eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Eosinophilic Folliculitis: Treatment & Medication

Author: Camila K Janniger, MD, Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, New Jersey Medical School
Coauthor(s): Rajendra Kapila, MD, MBBS, Professor of Medicine, Department of Medicine, UMDNJ, New Jersey Medical School; M Angelica Selim, MD, Associate Director of Dermatopathology, Departments of Pathology and Internal Medicine, Assistant Professor, Duke University Medical Center; Christopher R Shea, MD, Professor and Chief, Section of Dermatology, Department of Medicine, University of Chicago
Contributor Information and Disclosures

Updated: Jul 20, 2009

Treatment

Medical Care

Numerous topical and systemic therapies are available for eosinophilic folliculitis. Treatment modalities are chosen based on disease severity, patient preference (including cost and convenience), and response.

  • Topical corticosteroids are the mainstay of treatment for eosinophilic folliculitis.
    • The mechanism of action of corticosteroids in eosinophilic folliculitis is not fully understood; the anti-inflammatory and immunosuppressive properties of these agents may contribute to their effect.
    • The potency of the steroid prescribed depends on the location of the skin lesions. In the scalp, potent steroids in alcohol solution, such as fluocinonide 0.05%, are frequently indicated. On the face and other sensitive body sites, a low-potency cream, such as hydrocortisone 1%, may suffice.
    • The typical regimen consists of twice-daily application of topical corticosteroids. This decreases the inflammation and plaques in most patients. Skin atrophy due to topical corticosteroid use is usually not a problem unless the medication is continuously applied after the skin has normalized. Severe flares may be treated with short courses of oral prednisone.
  • Fukamachi et al (2009) evaluated the therapeutic effectiveness of various treatments for eosinophilic pustular folliculitis in 20 patients.15 Oral cyclosporine was markedly effective in all 11 patients treated with the drug, and topical tacrolimus ointment alleviated eosinophilic pustular folliculitis in 3 of 7 of the study participants. In addition to indomethacin or other oral nonsteroidal anti-inflammatory drugs (NSAIDs), oral cyclosporine and topical tacrolimus appeared to be beneficial in patients resistant to previous treatments.
  • Retinoids, such as isotretinoin, inhibit sebaceous gland function and keratinization. Clinical improvement occurs in association with a reduction in sebum secretion.
    • This effect is temporary and is related to the dose and duration of treatment.
    • Monitoring for hypertriglyceridemia and hepatotoxicity is required.
    • Common adverse effects include cheilitis and alopecia. Systemic retinoid therapy is teratogenic; it is indicated only in patients who have no reproductive potential.
    • Alternatives include indomethacin and dapsone.
  • In patients infected with HIV, treat mild eosinophilic folliculitis with topical steroids and oral antihistaminics. Treat moderate disease with oral itraconazole, isotretinoin, or phototherapy. Treat severe eosinophilic folliculitis with isotretinoin therapy for several months.
  • Potential treatments include oxyphenbutazone, colchicine, minocycline, acitretin, cyclosporine A, UV-B therapy,16,17 interferon alfa-2b, tacrolimus,18,19,20 doxycycline,21 and radiation therapy.22

Consultations

  • Consider referral to a dermatologist in the following settings:
    • If the diagnosis of eosinophilic folliculitis needs to be confirmed
    • If the response to treatment is inadequate
    • If the primary care physician is not familiar with the recommended treatment modality
    • If the patient has widespread or severe eosinophilic folliculitis

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

These agents have both anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids have profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.


Prednisone (Deltasone, Orasone, Liquid Pred)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Adult

5-60 mg/d PO

Pediatric

0.05-2 mg/kg/d PO

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Retinoids

These agents decrease cohesiveness of abnormal hyperproliferative keratinocytes and may reduce potential for malignant degeneration. They modulate keratinocyte differentiation. They also reduce the risk of skin cancer in patients who have undergone renal transplant.


Isotretinoin (Accutane)

Retinoid acid derivative reduces size of sebaceous gland and decreases sebum production. Also regulates cell differentiation and proliferation.

