| Question of the Month: January 2001 | ||||||||||||||||||
| Clinically expressed spontaneous pre-eclampsia-eclampsia appears to be specific of humans and higher primates. Some syndromes, involving the liver, the kidneys, and at times the neural systems affect pregnant sheep, goats, cattle, and possibly some wild quadrupeds. However, these conditions, generally labeled pregnancy toxemias, have somewhat clear metabolic and nutritionally deficient backgrounds not comparable to human pre-eclampsia. | ||||||||||||||||||
| Experimental pre-eclampsia-like syndromes have been induced in pregnant bitches, sheep, rats, and lower primates after very artificial diverse experimental interventions, that hardly can be expected to occur in human pre-eclampsia, and this fact has been the main barrier for the complete deciphering of the pre-eclamptic enigma. | ||||||||||||||||||
| The immunology of pregnancy in all mammals involves the maternal acceptance of foreign paternal materials as well as the creation of an efficient feto-maternal interface throughout the duration of pregnancy. So, what is present or what takes place in human pregnancy that does not occur in other species and may be responsible for the pre-eclamptic syndrome ?, or, what is present or what occurs in most non-human mammal pregnancies that cancels the possibility of a pre-eclamptic syndrome? Furthermore, can trophoblast distress, fragmentation and deportation as well as feto-maternal cell traffic, so prominent in hemochorial placentation, follow the same mechanisms with similar consequences in epithelio-chorial, syndesmo-chorial or endothelio-chorial placentation? | ||||||||||||||||||
| Before answering, it could be convenient to go to if villi could talk. | ||||||||||||||||||
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