Abstract Background.—Primary cutaneous T-cell–rich B-cell lymphoma is a relatively rare entity that has been diagnosed most commonly using immunohistochemical and molecular techniques. Flow cytometric immunophenotyping (FCI) has not been described in this entity. We report the demonstration of B-cell monoclonality by FCI in 3 cases of primary cutaneous T-cell–rich B-cell lymphoma. Methods.—Clinical and pathologic data were recorded for 3 cases of primary cutaneous T-cell–rich B-cell lymphoma. Immunohistochemical and FCI data were available in all cases; DNA analysis was performed in 1 case. Results.—Flow cytometric immunophenotyping revealed a monoclonal B-cell population exclusively in the monocyte (large cell) region in all 3 cases. Immunohistochemistry confirmed the T-cell richness of the infiltrates within the cutaneous lymphomas; T cells accounted for 65% to greater than 90% of the cells within the infiltrates. DNA analysis by polymerase chain reaction in 1 case did not demonstrate a monoclonal rearrangement of the immunoglobulin heavy-chain gene. Conclusions.—Flow cytometric immunophenotyping in primary cutaneous T-cell–rich B-cell lymphoma may be useful in demonstrating monoclonality in these cases, especially if there is selective gating on the relatively small population of cells in the large cell region. The FCI data should be correlated with histology and immunohistochemistry.
To compare Tzanck smears, viral cultures, and DNA diagnostic methods using the polymerase chain reaction (PCR) in detection of herpes simplex virus (HSV) or varicella-zoster virus (VZV) infection in clinically suspected cases.A 12-month trial comparing PCR with viral cultures and Tzanck smears in patients with clinically suspected HSV or VZV infection.Both ambulatory and hospitalized patients were recruited from a tertiary referral center and the Miami (Fla) Veterans Affairs Medical Center.Convenience samples of patients clinically suspected to have HSV (n = 48) or VZV (n = 35). To be included in the final analysis patients needed to have a positive Tzanck smear, viral culture, or PCR result. Patients who were clinically suspected to have HSV but had VZV by viral culture or PCR were analyzed in the VZV group. Similarly, patients who were clinically suspected to have VZV, but had HSV by viral culture or PCR were analyzed in the HSV group. Seventy-seven patients were available for final analysis: HSV (n = 30), VZV (n = 32), and 15 control cases who did not have evidence of viral infection.For HSV, PCR detected HSV DNA sequences in 73% of stained smears and 83% of unstained smears. For VZV infection, VZV DNA sequences were detected in 88% of stained smears and 97% of unstained smears. Viral DNA sequences were not detected in the 15 control cases. Viral cultures were positive in 83% and 44% of HSV and VZV cases, respectively. The Tzanck smear was positive in 60% and 75% of HSV and VZV cases, respectively.PCR is a reliable method for detecting HSV and VZV DNA sequences from single stained and unstained Tzanck smears. It is clearly superior to viral culture in identifying VZV infection and is equivalent to conventional culture techniques in identifying cases of HSV.
A 31-year-old man had a 4-year history of severe pemphigus vulgaris confirmed by histologic examination and direct and indirect immunofluorescence. His disease had been resistant to maximal doses and varying combinations of prednisone, oral gold, cyclosporine,methotrexate, azathioprine, pulse steroids, and pulse cyclophosphamide with methylprednisolone. Many adverse effects complicated his medical therapy, including renal insufficiency, hypertension, and a cushingoid appearance. At the time of initiation of photopheresis the patient had pemphigus lesions on 70% of his body surface (Fig. I). His treatment regimen included intramuscular methotrexate 20 mg weekly, azathioprine 100 mg daily, and oral prednisone 240 mg daily. He had been taking these medications for I month after failing to respond to monthly (eight) pulses of cyclophosphamide and methylprednisolone. Photopheresis was started with treatments on two consecutive days every 2 weeks. By the seventh cycle new blister formation had ceased and treatment frequency was reduced to every 3 weeks. His medications were slowly tapered with a greater than 80% reduction in his daily prednisone, discontinuation of methotrexate, and maintenance of azathioprine and gold at pretreatment doses. The patient tolerated photopheresis without complications and eventually all skin lesions healed with the exception of a few crusted erosionson his face (Fig. 2). Although the patient had one episode of a disseminated cutaneous herpetic infection that required intravenous acyclovir, he had had
Three patients, one healthy and two immunocompromised, developed cutaneous reactions that histologically mimicked granuloma annulare at sites of resolved varicella-zoster virus (VZV) reactivation infections. Variable latency periods between the infection and the granulomatous reaction were noted. As in other case reports, the presence of VZV DNA in these lesions was inconsistently demonstrated by the polymerase chain reaction (PCR) and appears more common in early, as opposed to late, post-zoster granulomas. In addition to various granulomatous reactions, vasculitic and neoplastic eruptions following resolved VZV infections have been described and are reviewed here. Therapeutically, topical, intralesional and systemic corticosteroids, as well as acyclovir, have been tried with inconsistent results. Although the pathogenesis remains unclear, the presence of VZV DNA in early lesions that histologically do not display viral cytopathic changes, suggests the virus induces an atypical delayed hypersensitivity reaction not affected by antiviral therapy.
