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). Over the past 2 decades, 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 infected with HIV. Note acneiform hyperpigmented papules. Photograph courtesy of Sarah A. Myers, MD.

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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.

Frequency

United States

The prevalence of eosinophilic folliculitis is unknown.

International

The classic form is most closely linked with persons of Japanese descent.^[4]

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.^[5]

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.^[6]

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.

Clinical Presentation

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Media Gallery

Eosinophilic pustular folliculitis in a patient infected with HIV. Note acneiform hyperpigmented papules. Photograph courtesy of Sarah A. Myers, MD.
Eosinophilic pustular folliculitis in a patient who is HIV-positive. Note follicular-based excoriated papules and pustules on the trunk. Photograph courtesy of Sarah A. Myers, MD.
Eosinophilic folliculitis (low-power). Note eosinophilic spongiosis, particularly involving the infundibular region of the hair follicle.
Eosinophilic folliculitis (high-power). In addition to the abundant eosinophils, note the variable numbers of neutrophils and mononuclear cells.

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Author

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, Rutgers New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

M Angelica Selim, MD, MD Director of Dermatopathology, Departments of Pathology and Internal Medicine, Associate Professor, Duke University Medical Center

Disclosure: Nothing to disclose.

Christopher R Shea, MD Eugene J Van Scott Professor in Dermatology, Chief, Section of Dermatology, Department of Medicine, University of Chicago, The Pritzker School of Medicine

Christopher R Shea, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society of Dermatopathology, Arthur Purdy Stout Society, Association of Professors of Dermatology, Chicago Dermatological Society, Dermatology Foundation, Illinois Dermatological Society, International Society of Dermatopathology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Joseph F John, Jr, MD, FACP, FIDSA, FSHEA Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Joseph F John, Jr, MD, FACP, FIDSA, FSHEA is a member of the following medical societies: Charleston County Medical Association, Infectious Diseases Society of America, South Carolina Infectious Diseases Society

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Rajendra Kapila, MD, MBBS † Professor, Department of Medicine, Rutgers New Jersey Medical School

Rajendra Kapila, MD, MBBS is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, Infectious Diseases Society of New Jersey

Disclosure: Nothing to disclose.

Harry Dao, Jr, MD Assistant Professor, Department of Dermatology, Baylor College of Medicine

Harry Dao, Jr, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.