Case Report
A 49-year-old female was referred to us with a 4-day history of cutaneous manifestations on the trunk and extremities. The patient had been diagnosed with systemic lupus erythematosus (SLE) 2 months earlier according to the European League Against Rheumatism and the American College of Rheumatology (2019) criteria 6 and remained hospitalized. SLE was controlled well by a treatment with prednisolone at 0.7 mg/kg/day, mycophenolate mofetil at 2,000 mg/day, and hydroxychloroquine at 200 and 400 mg on alternate days. Four days before presentation, the patient developed red papules on the right lower jaw. Two days before, dyspnea with pyrexia occurred and, thus, the administration of oxygen was initiated. In the first visit, the eruptions became vesicles, which spread over the body (Figure 1 ). The Tzanck test and immunochromatography to detect VZV antigens (DermaQuick VZV; Marho, Osaka, Japan) for vesicles were both positive. In blood tests, VZV-specific IgM and VZV-specific IgG examined using enzyme-linked immunosorbent assays (ELISA) were 0.38 (negative range, <0.8) and <2.0 (negative range, <2.0), respectively, while a CMV antigen-detecting test using the C7 horseradish peroxidase method was positive (4 positive cells per 50,000 white blood cells). Bilateral ground-glass opacities were observed on chest computed tomography (CT) (Figure 2 ).
A histopathological examination revealed intraepidermal blisters with large multinucleated giant cells and intranuclear inclusion bodies (Figure 3a ). There were no vascular changes in the dermis, such as endothelial swelling suggestive of CMV infection, the so-called owl’s eye sign. An immunohistochemical examination of vesicle tissue showed VZV antigens in keratinocytes on the adjacent side of blisters (Figure 3b ), but failed to detect CMV antigens. Based on these findings, we diagnosed the patient with adult varicella due to primary VZV infection and CMV pneumonia. We administered acyclovir (ACV) at 10 mg/kg/day and added a dose of valganciclovir (VGCV) at 1,800 mg/day.
Eight days after the first visit, vesicles became crusted through the administration of ACV and ELISA for VZV-specific IgM and IgG were 1.50 and 52.6, respectively. Fourteen days later, ELISA for VZV-specific IgM and IgG were 1.25 and 1,080, respectively. Eighteen days later, the attenuation of dyspnea was noted and, thus, oxygen inhalation and VGCV were stopped.