[Genesis and importance so-called inflammatory infiltration of the placenta. II. Immunohistochemical findings]. / Zur Genese und Bedeutung der sogenannten Asphyxieinfiltrate der Plazenta. II. Immunhistochemische Befunde.

We investigated the morphologically distinct forms of inflammatory infiltration of the placenta both histologically and immunohistologically (n = 24). Our material included cases of membraneous inflammation (chorioamnionitis), inflammatory infiltration of arteries in the chorionic membrane, basal and intervillous placentitis. NACE staining was used to detect myeloid cells and monoclonal antibodies (LCA, CD3, CD8, CD20, CD68). To detect lymphoid and macrophageal cells we also measured the proliferation activity with MiB 1. In cases of chorioamnionitis and subchorial demarcation and in the arteries of the chorionic membranes the main inflammatory cell is the myeloid cell (most often the mature neutrophil granulocyte). T-lymphocytes were only occasionally found. In cases of intervillous placentitis, on the other hand, lymphocytic infiltration predominates, consisting of T-lymphocytes which are mostly CD8 negative, and some monocytes and macrophages. Basal inflammation in the demarcation zone was characterized by T-lymphocytes. We interpret this as indicating basal demarcation. According to our histological and immunohistological observations, "asphyxial infiltrates" are abortive forms of a placental (bacteriological) inflammation, possibly infective in origin. We do not consider asphyxial infiltration to be a separate entity with its own causal pathogenesis.

[Genesis and significance of so-called asphyxial infiltrates in the placenta. I. Histologic results]. / Zur Genese und Bedeutung der sogenannten Asphyxieinfiltrate der Plazenta. I. Histologische Befunde.

The conventional conception of the cause and formal pathogenesis of so-called "asphyxial infiltrates" of the placenta is presented. Morphological examples are given. Our study included 561 newborn cases. Eighty two cases (14.6%) had such cell infiltrates, and there were 6 cases with phlegmoneous inflammation of the fetal membranes. These morphological findings correlated with the following clinical characteristics: term of birth, weight classes of newborns, Clifford-signs, clinical risks with respect to hypertension, the course of pregnancy and particularly the risk of inflammation. Additional correlates were the clinical statement of hypoxia and acidosis in newborns. We discovered relationships between these cell infiltrates and the Clifford-signs, and to some clinical risks (especially those for inflammation), but not to hypoxia and acidosis of the newborn. Our results show, that there are no relations between the conventional "Asphyxial infiltrates" of the placenta and the hypoxia and acidosis observed in newborns.