LETTER TO THE EDITOR

Disseminated Cutaneous Herpes Zoster and Immune Thrombocytopenic Purpura To the Editor: Herpes zoster (HZ) is a clinical syndrome caused by the reactivation of latent varicella-zoster virus (VZV) in the sensory ganglia. Waning of cell-mediated immunity is thought to be one of the causes of VZV reactivation. Most patients will present with a localized vesicular rash in a dermatomal distribution. Disseminated cutaneous HZ is uncommon in the immunocompetent patient, and only a limited number of cases have been described in the literature. In contrast, disseminated cutaneous HZ has a high incidence among immunocompromised patients. Recently, in an effort to identify conditions that can compromise VZV-specific immunity and predispose seemingly immunocompetent patients to disseminated cutaneous HZ, we read with great interest the article by Moquete and colleagues entitled ‘‘Herpes Zoster with Cutaneous Dissemination in a Patient 21 Years after Splenectomy for Idiopathic Thrombocytopenic Purpura’’ published in the Journal of Cutaneous Medicine and Surgery.1 The authors of this article describe a case of a 46-year-old immunocompetent woman with a disseminated cutaneous HZ infection. This patient had a previous medical history of idiopathic thrombocytopenic purpura (ITP). The authors suggested that patients with a history of splenectomy appear to be at increased risk for cutaneous dissemination of HZ, similar to what Manning and colleagues suggested, who reviewed 102 patients with splenectomy for nonmalignant disease.2 Nonetheless, in their study, Manning and colleagues did not find an increased incidence of HZ among splenectomy patents. The only two patients who had disseminated HZ also had a history of ITP, similar to the Moquete and colleagues findings. As no other splenectomized patients without a history of ITP developed disseminated HZ, it is possible that ITP is a risk factor for disseminated HZ and the lack of a spleen is a cofounder. Yu and colleagues suggested that functional defects in regulatory T cells might play a role in the pathogenesis of ITP.3 They also suggested that

diverse mechanisms may play a role in the pathogenesis of ITP. Although the mechanism of reactivation of VZV is not clear, it is possible that in patients with an immunologic condition such as ITP, VZV-specific immunity is affected. The different levels of immunodeficiency may be important in the development of more or less severe HZ disease. We believe that the underlying immune condition was the reason for dissemination rather than the splenectomy itself. We suggest that the term immunocompetent be used with caution in patients with immunologic conditions when referring to HZ infection. Specifically, ITP may affect VZV-specific immunity and predispose to cutaneous dissemination. Additional research is needed to further link these two conditions.

Acknowledgment Financial disclosure of authors and reviewers: None reported. Ivan Chernev West Virginia School of Osteopathic Medicine, Lewisburg, WV, Department of Medicine, Appalachian Regional Healthcare, Beckley, WV Eric Gomez Department of Medicine, Appalachian Regional Healthcare, Beckley, WV

References 1. Moquete RA, Hartman B, Granstein RD. Herpes zoster with cutaneous dissemination in a patient 21 years after splenectomy for idiopathic thrombocytopenic purpura. J Cutan Med Surg 2012;16: 368–71. 2. Manning DM, Luparello FJ, Arena VC Jr. Herpes zoster after splenectomy. A study of patients without malignancy. JAMA 1980; 243:56–8, doi:10.1001/jama.1980.03300270044028. 3. Yu J, Heck S, Patel V, et al. Defective circulating CD25 regulatory T cells in patients with chronic immune thrombocytopenic purpura. Blood 2008;112:1325–8, doi:10.1182/blood-2008-01-135335.

DOI 10.2310/7750.2014.13199 # 2014 Canadian Dermatology Association

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Canadian Dermatology Association | Journal of Cutaneous Medicine and Surgery, Vol 18, No 5 (September/October), 2014: pp 298

Disseminated cutaneous herpes zoster and immune thrombocytopenic purpura.

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