Herpes zoster occurring as a solitary vesicular in malignant lymphoma

ARTICLE

Auteur(s) : Natsuko Ishida, Daisuke Watanabe, Tomoe Kuhara, Hiromichi Takama, Yasuhiko Tamada, Yoshinari Matsumoto

Department of Dermatology, Aichi medical University, Nagakute, Aichi, 480-1195 Japan

Herpes zoster is caused by the reactivation of varicella zoster virus (VZV) from the nerve cell body in the sensory ganglia. It predominantly affects immunocompromised people or those receiving immunosuppressive drugs as well as elderly people [1]. Usually, the clinical feature of herpes zoster is painful vesicular affecting a single dermatome. However, atypical clinical presentations are sometimes observed in immunosuppressed patients and transplant recipients [2]. We report a case of solitary herpes zoster in non-Hodgkin lymphoma patient.

A 72-year-old Japanese male who was receiving chemotherapy with rituximab for a non-Hodgkin B cell lymphoma (Mantle cell lymphoma, stage IV), presented with a painless necrotic vesicular on his right femur. The lesion was accompanied by red halo of 15 mm diameter (figures 1A,B). He had a history of recurrent varicella two years previously, after receiving chemotherapy for 5 months. Tzanck test revealed multinucleated giant cells. A clinical diagnosis of herpes simplex virus (HSV) infection was made. A biopsy specimen from the lesion showed multinucleated giant cells with a ground-glass appearance of nuclei within hair follicles (figures 2A,B) and the eccrine gland (figure 2D) The epidermis was peeled off during biopsy. Immunohistochemical staining for VZV was positive in the same area (figures 2C,E). No HSV antigen was detected. PCR analysis from vesicular fluid exhibited a positive band for VZV, but negative for HSV (data not shown). Serum anti-VZV IgM and IgG titer was 0.19 and 3.8. Antiviral treatment was started with 3000 mg of daily valacyclovir for 3 weeks, but the lesion remained (figure 1C). VZV-DNA was still positive from fluid of the lesion. Then external application with vidarabin ointment was added. At day 40, the lesion was healed and VZV-DNA was no longer detected (figure 1D). Serum anti-VZV IgM and IgG titer at this time was 0.18 and 6.5.

Cutaneous eruptions caused by HSV1/2 and VZV represent common dermatoses. In most cases, a correct diagnosis can be made by those characteristic clinical features. But in some cases, especially in patients with immunosuppression or with hematopoietic disorders, cutaneous herpes infections can present with atypical clinical presentations [1, 2]. It is also well known that HSV and VZV affect not only the epidermal keratinocytes but also epithelial structures of the adnexa. These involvements of the hair follicles and the eccrine glands by herpesvirus infection are called herpes folliculitis or herpetic sycosis. Herpes folliculitis is much more commonly seen in VZV infections. Clinically, it often lacks vesicles or pustules. Histopathological features of herpes folliculitis often lack ballooning, multinucleated giant cells, but have dense lymphoid infiltrates simulating malignant lymphoma [3]. Herpetic sycosis is a rare manifestation of VZV infection in HIV or Hodgkin disease patients. In herpetic sycosis, epidermal damage by herpetic infection was noted concomitantly with the eccrine involvement [4].

To date, there are only two cases presenting solitary lesions by herpes zoster. One is a painful nodule on the index finger of a healthy woman showing intraepidermal blisters [5]. Histopathologically, the lesion shows intraepidermal blisters containing degenerated keratinocytes and multinucleated giant cells. Another case is herpetic sycosis without epidermal damage in a Burkitt lymphoma patient [6]. In our case, atypical herpes zoster presented as a solitary vesicular lesion, and histopathologically, VZV infection was observed both in epithelial cells and hair follicles. It was also interesting that the skin lesion in our case was persistent in spite of antiviral treatment and that the anti-VZV antibody titer was not elevated. Hematopoietic disorder and anti-CD20 antibody therapy might be the reason why such an atypical lesion occurred in this case.

Acknowledgements

References

2 Ahmed AM, Brantley JS, Madkan V, Mendoza N, Tyring SK. Managing herpes zoster in immunocompromised patients. Herpes 2007; 14: 32-6.

3 Böer A, Herder N, Winter K, Falk T. Herpes folliculitis: clinical, histopathological, and molecular pathologic observations. Br J Dermatol 2006; 154: 743-6.

4 Sangueza OP, Gordon MD, White Jr. CR. Subtle clues to the diagnosis of the herpesvirus by light microscopy. Herpetic syringitis. Am J Dermatopathol 1995; 17: 163-8.

5 Izu K, Yamamoto O, Yasumoto S, Hashimoto T, Sata T, Tokura Y. Herpes zoster occurring as a solitary nodule on the index finger. Br J Dermatol 2004; 150: 365-6.

6 Alonso-Pérez A, Fraga J, Delgado Y, Aragüés M, Nam-Cha S, García-Díez A. Nodular herpes zoster with herpetic syringitis and no epidermal involvement in a patient with Burkitt lymphoma. Am J Dermatopathol 2006; 28: 194-6.