Three Kinds of Foamy Cells in the Spleen: Comparative Histochemical and Ultrastructural Studies |
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Authors: | Tokuhiro Ishihara Yoshimi Yamashita Yoshiko Okuzono Tadaaki Yokota Mutsuo Takahashi Toshiaki Kamei Fumiya Uchino Noboru Matsumoto Shiro Miwa Hisaichi Fuji Takeshi Kozaki |
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Affiliation: | a The First Department of Pathology, Yamaguchi University School of Medicine, Ube, Japanb The School of Allied Health Sciences, Yamaguchi University School of Medicine, Ube, Japanc Department of Internal Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japand Department of Pediatrics, Nagoya National Hospital, Nagoya, Japan |
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Abstract: | By light and electron microscopy, we observed foamy cells in the spleens from a patient with hemolytic anemia due to red cell adenosine deaminase (ADA) overproduction, a patient with rheumatoid arthritis (RA) treated with gold, and patients with idiopathic thrombocytopenic purpura (ITP)
The foamy cells associated with red cell ADA overproduction were essentially similar to Gaucher-like cells described in patients with thalassemia, and it was suggested that the accelerated destruction of red cells was one of the factors responsible for the development of foamy cells. Foamy cells in ITP and RA were closely associated with an increased destruction of platelets in the spleen. Morphologic transitions between phagocytosed platelets and myelinlike materials were traced in these disorders. In RA, however, foamy cells were heterogeneous from an ultrastructural standpoint, with different cytoplasmic inclusions. In addition to myelinlike materials, dense bodies, vacuoles with flocculent materials, and gold were noted in most of foamy cells. As gold compounds are known to inhibit lysosomal enzymes, we surmise that an acquired disturbance in lysosomal digestion is partially responsible for the accumulation of intermediate metabolites.
In the pathogenesis of foamy cells associated with blood cell dyscrasia, the accelerated destruction of blood cells and/or acquired disorders in catabolic pathways within the macrophages are suggested to be the underlying mechanism of an intralysosomal accumulation of incompletely degraded cellular debris. |
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Keywords: | foamy cells RBC adenosine deaminase overproduction rheumatoid arthritis gold idiopathic thrombocytopenic purpura |
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