Search PubMed⌕ Search

PubMed · 14014867

[Polyneropathy. III].

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D BRAGE. 1962-07-30. [Polyneropathy. III].. https://pubmed.ncbi.nlm.nih.gov/14014867/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Inappropriately low reticulocytosis in severe malarial anemia correlates with suppression in the development of late erythroid precursors.

Inappropriately low reticulocytosis may exacerbate malarial anemia, but the under-lying mechanism is not clear. In this study, naive and infected mice were treated with recombinant murine erythropoietin (EPO), and the upstream events of erythropoiesis affected by blood-stage Plasmodium chabaudi AS were investigated. Malaria infection, with or without EPO treatment, led to a suboptimal increase in TER119(+) erythroblasts compared with EPO-treated naive mice. Furthermore, a lower percentage of TER119(+) erythroblasts in infected mice were undergoing terminal differentiation to become mature hemoglobin-producing erythroblasts. The impaired maturation of erythroblasts during infection was associated with a shift in the transferrin receptor (CD71) expression from the TER119(+) population to B220(+) population. Moreover, the suboptimal increase in TER119(+) erythroblasts during infection coincided with a blunted proliferative response by splenocytes to EPO stimulation in vitro, although a high frequency of these splenocytes expressed EPO receptor (EPOR). Taken together, these data suggest that during malaria, EPO-induced proliferation of early EPOR-positive erythroid progenitors is suppressed, which may lead to a suboptimal generation of TER119(+) erythroblasts. The shift in CD71 expression may result in impaired terminal maturation of these erythroblasts. Thus, inadequate reticulocytosis during malaria is associated with suppressed proliferation, differentiation, and maturation of erythroid precursors.

Anemia↗

Spontaneous subacute intratumoral hemorrhage of hepatic cavernous hemangioma.

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.

Anemia↗

Pneumococcus-induced T-antigen activation in hemolytic uremic syndrome and anemia.

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.

Anemia↗