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-1b, 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.3-5 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.