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Fig 1. Disseminated HSV infection in a patient treatedwith ruxolitinib. Subcutaneous edema of the face, bifrontalscalp ulcerations, and hemorrhagic crusting of theconjunctival, nasal, and oral mucosae.

Fig 2. Disseminated HSV infection in a patient treatedwith ruxolitinib. Necrotizing inflammation with numerousfoci of necrosis in the dermis, confluent epidermal necro-sis, and fibrinopurulent exudate. Arrow indicates viralinclusion within a keratinocyte. Hematoxylin-eosin stain;340.

Reactivation of herpes simplex virus infectionin a patient undergoing ruxolitinib treatment

To the Editor: Ruxolitinib (Jakafi), a selective JAK-1and -2 inhibitor, is the first agent approved by theFood and Drug Administration for myelofibrosis.1

Previously noted side effects include anemia, throm-bocytopenia, and neutropenia. It is also known thatruxolitinib can predispose to serious infections withvaricella zoster virus (VZV).

A 67-year-old African American man was startedon ruxolitinib for treatment of myelodysplastic syn-drome at an outside hospital; he had not previouslyreceived any other immunosuppressants. Four daysafter starting ruxolitinib, swelling, blisters, and painof the oral mucosa developed, followed by involve-ment of the conjunctival, nasal, and genital mucosae.Treatment at the outside hospital consisted ofintravenous antibiotics for presumed angioedemawith bacterial superinfection and methylpredniso-lone for possible Stevens-Johnson syndrome. Hiscondition continued to deteriorate, but becausethere was no dermatology service available at theoutside hospital, a biopsy was not performed. Onemonth later, he presented to us with diffuse erosions,ulcerations, and hemorrhagic crusting of theconjunctival, nasal, oral, and genital mucosae(Fig 1). He was admitted.

Magnetic resonance imaging of the face and orbitsshowed extensive subcutaneous edema with bothenhancing and nonenhancing foci, suggestive oftissue necrosis and pus. A left cheek punch biopsyspecimen showed necrotizing inflammation withnumerous foci of necrosis in the dermis, confluentepidermal necrosis, fibrinopurulent exudate, andscattered viral inclusions characteristic of herpessimplex virus (HSV) in both hair follicles andepidermis (Fig 2). Although a diagnosis of Stevens-Johnson syndrome was not favored, it could not beruled out. Subsequent viral cultures of the lip werepositive for HSV-1, confirming the diagnosis of peri-orificial HSV. The patient was started on acyclovir720 mg intravenously every 8 hours; his conditionnotably and rapidly improved. Within 3 weeks, mostof the skin and mucosae had reepithelialized.Unfortunately, the extensive conjunctival involve-ment led to permanent vision loss in both eyes.

HSV reactivation is often seen in immunocompro-mised patients, such as those with organ transplan-tation, corticosteroid use, or chemotherapy.2 Lesionstypically appear on the lips, posterior pharynx, oral

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mucosa, and perioral skin.3 Furthermore, HSV candisseminate in immunocompromised patients andpresent with visceral involvement, such as HSVhepatitis.4,5 This may be due to impaired T-cell andmacrophage immunity.5 Reactivated HSV often pre-sents with nonspecific findings such as fever, leuko-penia, and elevated aminotransferases. Definitive

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Fig 1. Psoriasis vulgaris. Erythematosquamous lesions onboth lower extremities.

Fig 2. Psoriasis vulgaris. Regression of psoriatic lesionsafter therapy.

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diagnosis can be made with biopsy of mucocuta-neous lesions, polymerase chain reaction, or directantigen assay. Serum serologies and radiographicfindings are typically noncontributory.5

Prompt diagnosis and treatment of HSV reactiva-tion is paramount because disseminated HSV canlead to rapid multisystem organ failure and death.HSV prophylaxis might be considered for patientsstarting ruxolitinib therapy, especially in those with ahistory of infection with human immunodeficiencyvirus. This case underscores the possibility of thisdevastating complication from use of this drug.

Lana X. Tong, BA, Julie Jackson, MD, JustinKerstetter, MD, and Scott D. Worswick, MD

Division of Dermatology, Department of Medicine,David Geffen School of Medicine at the Univer-sity of California, Los Angeles

Funding sources: None.

Conflicts of interest: None declared.

Correspondence to: Scott D. Worswick, MD, Divi-sion of Dermatology, Department of Medicine,David Geffen School of Medicine at UCLA, 200Medical Plaza, Suite 450, Los Angeles, CA 90095

E-mail: sworswick@mednet.ucla.edu

REFERENCES

1. Deisseroth A, Kaminskas E, Grillo J, Chen W, Saber H, Lu HL,

et al. US Food and Drug Administration approval: ruxolitinib

for the treatment of patients with intermediate and high-risk

myelofibrosis. Clin Cancer Res 2012;18:3212.

2. Kaufman B, Gandhi SA, Louie E, Rizzi R, Illei P. Herpes simplex

virus hepatitis: case report and review. Clin Infect Dis 1997;24:

334-8.

3. Zamora MR. DNA Viruses (CMV, EBV, and the herpesviruses).

Semin Respir Crit Care Med 2011;32:454-70.

4. Maalouf E, Moutran R, Maatouk I. Letter: disseminated primary

HSV-2 infection of the face. Dermatol Online J 2012;18:15.

5. Arkin LM, Castelo-Soccio L, Kovarik C. Disseminated herpes

simplex virus (HSV) hepatitis diagnosed by dermatology

evaluation. Int J Dermatol 2009;48:1020-1.

http://dx.doi.org/10.1016/j.jaad.2013.09.035

Management of psoriasis vulgaris and multiplesclerosis with fumaric acid

To the Editor: Psoriasis vulgaris has not only beenassociated with several comorbidities like metabolicsyndrome and cardiovascular disease, but also withneurologic disorders like multiple sclerosis (MS).1

New-onset psoriatic lesions and exacerbations havebeen described after treatment with biologics forMS, mainly interferon-beta (INF-�) as well as withother biologics such as natalizumab.2 INF-� is thefirst-line treatment for clinically isolated syndrome

with the high risk for MS development or forrelapsing-remitting multiple sclerosis (RR-MS).Fumaric acids have been a well-established therapyfor psoriasis vulgaris, mainly in Germany under thetrade name Fumadermea mixture of dimethylfumarate (DMF) and 3 salts of ethyl hydrogenfumarate, with DMF considered to be the activeingredient. In recent years, DMF BG-12 was alsoinvestigated for the treatment of MS. The results ofphase 2 and 3 trials showed successfully reducedrelapse rates and time of disability progression inpatients with MS.3,4

We report a case of a 26-year-old woman inwhom optic neuritis developed. Cerebrospinalfluid contained 9 oligoclonal bands and multifocalhemispheral inflammatory lesions typical of MSwere seen on magnetic resonance imagining(MRI) of the brain. The diagnosis was clinicallyisolated syndrome with a high risk for MS devel-opment. She was initially treated with systemiccorticosteroids and 2 months later INF-� treatmentwas started. Within half a year, an inflammatoryreaction appeared at the site of injection, whichdeveloped into psoriasiform plaque with gradualprogression to generalized psoriatic lesions (Fig 1).