par Wilkin, Paul 
Référence Irish journal of medical science, 36, 5, page (200-210)
Publication Publié, 1961
Référence Irish journal of medical science, 36, 5, page (200-210)
Publication Publié, 1961
Article révisé par les pairs
| Résumé : | In summing up the few facts shown in this contribution, we may say that the clinical syndrome known as “placental insufficiency” or better, “nutritive placental hypofunction”, includes a primary type, presumably of genetic origin, which frequently leads to carly spontaneous abortion; and a secondary type which leads to the birth of an immature foetus or even to foetal death in utero. This secondary type of placental insufficiency is, in the majority of cases, the result of toxaemia, hypertension, renal disease with or without superimposed toxaemia. All these causes diminish the nutritive placental function by reducing the maternal placental blood-flow, the placental growth and by injuring the placental barrier. The placental lesion most commonly found is the true infaret. Incidentally, the cause of the secondary placental insufficiency remains unknown, and the placental pathology may be the same as in the other cases or may be characterised by diffuse lesions of premature or excessive ageing (I.N.F.D.). The clinical diagnosis of placental insufficiency, in the absence of an easy and accurate permeability test, may be aided by various hormonal assays, the urinary oestriol being most reliable. The determination of different kinds of enzymatic activities related with placental function (L.A.P. or C.A.P.) or placental welfare (L.D.H. or S.D.H.) may become, in the near future, useful in the detection of placental insufficiency. © 1961, Springer. All rights reserved. |
