PubMed · 14274607
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Kh E GADZHIEV. 1965. [NUTRITIVE MACROCYTIC ANEMIA].. https://pubmed.ncbi.nlm.nih.gov/14274607/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
We report a case of giant hepatic cavernous hemangioma associated with spontaneous subacute intratumoral hemorrhage. Magnetic resonance imaging showed an oval, homogeneous, high-intensity lesion with a low-intensity rim in the original high-intensity tumor on T2-weighted images. On T1-weighted images, this oval lesion showed heterogeneous high intensity with peripheral higher intensity. The histologic specimen confirmed hepatic hemangioma with intratumoral hemorrhage.
The hemolytic uremic syndrome (HUS) is most commonly associated with Escherichia coli, but has been associated with other infections such as Streptococcus pneumoniae. Pneumococcus-induced HUS carries an increased risk of mortality and renal morbidity compared with E. coli-induced HUS. The pneumococcal organism produces an enzyme, which can expose an antigen (T-antigen) present on erythrocytes, platelets, and glomeruli. Antibodies to the T-antigen, normally found in human serum, bind the exposed T-antigen, and the resultant antigen-antibody reaction (T-activation) can lead to HUS and anemia. Clinicians need to be aware to request specific testing when pneumococcus-induced HUS/anemia is suspected, as current blood banking techniques do not routinely test for the presence of the T-antigen. Once this association is documented, washing all blood products and avoiding plasma products, if possible, is recommended. Plasmapheresis can be considered for the more critically ill patient. The incidence of pneumococcus-induced HUS may be increasing. We report six cases of pneumococcus-induced HUS/anemia presenting at our hospital.
Clearance of apoptotic cells by macrophages is considered important for prevention of inflammatory responses leading to tissue damage. The phosphatidylserine receptor (PSR), which specifically binds to phosphatidylserine (PS) exposed on the surface of apoptotic cells, mediates uptake of apoptotic cells in vitro, yet the physiologic relevance of PSR remains unknown. This issue was addressed by generating PSR-deficient (PSR(-/-)) mice. PSR(-/-) mice exhibited severe anemia and died during the perinatal period. In the PSR(-/-) fetal livers, erythroid differentiation was blocked at an early erythroblast stage. In addition, PSR(-/-) embryos exhibited thymus atrophy owing to a developmental defect of T-lymphoid cells. Clearance of apoptotic cells by macrophages was impaired in both liver and thymus of PSR(-/-) embryos. However, this did not induce up-regulation of inflammatory cytokines. These results indicate that during embryonic development, PSR-mediated apoptotic cell uptake is required for definitive erythropoiesis and T lymphopoiesis, independently of the prevention of inflammatory responses.