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Sweet Syndrome Induced by Oral Acetaminophen-Codeine Following Repair of a Facial Fracture

Cutis. 2017 September;100(3):E20-E23
October 4, 2017|Cutis
Laurence M. Bradley, MD;Shauna P. Higgins, MD;Monee M. Thomas, MD;Ife J. Rodney, MD;Rebat M. Halder, MD
Author and Disclosure Information

Drs. Bradley, Thomas, Rodney, and Halder are from the Department of Dermatology, Howard University Hospital, Washington, DC. Dr. Higgins is from the Department of Dermatology, Keck School of Medicine of the University of Southern California, Los Angeles.

The authors report no conflict of interest.

Correspondence: Laurence M. Bradley, MD, Howard University Hospital, Department of Dermatology, Ste 2107, 2041 Georgia Ave NW, Washington, DC (lmbradley@huhosp.org).

Sweet syndrome (SS), also known as acute febrile neutrophilic dermatosis, is an uncommon condition that is clinically characterized by painful, well-demarcated, indurated, erythematous plaques or nodules that typically favor the head, neck, and arms, and are accompanied by fever. The disease is divided into several categories based on the underlying etiology, with the drug-induced variant comprising a rising number of the total cases and being reported in association with an increasing number of medications. We report a rare case of SS induced by an oral acetaminophen-codeine suspension and tablets. The importance of this case lies in the ability to educate both physicians and pharmacists alike regarding a newly recognized cutaneous adverse effect of acetaminophen-codeine so that the medication may be discontinued or substituted upon recognition of this adverse reaction to decrease patient morbidity.

Practice Points

  • The rate of medication-induced Sweet syndrome is on the rise.
  • Oral acetaminophen-codeine may induce Sweet syndrome.

Comment

Although SS itself is relatively rare, there has been an increasing incidence of the drug-induced subtype, most often in association with use of granulocyte colony-stimulating factor and granulocyte monocyte-stimulating factor. There also have been reported associations with a growing number of medications that include antibiotics, antiepileptic drugs, furosemide, hydralazine, and all-trans retinoic acid.11-19 Moghimi et al11 also reported an association with antivirals, cancer biotherapies, nonsteroidal anti-inflammatory drugs, psychotropes, azathioprine, oral contraceptives, and propylthiouracil.10,20-26 Moghimi et al11 further reported an association with several vaccines.

Several therapies for advanced melanoma also have been reviewed in the literature, including ipilimumab and vemurafenib,27-30 as have several medications for the treatment of myelodysplastic syndrome including azacitidine.31,32 A severe episode of drug-induced SS, predominantly on the legs, has been reported in association with lenalidomide, an immunomodulatory agent used in the treatment of myelodysplastic syndrome.33

Additional medications more recently involved in the pathogenesis of drug-induced SS include the chemotherapeutic agents topetecan, mitoxantrone, gemcitabine, and vorinostat.34-37 The antimalarial medication chloroquine also has been implicated, as have selective cyclooxygenase-2 inhibitors, hypomethylating agents, the tumor necrosis factor inhibitor adalimumab, IL-2 therapies, aripiprazole, and several other medications.38-49

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Despite drug-induced SS being reported in association with an increasing number of medications, there had been a lack of appropriate diagnostic criteria. To that end, Walker and Cohen50 proposed 5 specific diagnostic criteria in 1996, including abrupt onset of painful erythematous plaques or nodules, histopathologic evidence of a dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis, pyrexia (temperature >38°C), temporal relationship between drug ingestion and clinical presentation or temporally related recurrence after oral rechallenge, and temporally related resolution of lesions after drug withdrawal or treatment with systemic corticosteroids.50,51 Our patient met all of these criteria.

Conclusion

The number of cases of drug-induced SS in the literature continues to climb; however, the association with acetaminophen-codeine is unique. The importance of this case lies in educating both physicians and pharmacists alike regarding a newly recognized adverse effect of acetaminophen-codeine. Because acetaminophen-codeine often is used for its analgesic properties, and the predominant symptom of the cutaneous eruption of SS is pain, the therapeutic value of acetaminophen-codeine is substantially diminished in acetaminophen-codeine–induced SS. Accordingly, in these cases, the medication may be discontinued or substituted upon recognition of this adverse reaction to reduce patient morbidity.

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