[The pathophysiology of aplastic anemia].
It is the conventional opinion that acquired aplastic anaemia is a heterogeneous disease including basically different conditions, such as idiopathic or virus induced pancytopenia, toxic-allergic marrow damage or autoimmunity. Here, an alternative concept is proposed, according to which aplastic anaemia is one disease, but multifactorial in all patients, apparent differences being due to the relative prevalence of one or the other pathological component in individual patients. Bone marrow from patients in the severe phase of aplastic anaemia does not grow in culture and is therefore not suitable for experimentation. Alternatively, bone marrow from patients who have resumed some degree of autologous bone marrow function, but still have residual signs of the disease after non-invasive therapy, offers the possibility to study pathological mechanisms in vitro. The majority of experiments presented have been done in such patients, assuming that their status of disease in some way reflects the original, more serious pretreatment condition. Three major pathophysiological components will be discussed, and it will be proposed how these factors act in concert to cause or aggravate aplasia.
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Nissen
D000741:Anemia, Aplastic / Q000097:blood / Q000276:immunology / Q000503:physiopathology*; D001853:Bone Marrow / Q000503:physiopathology; D006410:Hematopoiesis / Q000276:immunology; D006412:Hematopoietic Stem Cells / Q000276:immunology / Q000502:physiology; D006801:Humans
Patofiziologiia aplasticheskoĭ anemii.