Ultrasonographic findings of gall bladder in acute viral hepatitis

Thirty patients with acute viral hepatitis were studied for ultrasonographic findings of the gall bladder [GB] and for detection of patients with cholecystitis-like presentations within the first week of diagnosis. Patients were subjected to full history taking, clinical examination, laboratory and serological investigations, in addition to real time abdominal ultrasonography. Serologically, patients were classified into 3 groups: hepatitis-A virus [HAV] group; 16 patients [53%], hepatitis-B virus [HBV] group; 8 patients [27%], and hepatitis-C virus [HCV] group; 6 patients [20%]. The commonest ultrasonographic finding was increased GB wall thickness [GBWT], in 23 / 30 patients [76.7%]. It was more evident in patients with HAV. Twenty out of 23 patients [86.9%] with GBWT,exhibited clinical presentation similar to that of acute noncalcular cholecystitis, the so called; cholecystitis-like presentations. It was concluded that; GB wall thickening with cholecystitis - like presentations seemed to be more common in patients with acute viral hepatitis, particularly; HAV infection. Acute viral hepatitis must be considered as an underlying cause in patients with ultrasonographic diagnosis of acute non-calcular cholecystitis. Ultrasonography follow-up of GB changes associated with acute viral hepatitis is recommended

role of interleukin 16 in the immunopathogenesis of rheumatoid arthritis

Rheumatoid Arthritis [RA] is a chronic inflammatory disease characterized by hyperplasia of the synovium and excessive cellular infiltration, which leads to progressive joint destruction. We analyzed, interleukin 16 [IL16], in relation to disease activity to characterize its biologic function in RA. Secreted IL-16 was measured by enzyme immunoassay in sera from 30 RA patients and 30 healthy controls [HC], and also in synovial fluid [SF] from 16 RA patients and 15 patients with non-RA synovitis as controls. IL-16 expression in peripheral blood mononuclear cells [PBMC] was characterized by flow cytometric analysis after intracellular cytokine staining for IL-16. In synovial tissue specimens, both were done: Immunohistochemistry for localization of IL-16, and histopathology, in which the tissue scored semiquantitatively for synovial hyperplasia and cellular infiltration. IL-16 was detected at significantly higher levels in sera and SF of RA patients in comparison to HC and non-RA synovitis [p<0.001 and p<0.0001 respectively]. Also, IL-16 was detected significantly higher in SF in comparison to sera in RA patients [p<0.001]. Flow cytometry of PBMC showed that a great proportion of both CD4+ and CD8+ cells expressed IL-16 protein. Also, immunohistochemistry revealed more CD4+ and less frequency of CD8+ cells in synovial infiltration. A significant correlation between IL-16 expression and local inflammatory activity could not be established [p>0.21] by microscopic analysis of the synovial cells infiltrate. In addition, no significant association was observed between serum, SF, and synovial tissue expression of IL-16 and clinical disease activity in RA [p>0.61, p>0.5 and p>0.42 respectively]. This indicated that, IL-16 played a regulatory rather than a proin-flammatory role in the immunopathogenesis of RA