[Histochemical and immunohistochemical analysis of ruptured atherosclerotic abdominal aortic aneurysm wall].

BACKGROUND/AIM: The main complication of the atherosclerotic abdominal aortic aneurysm (AAA) is her rupture that begins with lesion in intima and rupture. The purpose of this work was to determine immunocytochemical and morphofunctional characteristics of the cells in aortic wall in ruptured atherosclerotic abdominal aortic aneurysm. METHOD: During the course of this study, 20 samples of atherosclerotic AAA were analyzed, all of them obtained during authopsy. The samples were fixed in 4% formalin and embedded in paraffin. Sections of 5 microm thickness were stained histochemically (of Heidenhain azan stain and Periodic acid Schiff--PAS stain) and immunocytochemically using a DAKO LSAB+/HRP technique to identify alpha-smooth muscle actin (alpha-SMA), vimentin, myosin heavy chains (MHC), desmin, S-100 protein, CD45 and CD68 (DAKO specification). RESULTS: The results of our study showed that ruptured atherosclerotic AAA is characterized by a complete absence of endothelial cells, the disruption of basal membrane and internal elastic lamina, as well as a presence of the remains of hypocellular complicated atherosclerotic lesion in intima. On the plaque margins, as well as in the media, smooth muscle cells (SMCs) are present, which express a alpha-SMA and vimentin (but without MHC or desmin expression), as well as leukocyte infiltration, and a large number of foam cells. Some of the foam cells show a CD68- immunoreactivity, while the others show vimentin- and S-100 protein-immunoreactivity. Media is thinned out with a disorganized elastic lamellas, while adventitia is characterized by inflammatory inflitrate (infection). CONCLUSION: Rupture of aneurysm occurs from the primary intimal disruption, which spreads into thinned out media and adventitia. Rupture is caused by unstable atherom, hypocellularity, loss of contractile characteristics of smooth muscle cells in intima and media, neovascularization of the media, as well as by the activity of the macrophages in the lesion.

[Immunocytochemical characteristics of submucosal uterine myomas].

BACKGROUND/AIM: Myomas of the uterus, the most common benign tumors, have been studied for decades from the aspects of different basic and clinical disciplines. Despite this fact, their pathogenesis is still poorly understood. The aim of this study was to determine immunocytochemical characteristics of smooth muscle cells and connective tissue components of submucosal myomas of the uterus. METHOD: During the course of this study, 25 samples of submucosal myomas of the uterus were analyzed, all of them obtained during the surgery, after abdominal histerctomy by Aldridge. The samples were fixed in 4% formalin and embedded in paraffin. Sections of 5 microm thickness were stained immunocytochemically using the DAKO LSAB+/HRP technique to identify alpha-smooth muscle actin (alpha-SMA), vimentin, desmin, CD34, CD45, CD68 and PCNA (DAKO specification). RESULTS: Our results suggest that submucosal myomas of the uterus are build-up of smooth muscle cells which are immunoreactive to alpha-SMA and desmin, but also to a certain number of smooth muscle cells which are immunoreactive to alpha-SMA and vimentin. Some of vimentin-immunoreactive cells also show an immunoreactivity of PCNA. In the build-up of connective stroma CD34-immunoreactive fibroblasts and neovascular formations are also present. By examining the distribution of CD45 antigen, at all the analyzed samples we observed a weak reaction. CONCLUSION: Submucosal myomas of the uterus are made-up of smooth muscle cells of the highly differentiated contractile phenotype (alpha-SMA- and desmin-immunoreactivity), as well as smooth muscle cell of the synthetic phenotype which proliferate (alpha-SMA-, vimentin- and PCNA-immunoreactivity). In submucosal myoma of the uterus there is a significant presence of connective tissue as a result of synthetic activity of fibroblasts, which clearly differ in their immunocytochemical characteristics from smooth muscle cells of the synthetic phenotype.