eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses

Acute Febrile Neutrophilic Dermatosis: Treatment & Medication

Author: Yoon-Soo Bae-Harboe, MD, General Surgery Intern, New York-Presbyterian Hospital of Weill Cornell Medical College
Coauthor(s): Sharon A Salter, MD, Staff Physician, Department of Psychiatry, Tufts-New England Medical Center; Alexa F Boer Kimball, MD, MPH, Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Jul 31, 2009

Treatment

Medical Care

  • In most cases of acute febrile neutrophilic dermatosis (Sweet syndrome), prednisone is extremely and rapidly effective, in doses of 1 mg/kg/d.1,40
    • Pulmonary infiltrates also tend to respond promptly to prednisone.25
    • However, despite the initial excellent response, recurrences of neutrophilic dermatitis are common and generally develop as steroid use is being tapered. If the underlying disease flares, it may take longer to effectively taper therapy.1
    • High-potency topical steroids (eg, clobetasol propionate 0.05%) or intralesional glucocorticoids (eg, triamcinolone acetonide 3.0-10 mg/mL) may also be useful in localized lesions.4
  • For long-term management, numerous drugs may be helpful. Many of the medications work by inhibiting neutrophil chemotaxis, but none have been shown to be better than corticosteroids.1,4
    • Indomethacin, colchicine, and potassium iodide were helpful in small series of patients.1,62,63
    • Dapsone, cyclosporine, etretinate, pentoxifylline, and clofazimine also have been used, with anecdotal success.1,37,40,64
    • Doxycycline, metronidazole, isotretinoin, methotrexate, cyclophosphamide, chlorambucil, adalimumab, infliximab, intravenous immunoglobulin (IVIG), pulse doses of methylprednisolone, and interferon alfa are also reportedly successful.1,37,40,64,65,66
  • If an underlying cause can be identified, it should be treated, eg, by means of resection of solid tumors, treatment of infections, and discontinuation of causative medication. Successful therapy of the underlying disorder may promote resolution of Sweet syndrome and prevent recurrences.3,4
  • Etanercept has been reported to control the skin manifestations of Sweet syndrome in a small case series of rheumatoid arthritis patients.67
  • In the pediatric population, long-term use of corticosteroids can cause problems with linear growth, blood pressure, and blood glucose levels. Children may also have social sequelae associated with their use. Therefore, attempts are usually made to treat children with steroid-sparing drugs.13

Consultations

  • Consultation with a dermatologist is indicated for the diagnosis and evaluation of underlying causes of acute febrile neutrophilic dermatosis (Sweet syndrome).
  • An internal medicine specialist may be consulted to evaluate any underlying or triggering diseases.

Medication

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

Corticosteroids

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.


Prednisone (Deltasone)

Useful in acute neutrophilic dermatitis because of its anti-inflammatory properties. Must be metabolized to the active metabolite prednisolone for effect. Conversion may be impaired in those with liver disease.

Adult

1 mg/kg/d qd; taper slowly over 4-6 wk to 10 mg/d (tapering may decrease adverse reactions)

Pediatric

0.5-1.5 mg/kg/d qd or divided bid/qid; taper over 4-6 wk, as symptoms resolve

Coadministration with estrogens may decrease clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase the metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics; coadministration with ritonavir may significantly increase serum concentrations of prednisone; concomitant therapy with montelukast may result in severe peripheral edema; clarithromycin may increase risk of psychotic symptoms
Postmarketing surveillance reports indicate that risk of tendon rupture may be increased in patients receiving concomitant fluoroquinolones and corticosteroids, especially elderly patients; administration of asparaginase concurrently with or before prednisone therapy may result in increased toxicity

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

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

May unmask hypertension or diabetes or exacerbate peptic ulcer disease and tuberculosis; long-term sequelae associated with long-term steroid use include osteoporosis, cataracts, and pituitary-hypothalamic axis suppression; with high doses, patients may develop a steroid psychosis and are at increased risk of infections, particularly when oral steroids are used in conjunction with other immunosuppressants; frequently monitor patient's blood sugar level, blood pressure, and weight; monitor for Cushing syndrome

Anti-inflammatories

These agents modulate events leading to inflammatory reactions.


