Abstract

Dissecting cellulitis (DSC) is a chronic inflammatory disease of hair follicles. Affected patients develop painful scalp nodules and sinus tracts. Although the precise cause is unknown, it is proposed that collapse of the hair follicle wall secondary to defective follicular support plays a role not only in DSC but also in conditions that make up the so-called follicular occlusion tetrad: DSC, hidradenitis suppurativa (HS), acne conglobata, and pilonidal cysts.1 Altered innate and adaptive immune responses may also be involved in the pathogenesis of DSC and HS.2 In HS, increased levels of tumor necrosis factor (TNF)-alfa, interleukin (IL)-10, IL-1β, and IL-17a have been documented. Treatments that inhibit the action of TNF-alfa, such as infliximab and adalimumab, are helpful for many patients with DSC and HS.3, 4, 5 How other immune mediators affect these diseases is not well understood. Here we present a case of DSC developing at site of trauma in a patient receiving interferon beta-1a therapy for multiple sclerosis. This case provides further insight into the possible pathogenesis of DSC.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call