Influence of Spleen Size and Portal Pressure on Erythrocyte Sequestration.
نویسندگان
چکیده
That a hemolytic process is one of the potential causes of anemia in cirrhosis of the liver has been well established by repeated demonstrations of decreased red cell survival time in a large proportion of patients (1-7). Shortened survival has been noted, not only with autologous cells, but also with transfused normal donor cells (1, 2). This would clearly establish the existence of an extracorpuscular factor. Moreover, Jandl (2) has pointed out that the exponential contour of disappearance curves observed in patients with cirrhosis suggests random fractional removal of cells by an organ such as the spleen. This of course is consistent with the widely accepted notion that the congestive splenomegaly of cirrhosis causes "hypersplenism." In previous studies employing thermally damaged Cr51-labeled red cells to assess the size of the spleen by a scanning procedure, both we (8) and Wagner and co-workers (9) found that the cells tended to disappear from circulating blood more rapidly in patients with cirrhosis than in control subjects. The present investigation was conducted in order that the rate of removal of thermally damaged cells might be measured definitively by analysis either of blood disappearance curves or of curves obtained by continuous recording of activity through an external probe placed over the spleen. It was expected that a sequestration function could be assessed in patients with cirrhosis and other disorders affecting the spleen if the corpuscular variable were minimized by introducing labeled red cells that had been subjected to standardized thermal damage. At the same time the size of the spleen could be estimated by the scanning procedure previously described (8).
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BACKGROUND/AIM Splenomegaly is a frequent finding in patients with liver cirrhosis and portal hypertension and may cause hypersplenism. The occurrence of thrombocytopenia in those patients can be considered as an event with multiple etiologies. Two mechanisms may act alone or synergistically with splenic sequestration. One is central which involves either myelosuppression because of hepatitis v...
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عنوان ژورنال:
- The Journal of clinical investigation
دوره 43 شماره
صفحات -
تاریخ انتشار 1964