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Extremely immature preterm infants rarely present with a leukocytosis exceeding 30,000/microL. The pathogenetic sequence leading to leukemoid reactions in non-malignant diseases remains to be elucidated. Potential triggers for leukemoid reactions in premature infants include prenatal corticosteroids, chorioamnionitis and funisitis or systemic infection. In the two-year period from 2006 to 2007 all infants with a gestational age of less than 26 weeks were screened for leukocytosis. Among our cases, one preterm infant presented with a leukocyte count of 229,300/microL at the age of 48 hours, lasting throughout the first three weeks of life. Impairment of microcirculation and resulting organ dysfunction were not observed. Thus, invasive therapeutic procedures, which are routinely initiated in hyperleukocytosis in accompanying malignant diseases, may not have the same significance in extremely immature preterm infants and should be executed in these patients on an individual basis and with extreme caution.

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.