Aims: Ovarian clear cell carcinoma has a unique stroma. Although a hyalinized or mucoid stroma is more common, the stroma sometimes shows a dense inflammatory infiltrate, simulating a dysgerminoma. The aim of this study was to analyse the character and significance of the inflammatory stroma. Methods and results: Twelve of 60 (20%) clear cell carcinomas showed an inflammatory stroma. The inflammatory stroma and hyalinized/mucoid stroma were mutually exclusive. Inflammatory cells were predominantly composed of CD138-positive plasma cells. As compared with the non-inflammatory cases, the epithelial component frequently showed a solid growth pattern and immunoreactivity for cyclooxygenase-2, one of the critical proinflammatory enzymes (P < 0.005). These findings were repeated after heterotransplantation of three clear cell carcinoma cell lines into athymic nude mice. In particular, xenografts of one cell line (JHOC-5) were infiltrated by mature plasma cells, indicating that plasma cell differentiation was stimulated by JHOC-5 cells, independently of T lymphocytes. Clinicopathologically, the frequency of International Federation of Gynaecology and Obstetrics stage III was higher in the cases with an inflammatory stroma than in those without it (P < 0.01). Conclusions: Clear cell carcinomas with an inflammatory stroma constitute a distinct clinicopathological subgroup. It is strongly suggested that tumour cells themselves are responsible for inducing inflammation and stimulating plasma cell differentiation in a paracrine manner.
We reported on a case of subcutaneous panniculitis-like T-cell lymphoma (SPTCL) with multiple erythematous nodular lesions on the extremities, trunk and face. Histological examination of an excised lesion revealed a dense infiltrate of markedly atypical T-lymphoid cells expressing the CD8+ phenotype located in the subcutaneous tissue with histiocyte-phagocytizing apoptotic cells. The 'bean-bag' histiocytic cells, the characteristic finding of SPTCL, are considered to be products of haemophagocytosis. In our case the 'bean-bag' cells were produced by phagocytosis of apoptotic bodies, as confirmed by electron microscopy. It is suspected that 'bean-bag' cells are related not to haemophagocytosis but to phagocytosis of apoptotic cells in the CD8+ T-cell type of SPTCL.
Giant serpentine aneurysm (GSA) is an entity defined on radiological and pathological grounds as a giant, partially thrombosed aneurysm containing tortuous vascular channels. We have had the opportunity to study two patients with GSAs, which has allowed for a complete comparative anatomical and radiological study. This report emphasizes the etiology of the GSAs. Twenty-two patients with GSAs have been reported in the literature, of which pathological studies were done in 10. In most of these, the aneurysm was found to be filled with an organized thrombus, but in our patients the aneurysm was filled with relatively new clot. The aneurysm enlarged and a change in the tortuous vascular channel was observed over a period of 1 year in the first patient, whereas a globoid aneurysm developed into a GSA in the brief period of just 2 weeks in the second patient. This rapid transformation of a globoid aneurysm into a GSA is of particular interest when the etiology of GSAs is considered. Our patients therefore shed some interesting light on the possible pathophysiology of GSAs. That is, the bloodstream may change dynamically in a giant aneurysm and may become a serpentine channel under conditions that lead to a "Coanda effect."
The pathological changes in the brains of seven patients who had been clinically diagnosed as normal pressure hydrocephalus (NPH) are described and the possible etiological mechanisms are discussed. The pathological findings in all cases consisted of demyelination akin to Binswanger's type of encephalopathy, especially in the frontal lobes. Arteriosclerosis accompanied by occasional organized thrombi and scattered microinfarcts in the periventricular white matter were seen. Focal leptomeningeal fibrosis, diminution of arachnoidal granulations, and non‐specific aging processes were noted. Among the above of particular interest, was the degeneration of both periventricular and deep white matters with microinfarcts, and moderate to severe arteriosclerosis. On the basis of these observations, we assume that the degeneration in the white matter is not merely a secondary change due to the result of enlargement of ventricle, but plays an important role in the development of NPH. The development of NPH requires not only the disturbance of cerebrospinal fluid, but also the pre‐or coexisting vulnerability in the white matter caused by variables such as ischemia, hypoxia, and trauma.
Giant serpentine aneurysm (GSA) is an entity defined on radiological and pathological grounds as a giant, partially thrombosed aneurysm containing tortuous vascular channels. We have had the opportunity to study two patients with GSAs, which has allowed for a complete comparative anatomical and radiological study. This report emphasizes the etiology of the GSAs. Twenty-two patients with GSAs have been reported in the literature, of which pathological studies were done in 10. In most of these, the aneurysm was found to be filled with an organized thrombus, but in our patients the aneurysm was filled with relatively new clot. The aneurysm enlarged and a change in the tortuous vascular channel was observed over a period of 1 year in the first patient, whereas a globoid aneurysm developed into a GSA in the brief period of just 2 weeks in the second patient. This rapid transformation of a globoid aneurysm into a GSA is of particular interest when the etiology of GSAs is considered. Our patients therefore shed some interesting light on the possible pathophysiology of GSAs. That is, the bloodstream may change dynamically in a giant aneurysm and may become a serpentine channel under conditions that lead to a “Coanda effect.”
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