PubMed · 14385436
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E M KNIGHTS, V CLERMONT, R M STURROCK, B J SCHULTZ. 1955. [Sickle cells studied by electron microscope].. https://pubmed.ncbi.nlm.nih.gov/14385436/
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Most patients suffering from chronic infections, chronic inflammatory diseases, and some malignancies develop a mild to moderate anemia designated anemia of chronic disease or anemia of inflammation. Patients with this anemia have low serum iron, low to normal transferrin, and high to normal serum ferritin concentration. The anemia is caused by increased inflammatory cytokines, especially IL-6, inducing increased production of the iron-regulatory hormone hepcidin by hepatocytes. Hepcidin blocks the release of iron from macrophages, hepatocytes, and enterocytes, causing the characteristic hypoferremia associated with this anemia and iron-deprivation of the developing erythrocytes.
Malaria kills approximately 1-2 million people every year, mostly in sub-Saharan Africa and in Asia. These deaths are at the most severe end of a scale of pathologies affecting approximately 500 million people per year. Much of the pathogenesis of malaria is caused by inappropriate or excessive immune responses mounted by the body to eliminate malaria parasites. In this review, we examine the evidence that immunopathology is responsible for malaria disease in the context of what we have learnt from animal models of malaria. In particular, we look in detail at the processes involved in endothelial cell damage leading to syndromes such as cerebral malaria, as well as generalised systemic manifestations such as anaemia, cachexia and problems with thermoregulation of the body. We also consider malaria in light of the variation of the severity of disease observed among people, and discuss the contribution from animal models to our understanding of this variation. Finally, we discuss some of the implications of immunopathology, and of host and parasite genetic variation, for the design and implementation of anti-malarial vaccines.
We reviewed 64 pregnancies in 26 women with Diamond-Blackfan anemia (DBA) included in the French and German DBA registries. Complications were seen in 42 pregnancies (66%) and included abortion, pre-eclampsia, in utero fetal death, intrauterine growth retardation, retroplacental hematoma, pre-term delivery and fetal malformations. Of the 34 children (53%) born alive, 13 had DBA. No correlations were found between pregnancy outcome and features of either maternal or child DBA. Pregnancies in DBA-affected women are at high risk, especially for complications likely to be of vascular-placental origin. Careful monitoring with prevention of severe anemia and early introduction of aspirin is suggested.