morphine and Vasculitis

Meconium-associated vascular necrosis (MAVN) is a histological abnormality of human placental chorionic vessels that is associated with poor neonatal outcome. We tested the hypothesis that MAVN shows apoptosis in the walls of chorionic vessels. Archival placental specimens with MAVN (n = 5) were compared with specimens from uncomplicated pregnancies at term (n = 5) and from placentas with intense chorionic vasculitis associated with acute chorioamnionitis with (n = 5) or without (n = 5) a clinical history of meconium in the amniotic fluid. Sections from all placentas were processed by the TUNEL method, and 2 observers who were blinded to specimen diagnosis quantified the immunofluorescent TUNEL staining in both the amnion-facing and villous-facing walls of the larger chorionic vessels in each specimen. Compared with the other 3 groups, only the amnion-facing wall of chorionic vessels in MAVN showed a significantly greater number of apoptotic cells. This was verified by morphological criteria and caspase 3 staining. There were limited or no detectable TUNEL-stained cells in either the villous-facing walls of vessels in the MAVN specimens or in any of the vessels of the placentas from uncomplicated pregnancies. There was a negligible level of apoptosis in chorionic vessels of placentas with intense chorionic vasculitis, with or without meconium, despite the inflammatory response or presence of meconium. We conclude that apoptosis contributes to the pathophysiology of MAVN.

Topics: Apoptosis; Blood Vessels; Caspase 3; Caspases; Chorion; Female; Humans; Immunohistochemistry; In Situ Nick-End Labeling; Meconium; Muscle Cells; Necrosis; Placenta; Placenta Diseases; Pregnancy; Vasculitis

Two hundred and eighteen cases of hemorrhagic endovasculitis (HEV), a recently recognized abnormality of human placentas, were identified from placentas submitted to the Michigan Placental Tissue Registry over a 2.5-year period. HEV appears to focus on fetal placental blood vessels with resultant fragmentation and destruction of fetal RBCs, hemorrhage into villous stroma, microthrombi in villous capillaries and non-exudative necrosis of medium sized chorionic vessels. Placentas without HEV submitted for evaluation from the same hospitals were selected for comparison. Women with HEV placentas were of similar age, race and parity as control women. The sex of the fetus of HEV cases was somewhat more often female (57% vs. 48%, P = 0.05). The presence of HEV appeared to have a deleterious effect on the outcome of pregnancy: 52% (112/218) of the HEV placentas were associated with stillborn infants, in contrast to only 22% (89/400) of control placentas. The difference in the proportion of stillbirths was greatest when the gestational age was 25 weeks or greater. Other significant positive associations with HEV included the presence of meconium staining, intrauterine growth retardation, smaller placentas, and maternal hypertension or toxemia. Pathologic findings associated with HEV were chronic villitis, erythroblastosis, thrombosis and cord abnormalities. No association was found with infant Apgar score or fetal anomalies. The association of HEV with a high proportion of stillbirths in the registry suggests that further understanding of this lesion might shed light on the problem of unexplained stillbirth.

Topics: Female; Fetal Death; Fetal Diseases; Hemorrhage; Humans; Infant, Newborn; Infant, Small for Gestational Age; Male; Meconium; Placenta Diseases; Pre-Eclampsia; Pregnancy; Registries; Risk; Vasculitis