Pitfalls in the diagnosis of thoracic aortic dissection at CT angiography.

Two hundred seventy-five computed tomographic (CT) angiograms of the thoracic aorta were obtained over a period of approximately 4 years in patients with suspected or known aortic dissection. In all cases, unenhanced images were initially obtained, followed by contrast material-enhanced images. A variety of pitfalls were encountered that mimicked aortic dissection. These pitfalls were attributable to technical factors (eg, improper timing of contrast material administration relative to image acquisition); streak artifacts generated by high-attenuation material, high-contrast interfaces, or cardiac motion; periaortic structures (eg, aortic arch branches, mediastinal veins, pericardial recess, thymus, atelectasis, pleural thickening or effusion adjacent to the aorta); aortic wall motion and normal aortic sinuses; aortic variations such as congenital ductus diverticulum and acquired aortic aneurysm with thrombus; and penetrating atherosclerotic ulcer. Although several of these pitfalls are easy to recognize and therefore unlikely to present a diagnostic problem, others are potentially confusing. Familiarity with these common pitfalls, coupled with a knowledge of normal intrathoracic anatomy, will facilitate recognition of true aortic dissection and help avoid misdiagnosis at thoracic aortic CT angiography.

Membrane protein pattern in hereditary spherocytosis in five subjects from north-east Italy obtained by SDS-PAGE using N,N'-diallyltartardiamide.

In the present study we examined five subjects affected by hereditary spherocytosis (three unsplenectomized and two splenectomized), coming from an area in the north-east of Italy where hereditary spherocytosis is an anaemic disease with very low incidence. All patients showed a low degree of spectrin deficiency (14%), detected with sodium dodecyl sulfate polyacrylamide gel electrophoresis. Moreover, when this analysis was performed with N,N'-diallyltartardiamide as cross-linking agent instead of N,N'-methylenbisacrylamide, some unusual bands appeared in the region between proteins 4.2 and 5, the three unsplenectomized and two splenectomized patients showing different patterns. We hypothesise that some alterations of proteins in this region (e.g. the 4.5 or 4.9 bands), possibly due to proteolysis, must have occurred in relation to the disease.

Epstein-Barr virus strains with latent membrane protein-1 deletions: prevalence in the Italian population and high association with human immunodeficiency virus-related Hodgkin's disease.

Six Epstein-Barr virus (EBV)-related lymphoproliferative disorders were investigated to verify whether the EBV strain harbored by neoplastic cells had the same EBNA-2 and latent membrane protein-1 (LMP-1) DNA sequences of the virus carried by normal lymphocytes of the same patients. Within each case, the analysis of neoplastic lymph nodes, reactive lymphadenopathies, and/or EBV+ spontaneous lymphoblastoid cell lines gave concordant results with respect to type-specific EBNA-2 region and LMP-1 gene. In particular, five cases showed the same deletion in the 3' end of the LMP-1 gene in both normal and neoplastic cells. We also determined the prevalence of LMP-1 deletions in a large series of normal peripheral blood mononucleated cells (PBMCs) from Italian individuals. The analysis showed that 50% (9 of 18) of PBMCs from human immunodeficiency virus (HIV)-seronegative donors carried a 30-bp deletion in the C-terminal portion of the LMP-1 gene, whereas a nondeleted fragment was amplified in about 44% (8 of 18) of the cases. Only one sample (5.6%) showed the amplification of a full-length LMP-1 band together with a deleted fragment. Similarly, PBMCs from HIV-infected patients showed an almost equivalent prevalence of full-length (17 of 37, 46%) and deleted (16 of 37, 43.2%) LMP-1 fragments, whereas about 11% of samples (4 of 37) showed evidence of double infections. Of note, deletions in the LMP-1 gene were detected with similar prevalence values in EBV+ Hodgkin's disease (HD) (13 of 30, 43.3%) and non-Hodgkin's lymphoma (NHL) (2 of 5, 40%) cases from HIV-seronegative patients and in HIV-related, EBV+ NHLs (4 of 7, 57.1%). Conversely, a 30-bp LMP-1 deletion was found in 10 of 12 HIV-associated HD cases (83%), a prevalence significantly higher than that detected in HIV-unrelated HD (P = .01). These findings indicate that: (1) the same EBV strain carrying LMP-1 deletions is harbored by normal and neoplastic cells of patients with EBV+ disorders, ruling out that these mutations might result from immunoselection phenomena; (2) in the Italian population, the prevalence of LMP-1 deletion mutants is comparable to that of EBV strains with full-length LMP-1; (3) HIV-induced immunosuppression is not associated with an increased prevalence of LMP-1 deletions in PBMCs; and (4) HIV-related HD cases, but not those of HIV-seronegative Italian patients, are closely correlated with the presence of LMP-1 deletions, suggesting that infection with these strains may increase the risk of developing HD in the HIV setting.

