[Preterm delivery: detection of risks and preventive treatment]. / El parto pretérmino: detección de riesgos y tratamientos preventivos.

Every year around the world some 13 million premature children are born. Most of these children are born in developing countries, and they account for the largest share of perinatal morbidity and mortality. This review study analyzed scientifically validated data on interventions to prevent at least some portion of these preterm deliveries and to lessen their impact on neonatal health. The Cochrane and MEDLINE bibliographic databases were consulted. Fifty review pieces and research articles were studied, relating to the following aspects of preterm delivery: risk factors and early detection of the risk of preterm delivery; preventing the risk of preterm delivery; treating preterm delivery once it has begun; and preventing neonatal respiratory distress syndrome. There were few successful approaches to the prediction, prevention, or early detection of the threat of preterm delivery. The only measures that can be recommended for all pregnant women are screening for and treating asymptomatic bacteriuria as a part of prenatal check-ups. Screening for bacterial vaginosis and treating it reduce the incidence of preterm births in pregnant women with a history of premature delivery. In addition, prophylactic cerclage decreases the incidence of premature births in pregnant women who have had more than three preterm births. To treat a delivery that starts early, with or without premature membrane rupture, the interventions that have proved to be effective are administering betamimetics to the parturient woman in order to delay delivery for 48 hours, and using indomethacin for the same purpose, as the second-choice drug. The prenatal administration of corticosteroids to the pregnant woman can induce lung maturation in the fetus and reduce respiratory distress syndrome and ventricular hemorrhage, thus decreasing neonatal mortality. There is a need to continue and support basic and epidemiological research in order to develop new knowledge on the causes and mechanisms of preterm delivery and on preventing the morbidity and mortality that preterm delivery produces.

Placental lesions in maternal autoimmune diseases.

We have investigated the presence and clinical implications of maternal vascular lesions and chronic villitis of unknown etiology (CVUE) in 18 placentas of 15 mothers with several autoimmune diseases (AD), including, for the first time, idiopathic thrombocytopenic purpura, autoimmune thyroid diseases, and multiple sclerosis. The group with AD had significantly more maternal vascular lesions and CVUE than the control group. We did not find lesions that could be attributed to any of the diseases in particular. The histopathologic picture was similar in these diseases, although there appears to be a spectrum in severity. Placental vascular damage with deposits of IgM, C3, and C1q was more prominent in systemic lupus erythematosus and in a patient with systemic sclerosis. In both of these diseases but not in the other conditions, these lesions were related to poor fetal outcome. Although the precise role of each of these autoimmune diseases in pregnancy and fetal outcome remains to be established, there appears to be at least one link between them represented by the presence of severe acute atherosis and heavy granular vascular deposits of IgM, C3, and C1q associated in some with poor fetal outcome. The role of CVUE remains speculative.

Intrauterine growth retardation of unknown etiology: II. Serum complement and circulating immune complexes in maternal sera and their relationship with parity and chronic villitis.

Significantly lower CH50 levels were found in women with small for gestational age (SGA) infants. The lowest values corresponded to nulliparous with placental chronic villitis (124.0 +/- 10.6). Three out of five mothers with circulating immune complexes from SGA group were nulliparous, having placental chronic villitis. An immunological derangement in women with SGA infants is proposed for the development of placental lesions, mainly in nulliparous mothers with a lower previous exposure to fetal antigens.

Primary chronic abortion, preeclampsia, idiopathic intrauterine growth retardation, hydatidiform mole, and choriocarcinoma: a unifying concept.

Different degrees of maternal hyporesponse, as far as blocking activity is concerned, are proposed for primary chronic abortion, preeclampsia, and idiopathic intrauterine growth retardation. On the other hand, a maternal hyperresponse to fetal antigens with a higher production of blocking antibodies may be related to an unusual proliferation of the trophoblast in cases of hydatidiform mole and choriocarcinoma.