestyle elements significantly increase the risk of developing or worsening HS, particularly cigarette smoking and obesity. Studies indicate that 70% to 90% of individuals with HS are current or past smokers.
Diagnosis and Treatment Approaches
Diagnosis of HS is primarily clinical, relying on a healthcare provider’s examination of the characteristic lesions in the typical locations. Because the symptoms can resemble other conditions like acne or boils, diagnosis is often delayed. While no specific laboratory test exists for HS, a sample of drainage may be tested to check for a secondary bacterial infection.
The goals of managing HS are to reduce pain, prevent the formation of new lesions, and stop the progression to deep tunneling and scarring. Treatment strategies are tailored to the Hurley stage.
Mild cases may include topical antibiotics like clindamycin. For moderate or severe disease, treatment may involve systemic medications such as oral antibiotics, hormonal therapies, or advanced biologic drugs that target the underlying inflammatory pathways. In cases with persistent or advanced tunneling, surgical intervention, such as unroofing the tracts or removing the affected skin, is often necessary.