J. W. Keeling

Prostaglandins, chorioamnionitis and preterm labour

Summary. The production of prostaglandin E (PGE) and leukotriene B4 (LTB4) by amnion was measured in vitro in 12 women delivered after spontaneous preterm labour and in 15 women delivered after spontaneous labour at term. The placenta and fetal membranes were examined histologically in all cases. PGE output (fmol/mg dry weight/2 h) in the amnions from uncomplicated preterm deliveries was low (median 486, range 232–3203, n= 7) compared with the values obtained after spontaneous labour at term (5529, 1722–14226, n= 15). In amnions from preterm deliveries complicated by acute chorioamnionitis or round cell infiltration there was massive release of PGE (15 262,10 905–27 640, n= 5) which was accompanied by an increase in LTB4 production. Inflammatory infiltration of the fetal membranes results in a huge increase in PG production which could cause preterm labour.

Quantitative structural studies on placentas from pregnancies complicated by diabetes mellitus.

Summary. Fourteen placentas from pregnancies complicated by insulin‐dependent diabetes mellitus have been examined by quantitative morphometry. The results have been compared with those from 22 placentas of comparable gestation from uncomplicated pregnancies. The volume of parenchymatous tissue in the placentas from diabetic mothers was significantly increased while the volume of non‐parenchyma was decreased. The villous surface area was increased in placentas from the diabetic group, the mean value being 17·3 m2 compared with the 11·4 m2of the normal group. This increase was larger than would be expected when the increase in fetal weight of some babies born to diabetic mothers is taken into account.

Placental leukotriene B4 release in early pregnancy and in term and preterm labour

The production of leukotriene B4 (LTB4) by the human placenta in vitro was measured by radioimmunoassay. In early pregnancy (7-12 weeks gestation) LTB4 production rate (pmol/mg dry weight/2 h) was 3.7 (2.6-4.7) (median and range; n = 9) and at term it was 0.7 (0.4-2.3; n = 10) in placental tissue obtained at elective caesarean section, and 2.7 (1.3-3.6; n = 10) in samples following labour of spontaneous onset and vaginal delivery. In spontaneous preterm labour (26-36 weeks gestation) with normal placental histology LTB4 production was 0.7 (0.3-1.7; n = 14), but it was significantly higher in preterm placentas with inflammatory infiltration: 3.1 (0.8-4.8; n = 6). These data show that the production of LTB4 by human placenta is high in early pregnancy, but remains low during the third trimester, with a significant increase in spontaneous labour at term. LTB4 output is low in uncomplicated preterm labour but markedly increased in chorioamnionitis-associated preterm labour.

Congenital Malformations, Prenatal Diagnosis and Fetal Examination

Congenital malformations are an important cause of perinatal and infant mortality and morbidity. Three per cent of newborns have a single major malformation and 0.7% have multiple major defects. They have fascinated curious individuals for centuries but during the past 50 years infants with major anomalies have become the focus of increasing and diverse professional expertise and consume a large slice of health budgets in developed countries. Their importance as a cause of perinatal mortality has grown as deaths from intrapartum problems have declined and better neonatal care has improved the survival of normally formed low birth weight babies (see Chapter 8). Clinical interest in malformations has been enhanced because sophisticated surgical and anaesthetic management makes correction of some major defects possible. This and the recognition of syndromes, their mode of inheritance and sometimes their aetiology requires detailed information from the pathologist in respect of those babies who die.

Dispermic origin of a 69,XXY triploid

SummaryTriploidy, 69,XXY, was found in a newborn with multiple abnormalities. Conception had occurred shortly after the mother ceased taking an oral contraceptive. The infant carried a pair of 21s with giant satellites; of the parents, only the father carried a giant-satellited 21. This, together with the XXY constitution, suggested a dispermic origin of the triploidy.

LIPID-CONTAINING CELLS IN THE BRAIN IN SUDDEN INFANT DEATH SYNDROME

The authors report a semi‐quantitive autopsy study on the content of lipid‐containing cells (LCC) in corpus callosum and periventricular frontal white‐matter from the brains of 96 infants. These were 55 cases of sudden infant death syndrome (SIDS), 28 with conditions expected to have caused hypoxia (hypoxic control), and 13 with conditions not expected to have caused more than brief, terminal hypoxia (non‐hypoxic control). Appreciable numbers of LCC were found in the non‐hypoxic control cases, but significantly more LCC were found in the hypoxic controls. LCC in SIDS cases were intermediate between the non‐hypoxic and hypoxic controls. The findings are discussed in the light of an experimental primate study. The authors conclude that the slight excess of LCC in SIDS cases is more likely to be an exaggeration of normal developmental LCC accumulation than evidence of pre‐terminal episodes of hypoxia.

Congenital Abnormalities and the Examination of the Fetus Following Prenatal Suspicion of Congenital Abnormality

Congenital malformations are an important cause of prenatal, perinatal, infant mortality and morbidity. Three percent of newborns have a single major malformation and 0.7% have multiple major defects. The frequency is much higher prenatally, the majority aborting spontaneously. They have fascinated curious individuals for centuries but during the past 50 years infants with major anomalies have become the focus of increasing and diverse professional expertise and consume a large slice of health budgets in developed countries. Their importance as a cause of perinatal mortality has grown as deaths from intrapartum problems have declined and better neonatal care has improved the survival of normally formed low-birthweight babies (see Chap. 8). Clinical interest in malformations has been enhanced because sophisticated surgical and anaesthetic management makes correction of some major defects possible.

Prostaglandin E production by the fetal membranes in unexplained preterm labour and preterm labour associated with chorioamnionitis

The production of prostaglandin E (PGE) by amnion, choriodecidua and placenta was measured in 45 women delivered after spontaneous preterm labour, in 10 women delivered electively preterm, in 30 women at elective caesarean section at term, and in 28 women after spontaneous labour at term. In the preterm labour group 24 women had normal placental histology, and gestational age was 34 (31-36) weeks (median and range); 18 women had evidence of chorioamnionitis and gestational age was significantly shorter, 30 (24-36) weeks; three other patients had placental abruption. In the absence of inflammatory infiltration of these tissues the highest PGE output (fmol/mg dry weight/2 h) was found after labour at term and the lowest after uncomplicated preterm labour: 2640 (360-15,580) (median and range) compared with 1414 (164-11,045) in amnion, 677 (100-3245) compared with 308 (39-1086) in choriodecidua, and 1200 (520-3022) compared with 578 (150-1859) in placenta, respectively. Tissues showing chorioamnionitis produced much higher outputs of PGE from amnion (12,278, 1799-82,617) and from choriodecidua (1018, 216-11,768), but not from placenta (616, 89-4131). Chorioamnionitis seems to cause very early preterm labour by increasing PG production in the amnion and choriodecidua.

Prostaglandins, Chorioamnionitis and Preterm Labour

The production of prostaglandin E (PGE) and leukotriene B4 (LTB4) by amnion was measured in vitro in 12 women delivered after spontaneous preterm labour and in 15 women delivered after spontaneous labour at term. The placenta and fetal membranes were examined histologically in all cases. PGE output (fmol/mg dry weight/2 h) in the amnions from uncomplicated preterm deliveries was low (median 486, range 232-3203, n = 7) compared with the values obtained after spontaneous labour at term (5529, 1722-14,226, n = 15). In amnions from preterm deliveries complicated by acute chorioamnionitis or round cell infiltration there was massive release of PGE (15,262, 10,905-27,640, n = 5) which was accompanied by an increase in LTB4 production. Inflammatory infiltration of the fetal membranes results in a huge increase in PG production which could cause preterm labour.