Distribution of HHV-6 variants in human tissues.

Human herpesvirus (HHV)-6 strains segregate into two variants (HHV-6A and HHV-6B), closely related to each other but clearly and easily distinguishable. These two HHV-6 variants differ in their ability to grow in T-cell lines, have distinctive patterns of DNA restriction fragments, and show specific reactivities with some monoclonal antibodies. The degree of DNA homology between variants ranges from 97% in the most conserved region to 75% in the immediate early region 1. HHV-6B is the etiologic agent of exanthema subitum but HHV-6A has not yet been clearly associated with any human pathology. HHV-6 sequences are frequently detected by the polymerase chain reaction (PCR) in healthy and pathological tissues. HHV-6B is more prevalent in peripheral blood mononuclear cells and in lymphatic tissue. The prevalence of HHV-6A may be greater in some pathological conditions such as Kaposi's sarcoma, and in skin biopsies. Results so far available support the hypothesis that HHV-6 variants may have different epidemiologies.

Human herpesvirus 8 is present in the lymphoid system of healthy persons and can reactivate in the course of AIDS.

In this study the prevalence of human herpesvirus (HHV) 8 DNA was determined in biopsies from persons with lymphoproliferative disorders and in peripheral blood mononuclear cells (PBMC) from human immunodeficiency virus (HIV)-seronegative and HIV-infected persons. The results show that HHV-8 is present in 10% of biopsies from HIV-seronegative persons: HHV-8 is detected with similar prevalence values in HIV-infected patients with lymphoproliferative diseases, but the virus load is higher. HHV-8 was also found in PBMC. The presence of monoclonal Epstein-Barr virus (EBV) genomes in malignant lymphoproliferations was only infrequently associated with HHV-8 infection. Therefore, HHV-8 is fairly common in the population, and the lymphoid system could represent a reservoir of latently infected cells from which the virus may reactivate in conditions of immunodepression; furthermore, HHV-8 and EBV do not seem to act in conjunction in lymphomagenesis.

Chimeric BK virus DNA episomes in a papillary urothelial bladder carcinoma.

BK virus (BKV) DNA sequences were identified in a papillary urothelial bladder carcinoma by Southern blot hybridization. The carcinoma contained both integrated and extrachromosomal DNA. Integrated sequences had a clonal restriction pattern, suggesting that BKV was integrated at some early stage of neoplastic initiation or progression. Viral episomes consisted of a population of covalent polymers based on a high-molecular-weight DNA unit, about 11-12 kb in size. DNA sequences non-homologous to the BKV genome were encompassed within DNA episomes, suggestive of acquisition of cellular sequences by viral DNA replication at the integration site. Extrachromosomal, chimeric DNA molecules were present at an average level of about 50 copies per cell, but their size, apparently incompatible with viral assembly, showed that BKV productive infection was impaired. The data suggest that infected cells underwent reversible changes affecting autonomous BKV DNA replication.