We encountered two cases of ruptured anastomotic pseudoaneurysms 47 and 77 months after surgery for atherosclerotic thoracic aortic aneurysms. Autopsy was performed in one case and emergency re-operation was performed in the other case. We gained some interesting findings in the autopsy and the re-operation. The anastomotic sites were sustained by sutures only, and there was no evidence of tissue supplementation at the anastomotic sites in macroscopic observation. Microscopic findings demonstrated endothelium healing on the internal side of the prosthesis near the anastomotic site. There was no tissue connection between the prostheses and the native aortic walls, although over four or six years had passed after the previous anastomoses. Anastomotic pseudoaneurysms may occur even in a long time after surgery. Careful operative procedures and long-term computed tomography or magnetic resonance imaging follow-up are crucial.
MCL and FCL differ substantially in their features of presentation, response to chemotherapy, and long-term prognosis. The extent of residual disease after completion of chemotherapy discriminates patients with different prognosis and may be used for the stratification of postremission strategies.
Paroxysmal nocturnal haemoglobinuria (PNH) is now generally accepted as a disease in which bone marrow derived cells are deficient in phosphatidylinositolglycan (PIG)-anchored surface molecules. A series of new monoclonal antibodies detecting PIG-anchored surface structures on human leucocytes (CD48, CD55, CD59) has recently been described. In the present study 12 patients with the diagnosis PNH and a positive Ham test were examined for PIG-anchored surface antigen expression on various cell lineages using immunofluorescence. In all patients deficient cells were detected in erythrocyte, granulocyte and monocyte analysis. A deficient lymphocyte subset was also observed in all but one of these patients. Using two-colour analysis, all lymphocyte subpopulations such as T, B and NK cells were found to be affected. In addition, peripheral blood cells of 22 patients with severe aplastic anaemia (SAA) were tested for the PIG-anchoring defect. In five of these patients the defect was detected, and in four of the five the lack of PIG-anchored molecules was confined to the granulocyte and monocyte lineages apparently without affecting the erythrocytes. The results of these studies demonstrate that cytofluorographic testing of peripheral blood cells provides a simple and reliable method for establishing the diagnosis of PNH. Furthermore, especially in the case of aplastic anaemia patients, the sensitivity of immunophenotyping might be superior to conventional laboratory tests.
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