Eosinophilic Folliculitis

Updated: Apr 04, 2025
  • Author: Camila K Janniger, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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Overview

Background

Eosinophilic folliculitis (EF) is a recurrent skin disorder of unknown etiology. In 1965, Ise and Ofuji reported a case of recurrent follicular pustules and eosinophilia in a Japanese woman. [1] Five years later, and after 3 additional cases, Ofuji named this skin condition eosinophilic pustular folliculitis (EPF). [2] Orfanos and Sterry argued that the name sterile eosinophilic pustulosis might be more appropriate because this lesion is not restricted to the hair follicle. Other names have also been proposed (eg, classic form of eosinophilic folliculitis, Ofuji disease, eosinophilic pustular dermatosis). Since the 1990s, the spectrum of eosinophilic folliculitis has expanded to pediatric populations, transplant recipients, and persons with HIV and hematopoietic disorders.

Eosinophilic folliculitis is a noninfectious eosinophilic infiltration of hair follicles. The 3 variants of eosinophilic folliculitis include classic eosinophilic pustular folliculitis, immunosuppression-associated eosinophilic folliculitis (mostly HIV-related), and infancy-associated eosinophilic folliculitis. [3]

Eosinophilic folliculitis has been classified as an AIDS-defining illness. In both children and adults, eosinophilic pustular folliculitis should be viewed as a possible cutaneous sign of immunosuppression. However, eosinophilic folliculitis may also develop in immunocompetent persons.

Eosinophilic pustular folliculitis in a patient inEosinophilic pustular folliculitis in a patient infected with HIV. Note acneiform hyperpigmented papules. Photograph courtesy of Sarah A. Myers, MD.

Pathophysiology

Although the exact etiology of eosinophilic folliculitis remains obscure, studies have favored an autoimmune process directed against sebocytes or some component of sebum. Markers of acute inflammatory activation of the epithelia, such as ICAM-1 and MAC 387, are strongly positive in sebocytes of eosinophilic folliculitis lesions but only weakly reactive in the follicular epithelium. Antibody formation and the creation of immune complexes are believed to directly or indirectly mediate clinical manifestations. Patients with eosinophilic folliculitis create antibodies to the intercellular substance of the lower epidermis and the outer root sheath of the hair follicle. An abnormal Th2-type immune response to a follicular antigen, such as caused by Demodex species, may be responsible for HIV-associated eosinophilic folliculitis.

Members of the interleukin (IL)-36 family, IL-36α, IL-36β and IL-36γ, are potent chemoattractive cytokines for neutrophils and eosinophils. [4] IL-36 receptor antagonist (IL-36Ra) inhibits IL-36α, IL-36β and IL-36γ activity. However, before the late 1990s, the immunohistological expression of IL-36α, IL-36β, IL-36γ and IL-36Ra had never been addressed in normal follicles, folliculitis or eosinophilic pustular folliculitis (EPF).

Therefore, researchers performed immunohistochemical staining for IL-36α, IL-36β, IL-36γ and IL-36Ra using 10 cases of EPF, nine of non-specific folliculitis, 10 normal skin samples, and 10 samples of normal follicles adjacent to a sebaceous naevus as a control. Two dermatologists, who were blind to the patient records, evaluated all of the slides.

The immunoreactive IL-36α was hardly detected in the follicular epithelium and epidermis in the normal skin, folliculitis or EPF. The expression of IL-36β, IL-36γ and IL-36Ra was augmented in both folliculitis and EPF compared with that in normal follicles. Negative correlations were detected between IL-36β and IL-36Ra and between IL-36γ and IL-36Ra in normal follicles; however, these were absent in folliculitis. In contrast to normal follicles and folliculitis, a significant positive correlation between IL-36β/γ and IL-36Ra was shown in EPF.

The researchers concluded the overexpression of IL-36β, IL-36γ and IL-36Ra is an integral part of the inflammatory response of folliculitis and EPF. The coordinated expression of IL-36γ and IL-36Ra may be related to the pathomechanism of EPF.

Epidemiology

Frequency

United States

The prevalence of eosinophilic folliculitis is unknown.

International

The classic form is most closely linked with persons of Japanese descent. [5]

Mortality/Morbidity

Eosinophilic folliculitis is not disabling or life-threatening, but it may be intensely pruritic.

Race

Eosinophilic folliculitis is more common among Asian persons but also occurs among persons of Hispanic descent and in whites and blacks.

Sex

The male-to-female ratio of eosinophilic folliculitis is 5:1 in all 3 variants.

Classic type eosinophilic folliculitis was found to have no sexual predilection. [6]

HIV-associated eosinophilic folliculitis is more common among homosexual or bisexual men.

Age

Eosinophilic folliculitis is most common among persons aged 20-40 years.

In the pediatric population, eosinophilic folliculitis typically affects patients aged 5-10 months, although neonatal cases have been reported. A newborn was described with it. [7]

Prognosis

Eosinophilic folliculitis is a benign dermatologic disease; however, eosinophilic folliculitis is associated with advanced AIDS, and patients with HIV infection are at an increased risk of developing opportunistic infections.

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