Adult

0.5 mg/kg PO divided bid

Pediatric

Not established

Toxicity may occur with vitamin A coadministration; pseudotumor cerebri or papilledema may occur when coadministered with tetracyclines; isotretinoin may reduce plasma levels of carbamazepine

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May decrease night vision; inflammatory bowel disease may occur; may be associated with development of hepatitis; occasional exaggerated healing response of acne lesions (excessive granulation with crusting) may occur; diabetic patients may experience problems in controlling their blood sugar while on isotretinoin; avoid exposure to UV light or sunlight until tolerance achieved; discontinue treatment if rectal bleeding, abdominal pain, or severe diarrhea occur; mood swings or depression may occur; caution if history of depression

Nonsteroidal anti-inflammatory agents (NSAIDs)

These agents have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also exist (eg, inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, various cell-membrane functions).


Indomethacin (Indocin, Indochron ER)

Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.

Adult

75 mg PO divided bid/tid; not to exceed 200 mg

Pediatric

1-2 mg/kg/d PO divided bid; not to exceed 4 mg/kg/d

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; GI bleeding or renal insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, (discontinue with persistent leukopenia, granulocytopenia, or thrombocytopenia)

Antibiotics, sulfone; Leprostatic agents

These agents may improve the clinical stage of the disease.


Dapsone (Avlosulfon)

Bactericidal and bacteriostatic against mycobacteria; mechanism of action is similar to that of sulfonamides in which competitive antagonists of PABA prevent formation of folic acid, thus inhibiting bacterial growth.

Adult

100 mg PO qd

Pediatric

1-2 mg/kg PO qd; not to exceed 100 mg/d

May inhibit anti-inflammatory effects of clofazimine; hematologic reactions may increase with folic acid antagonists, eg, pyrimethamine (monitor for agranulocytosis during the second and third months of therapy); probenecid increases toxicity; trimethoprim with dapsone may increase toxicity of both drugs; because of increase in renal clearance, levels may significantly decrease when administered concurrently with rifampin

Documented hypersensitivity; known G-6-PD deficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform weekly CBC counts (first mo); then perform WBC counts monthly (6 mo); then semiannually; discontinue if significant reduction in platelets, leukocytes, or hematopoiesis is observed; caution in methemoglobin reductase deficiency, G-6-PD deficiency (patients receiving >200 mg/d), or hemoglobin M due to high risk for hemolysis and Heinz body formation; caution in patients exposed to other agents or conditions (eg, infection, diabetic ketosis) capable of producing hemolysis; peripheral neuropathy can occur (rare); phototoxicity may occur when exposed to UV light

More on Eosinophilic Folliculitis

Overview: Eosinophilic Folliculitis
Differential Diagnoses & Workup: Eosinophilic Folliculitis
Treatment & Medication: Eosinophilic Folliculitis
Follow-up: Eosinophilic Folliculitis
Multimedia: Eosinophilic Folliculitis
References
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References

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Further Reading

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Keywords

eosinophilic folliculitis, EF, eosinophilic pustular dermatosis, eosinophilic pustular folliculitis, EPF, Ofuji disease, Ofuji's disease, sterile eosinophilic pustulosis, immunosuppression-associated eosinophilic folliculitis, infancy-associated eosinophilic folliculitis, immunosuppression-associated EF, infancy-associated EF, pediatric eosinophilic folliculitis, infant eosinophilic folliculitis, pediatric EF, infant EF, neonatal eosinophilic folliculitis, neonatal EF, classic eosinophilic folliculitis, classic EF

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Contributor Information and Disclosures

Author

Camila K Janniger, MD, Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, 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)

Rajendra Kapila, MD, MBBS, Professor of Medicine, Department of Medicine, UMDNJ, 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, and Infectious Diseases Society of New Jersey
Disclosure: Nothing to disclose.

M Angelica Selim, MD, Associate Director of Dermatopathology, Departments of Pathology and Internal Medicine, Assistant Professor, Duke University Medical Center
Disclosure: Nothing to disclose.

Christopher R Shea, MD, Professor and Chief, Section of Dermatology, Department of Medicine, University of Chicago
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, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Joseph Richard Masci, MD, Chief of Infectious Diseases, Associate Director, Associate Professor, Department of Internal Medicine, Division of Infectious Diseases, Elmhurst Hospital Center, Mount Sinai School of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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