Letters to the Editor

of paramount importance, since a typical PR may develop during but independently from a therapy. In such a case, the drug (if indispensable for the health of the patient) may be cautiously continued, whereas in the case of PR-like eruptions it is preferable to withdraw the drug promptly lest more dangerous drug reactions develop. We are pleased to reply that in our experience the distinguishing criteria can exist. We studied 15 patients with PR-like eruptions from clinical, histopathologic and virologic points of view. None of these patients were taking immunosuppressive drugs or tumor necrosis factor-a (TNF-a). We found that in PR-like eruptions the lesions are more itchy, diffuse and confluent than in typical PR and the mucous membranes can be involved. There is not the herald patch and the patients never experience the prodromal symptoms, which are present approximately in 69% of typical PR.2 In addition, patients with PR-like eruption may have blood eosinophilia and their histopathology usually disclose eosinophils in the dermis, epidermal necrotic keratinocytes and junctional vacuolar degeneration. Lastly, there are no signs of HHV-6 and HHV-7 systemic reactivation in plasma and blood mononuclear cells that are usually present in typical PR.3 In fact PR has been ascribed to a HHV-6 and/or HHV-7 systemic reactivation. Opportunistic viral reactivation are a well-recognized complication of anti-TNFa therapy and cases of severe herpes virus reactivation have been described.4 In the patient described by Ohtsuka1, an HHV-6 and/or HHV-7 reactivation may be hypothesized causing the onset of typical PR. In this, as in other cases5 of typical PR described in the literature, the therapy can usually be continued under close surveillance of

the patient’s eruption and general condition. In conclusion, the clinical, histopathologic and virologic investigations may definitely help to distinguish typical PR from PR-like eruptions, even taking into account that virologic investigations are less likely to be performed routinely.

CONFLICT OF INTEREST:

None.

Francesco DRAGO, Giulia CICCARESE, Alfredo REBORA, Aurora PARODI DISSAL, Section of Dermatology, IRCCS Azienda Universitaria Ospedaliera San Martino-IST, Genoa 16132, Italy doi: 10.1111/1346-8138.12562

REFERENCES 1 Ohtsuka T. Pityriasis rosea-like arranged eruption after infliximab therapy in a patient with psoriasis vulgaris. J Dermatol 2014; 41: 354–355. 2 Drago F, Broccolo F, Rebora A. Pityriasis rosea: an update with a critical appraisal of its possible herpesviral etiology. J Am Acad Dermatol 2009; 61: 303–318. 3 Broccolo F, Drago F, Careddu AM et al. Additional evidence that pityriasis rosea is associated with reactivation of human herpesvirus-6 and -7. J Invest Dermatol 2005; 124: 1234–1240. 4 Ma C, Walters B, Fedorak RN. Varicella Zoster meningitis complicating combined anti-tumor necrosis factor and corticosteroid therapy in Crohn’s disease. World J Gastroenterol 2013; 19: 3347–3351. 5 Raipara SN, Ormerod AD, Gallaway L. Adalimumab-induced pityriasis rosea. J Eur Acad Dermatol Venereol 2007; 21: 1294–1296.

Reply to a letter from Dr Drago Dear Editor, Thank you for the interest of Dr Drago et al. to a letter about pityriasis rosea (PR)-like arranged eruption after infliximab therapy. They raised the question whether it is possible to distinguish between PR and PR-like eruption. They concluded that the clinical, histopathologic and virologic investigations might definitely help to distinguish typical PR from PR-like eruptions. They found that there were no signs of HHV-6 and HHV-7 systemic reactivation in plasma and blood mononuclear cells. In the case presented in the letter, histological examination showed no eosinophils in the dermis. Retrospectively studied HHV-6 and HHV-7 in plasma showed no systemic reactivation. Accordingly, PR-like eruption observed showed similarity in clinical symptoms, and in no HHV-6 and HHV-7 systemic reactivation. However, histological findings were different in that no eosinophil was observed. The clinical, histopathologic and virologic investigations may help to distinguish typical PR from PR-like eruptions, however, further studies should be done to make a definite conclusion.

A study investigated the short-term effect of infliximab on reactivation of several harmful latent viruses.1 All patients were negative for HHV-6, -7, and -8 at all time points. Another study analyzed the risk of reactivation of lymphotropic herpes viruses in rheumatoid arthritis treated with TNF-alpha agent.2 Viral reactivation related to infliximab treatment was not observed. Accordingly, infliximab treatment does not induce replication of human lymphotropic herpes viruses. A study described paradoxical clinical response cases, conducted a comprehensive analysis of the literature, explored possible immunologic mechanisms of action of this perplexing reaction, and recommended management options.3 The study concluded that TNF antagonist-induced psoriasis is a newly recognized adverse effect of these medications that typically does not require therapy cessation. Another study pointed out that genomic studies of affected patients may assist with identification of predisposed patients and elucidation of the molecular trigger of this perplexing response.4

Correspondence: Tsutomu Ohtsuka, M.D., Ph.D., Department of Dermatology, International University of Health and Welfare Hospital, 537-3, Iguchi Nasushiobara, Tochigi 329-2763, Japan. Email: [email protected]

© 2014 Japanese Dermatological Association

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Letters to the Editor

CONFLICT OF INTEREST:

None.

Tsutomu OHTSUKA Department of Dermatology, International University of Health and Welfare Hospital, Nasushiobara, Japan doi: 10.1111/1346-8138.12561

REFERENCES

 n JJ, Castro MC, Pe rez V, 2 Torre-Cisneros J, Del Castillo M, Casto Collantes E. Infliximab does not activate replication of lymphotropic herpesviruses in patients with refractory rheumatoid arthritis. Rheumatology (Oxford) 2005; 44: 1132–5113. 3 Collamer AN, Guerrero KT, Henning JS, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum 2008; 59: 996–1001. 4 Collamer AN, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: clinical features and possible immunopathogenesis. Semin Arthritis Rheum 2010; 40: 233–240.

1 Lavagna A, Bergallo M, Daperno M et al. Infliximab and the risk of latent viruses reactivation in active Crohn’s disease. Inflamm Bowel Dis 2007; 13: 896–902.

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© 2014 Japanese Dermatological Association

Reply to a letter from Dr Drago.

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