that EBV nuclear antigen 1-specific CD4+ T cells had the capa- bility of exerting immune control over all latently EBV- infected proliferating cells. This could explain the long-term survival in our patient without exacerbation or lymphomagen- esis because of the immunomodulatory role of CD4+ cell infiltration. In conclusion, the current case confirms that HV is an EBV- associated lymphoproliferative disease and that it may undergo an indolent clinical course that may be associated with CD4+ T-cell activation. J-L. X IE G-Y. C HEN Y. J IN X-D. Z HENG X-J. W EI Y-Y. Z HENG S-H. Z HANG Y-N. Z HANG X-J. Z HANG X-G. Z HOU Department of Pathology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China Correspondence: Xiao-Ge Zhou. E-mail: zhouxiaoge59@hotmail.com References 1 Goldgeier MH, Nordlund JJ, Lucky AW et al. Hydroa vacciniforme: diagnosis and therapy. Arch Dermatol 1982; 118:588–91. 2 Verneuil L, Gouarin S, Comoz F et al. Epstein–Barr virus involve- ment in the pathogenesis of hydroa vacciniforme: an assessment of seven adult patients with long-term follow-up. Br J Dermatol 2010; 163:174–82. 3 Iwatsuki K, Satoh M, Yamamoto T et al. Pathogenic link between hydroa vacciniforme and Epstein–Barr virus-associated hematologic disorders. Arch Dermatol 2006; 142:587–95. 4 De Pietro U, Simoni R, Barbieri C, Girolomoni G. Hydroa vaccini- forme persistent in a 60-year-old man. Eur J Dermatol 1999; 9:311– 12. 5 Gupta G, Man I, Kemmett D et al. Hydroa vacciniforme: a clinical and follow-up study of 17 cases. J Am Acad Dermatol 2000; 42:208– 13. 6 Cohen JI, Kimura H, Nakamura S et al. Epstein–Barr virus-associated lymphoproliferative disease in non-immunocompromised hosts: a status report and summary of an international meeting, 8–9 Sep- tember 2008. Ann Oncol 2009; 20:1472–82. 7 Iwatsuki K, Xu Z, Takata M et al. The association of latent Epstein– Barr virus infection with hydroa vacciniforme. Br J Dermatol 1999; 140:715–21. 8 Wu YH, Chen HC, Hsiao PF. Hydroa vacciniforme-like Epstein– Barr virus-associated monoclonal T-lymphoproliferative disorder in a child. Int J Dermatol 2007; 46:1081–6. 9 Iwatsuki K, Ohtsuka M, Harada H et al. Clinicopathologic manifes- tations of Epstein–Barr virus-associated cutaneous lymphoprolifera- tive disorders. Arch Dermatol 1997; 133:1081–6. 10 Cho K-H, Kim C-W, Heo D-S et al. Epstein–Barr virus-associated peripheral T-cell lymphoma in adults with hydroa vacciniforme- like lesions. Clin Exp Dermatol 2001; 26:242–7. 11 Nakata M, Kawasaki A, Azuma M et al. Expression of perforin and cytolytic potential of human peripheral blood lymphocyte sub- populations. Int Immunol 1992; 4:1049–54. 12 Krenacs L, Wellmann A, Sorbara L et al. Cytotoxic cell antigen expression in anaplastic large cell lymphomas of T- and null-cell type and Hodgkin’s disease: evidence for distinct cellular origin. Blood 1997; 89:980–9. 13 Hahn S, Gehri R, Erb P. Mechanism and biological significance of CD4-mediated cytotoxicity. Immunol Rev 1995; 146:57–79. 14 Heller K, Upshaw J, Seyoum B et al. Distinct memory CD4+ T-cell subsets mediate immune recognition of Epstein Barr virus nuclear antigen 1 in healthy virus carriers. Blood 2007; 109:1138–46. Funding sources: none. Conflicts of interest: none declared. Evaluation of Bowen disease by in vivo reflectance confocal microscopy DOI: 10.1111/j.1365-2133.2011.10563.x MADAM, Bowen disease (BD) is a form of epidermal carcinoma in situ, characterized histologically by proliferation of atypical, pleomorphic keratinocytes involving the whole epidermis. Dyskeratotic, mitotic and multinucleated cells frequently occur. 1 Clinically, BD should be differentiated from other non- melanoma skin cancers (NMSC) and from inflammatory dermatoses such as eczema or psoriasis. Although BD develops as an in situ carcinoma, it may progress into invasive squamous cell carcinoma (SCC) in 3–5% of cases, 2 with a potential risk for metastasis of up to 10%. 3 Dermatoscopy has been applied as an adjunct imaging technique for the diagnosis of pig- mented and nonpigmented BD, showing a peculiar dermato- scopic pattern characterized by glomerular vessels and a scaly surface in 100% and 90% of cases, respectively. 4 However, the diagnosis of BD is usually based on histological examina- tion of a skin biopsy. In vivo reflectance confocal microscopy (RCM) is a novel noninvasive diagnostic tool that has recently been applied for the evaluation of various skin diseases, including actinic keratosis, basal cell carcinoma and psoriasis. Here we report the RCM features of BD and correlate them to the corresponding histological features. Ten cases of BD (six male ⁄ four female) were studied. Approval was obtained by the local ethics committee of the Charite ´ Universita ¨tsmedizin Berlin, and written informed con- sent was obtained from each patient. All research was con- ducted according to the declaration of Helsinki principles. RCM evaluation was performed using a commercially available system (Vivascope 1500 Ò ; Mavig GmbH, Munich, Germany; Lucid-Tech Inc., Henrietta, NY, U.S.A.). A detailed description of the technique and the device used has been published pre- viously. 5–7 RCM imaging revealed superficial epidermal disruption in all cases, with single, detached and nucleated keratinocytes (n = 9), corresponding to parakeratosis. Neutrophils within the stratum corneum were detected in seven of 10 cases. At the granular ⁄ spinous layers of the epidermis all cases showed an atypical honeycomb pattern with great variations in cell and nuclear morphology. Remarkably, the atypical honeycomb pattern extended to the whole thickness of the epidermis, as Ó 2011 The Authors BJD Ó 2011 British Association of Dermatologists 2012 166, pp440–469 Correspondence 451