QUESTION OF THE MONTH
March  2002.
   Most evidence signals a generalized  vascular endothelial dysfunction as an intermediate but indispensable link in the pathophysiology of pre-eclampsia-eclampsia. This in turn seems to be the consequence of an aseptic inflammatory process generated at the fetomaternal interface with the trophoblast and neighboring elements releasing pro-inflammatory and potentially cytotoxic substances that access the systemic circulation via the uterine veins and the inferior cava vein.
   After reaching the systemic venous circulation, the first organs that face their presence are the lungs and after going back to the heart are distributed through the arterial system to all organs and regions of the body where these substances affect the vascular endothelium, most significantly in the liver and the kidneys because of their circulatory proximity to the aorta, their blood flow and the high levels of perfusion pressure, among other factors. Without medical intervention, the natural course of the disease process very frequently ends up in liver rupture, brain hemorrhage and diffuse bilateral cortical and/or tubular necrosis.
  If the lungs are the first organs to face the presence of these cytotoxic substances causing generalized vascular endothelial dysfunction followed by structural damage and rupture (micro to macro ruptures), why is it that the lungs, even though one can find evidence of intravascular coagulation in some arterioles and capillaries with occasional petechial hemorrhages, never show as spectacular lesions as the liver, the kidneys or the brain in autopsy material.?
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