No abstract

Hepatitis C virus (HCV) is the main cause of parenterally transmitted non-A, non-B viral hepatitis. In recent years, a significant association between lichen planus and chronic HCV infection has been reported. Anti-HCV antibody status was evaluated by ELISA in 54 patients with lichen planus and 54 patients with minor dermatological disorders. PCR was used to examine HCV RNA from serum and lesional and nonlesional cutaneous biopsy samples of HCV-infected patients. Seven patients with lichen planus (12.9%) and two patients in the control group (3.7%) were anti-HCV antibody positive. Five out of seven patients with anti-HCV antibodies had demonstrable HCV RNA in lesional skin biopsies. The viral RNA was absent in three out of four patients with lichen planus whose serum samples were positive for HCV RNA and agreed to biopsy of nonlesional skin. The prevalence of HCV infection is not increased in Turkish patients with lichen planus. However our findings suggest that the virus may play a potential pathogenic role by replicating in cutaneous tissue and triggering lichen planus in genetically susceptible HCV-infected patients.

Objective: To describe the clinical presentations, laboratory findings, prevalence and pattern of complications and the response to treatment of brucellosis in a 12-year period in a Turkish research hospital. Materials and Methods: Between 1996 and 2008, 231 patients were diagnosed with brucellosis and treated in our clinic. Medical records of 189 of the 231 patients with at least one demonstrable complication of the disease were reviewed for anamnesis, diagnosis, complications, treatment and clinical outcomes. Results: The decreasing order of the complications was: hematological, 104 (55%); osteoarticular, 70 (37%); hepatobiliary, 59 (31%), and gastrointestinal, 23 (12%). The most common laboratory findings were anemia, lymphomonocytosis, elevated sedimentation rate and C-reactive protein, and elevated aminotransaminases. Conclusion: The hematological, osteoarticular and hepatobiliary manifestations were predominant. Bursitis, synovitis, glomerulonephritis, cutaneous lesion and deep vein thrombosis were the rare complications observed in our study. In clinical practice, brucellosis should be considered in the differential diagnosis in the presence of infrequent complications.

Acinetobacter is a highly resistant microorganism, commonly isolated in intensive and post-operative care units. Although rarely reported, it may constitute 1 of the several causes of early prosthetic valve endocarditis. A diffuse, red maculopapular rash may be encountered in patients with Acinetobacter endocarditis. Here we present a case of early prosthetic valve endocarditis due to Acinetobacter baumannii and accompanied by a cutaneous eruption.

2a-1 ) 5¢ CTG GTC AGC TTT CGG TAC GA 3¢ , and (HSV Sir, gB 2a-2 ) 5¢ CAG GTC GTG CAG CTG GTT GC 3¢ . These Human herpesvirus 8 ( HHV-8) is the most recent putatprimers have been amplifying both types of HSV, namely types I and II. As a positive control specimen, cerebrospinal ive human herpesvirus. Evidence was obtained using uid of a patient with a clinical and serologically proven HSV molecular biology techniques (1). Speci c DNA encephalitis was used.sequences were rst identi ed in 1994 by Chang et al.(2) in Kaposi's sarcoma tissues from patients with AIDS using the representational diVerence analysis technique.RESULTS AND DISCUSSION In the vast majority of cases, HHV-8 DNA sequences can be shown by polymerase chain reaction (PCR) in Using PCR, we were able to amplify DNA speci c for classical, endemic, iatrogenic and AIDS-associated HSV from 16 of 50 MF patients ( 32%). Thirteen out of Kaposi's sarcoma (1). HHV-8 is also lymphotrophi c 16 HSV-positive samples were diagnosed as MF erythand has the ability to immortalize cells (3, 4). The virus ematous stage and 3 were MF plaque stage. All samples has been associated with peripheral T-cell lymphomas, lacked HHV-8 DNA by PCR. Neither HSV nor HHV-8 plaque parapsoriasis, lymphomatoid papulosis and cutawas detected in any of the control specimens. The neous T-cell lymphomas (CTCL), including mycosis representative positive PCR results are shown in Figs 1 fungoides (MF ) ( 5-7). Herpes simplex virus (HSV ) and 2. primarily targets epithelial and neural cells rather than HHV-8 is usually together with EBV as a dual infeclymphocytes. However, given the immunologic relationtion in body cavity lymphomas, AIDS-related nonship between T lymphocytes and the epidermis, and the Hodgkin's lymphomas and in non-malignant lymphoid fact that MF often appears to be initiated as a cutaneous lesions ( 10, 11 ). In HIV + patients, EBV and HHV-8 process, a potential role for HSV in the development or associated CTCL have been reported to take anaplastic progression of MF has been suggested (8).large cell morphology (12 ). However, there was no The purpose of this study was to elucidate a potential evidence for the presence of EBV (9) and HHV-8 in role for HHV-8 and HSV in the etiopathogenesis of MF.lesional samples of our patients. This nding is in accordance with that of previous studies (5-7, 13-15 ) revealing the absence of HHV-8 in MF and suggesting MATERIAL AND METHODS that HHV-8 can be excluded from the list of potential etiological factors in MF. Fifty formalin-xed paraYn-embedded samples from lesional skin of 50 Caucasian patients with MF were selected and The presence of both HSV-speci c antigens and HSV retrospectively collected from archival les of the Pathology DNA in lesions of CTCL has been reported previously Department. In a previous study performed in our department, (16, 17). However, no direct association between chronic these biopsy samples have been shown by PCR to be EBV HSV infection and the development of malignant negative (9). In all patients, the skin biopsi...