Dapsone (Avlosulfon)

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

Adult

100-200 mg/d qd; may use as monotherapy or in combination therapy

Pediatric

0.5 mg/kg/d; can increase to 2 mg/kg

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

Documented hypersensitivity; known G-6-PD deficiency (assay for G-6-PD activity prior to initiation of therapy)

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

Associated with a variety of systemic toxicities, including agranulocytosis, anemia, methemoglobinemia, hepatitis, and neuropathy; patients may experience headache and/or GI distress on initiation of therapy
Perform weekly blood counts (first mo), then monthly WBC counts (6 mo), then semiannual WBC counts; discontinue if a significant reduction in platelets, leukocytes, or hematopoiesis occurs; caution in methemoglobin reductase deficiency, G-6-PD deficiency, or hemoglobin M because of 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; pancreatitis may occur; various forms of renal complications including acute renal failure, acute tubular necrosis, and oliguria have occurred with dapsone use


Colchicine

Decreases leukocyte motility and phagocytosis in inflammatory responses. Has effects against neutrophils, which are probably involved in expression of cutaneous vasculitis; has been demonstrated to be steroid-sparing in open-label studies. The only double-blinded placebo-controlled trial failed to demonstrate its efficacy; however, several methodological errors occurred in this study. Not FDA approved in children.

Adult

0.6 mg/d PO

Pediatric

Not established

Sympathomimetic agent toxicity and effect of CNS and bone marrow depressants are significantly increased with colchicine; clarithromycin may cause significant increases in colchicine serum concentrations; may increase cyclosporine levels when concomitantly administered with colchicine

Documented hypersensitivity; severe renal, hepatic, GI, or cardiac disorders; blood dyscrasias

Pregnancy

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

Precautions

Risk of renal failure, hepatic failure, permanent hair loss, bone marrow suppression, numbness or tingling in hands and feet, disseminated intravascular coagulopathy, and decreased sperm count; may cause nausea, diarrhea, vomiting, or abdominal pain approximately 8-12 h after PO administration in 80% of patients, especially when maximal doses used (discontinue use at onset of gastrointestinal intolerance); may cause myopathy and myoneuropathy

More on Acute Febrile Neutrophilic Dermatosis

Overview: Acute Febrile Neutrophilic Dermatosis
Differential Diagnoses & Workup: Acute Febrile Neutrophilic Dermatosis
Treatment & Medication: Acute Febrile Neutrophilic Dermatosis
Follow-up: Acute Febrile Neutrophilic Dermatosis
Multimedia: Acute Febrile Neutrophilic Dermatosis
References
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References

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Further Reading

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Keywords

acute febrile neutrophilic dermatosis, Sweet syndrome, Sweet disease, Sweet's syndrome, Sweet's disease, neutrophilic dermatitis, Gomm-Button disease, granulocyte colony-stimulating factor, G-CSF

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Contributor Information and Disclosures

Author

Yoon-Soo Bae-Harboe, MD, General Surgery Intern, New York-Presbyterian Hospital of Weill Cornell Medical College
Yoon-Soo Bae-Harboe, MD is a member of the following medical societies: American Medical Student Association/Foundation
Disclosure: Nothing to disclose.

Coauthor(s)

Sharon A Salter, MD, Staff Physician, Department of Psychiatry, Tufts-New England Medical Center
Sharon A Salter, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Obstetricians and Gynecologists
Disclosure: Nothing to disclose.

Alexa F Boer Kimball, MD, MPH, Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital
Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Timothy McCalmont, MD, Director, UCSF Dermatopathology Service, Professor of Clinical Pathology and Dermatology, Departments of Pathology and Dermatology, University of California at San Francisco
Timothy McCalmont, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society of Dermatopathology, California Medical Association, College of American Pathologists, and United States and Canadian Academy of Pathology
Disclosure: Apsara Consulting fee Independent contractor

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Rosalie Elenitsas, MD, Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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