Retrospective examinations of 8,139 placentae were performed to clarify the relationship between placental disorders with massive intervillous fibrin deposition (MIFD) and intrauterine growth retardation (IUGR). Although the incidence of MIFD was low (0.4%), the small-for-date (SFD) birth rate in the MIFD group was significantly higher than that in the control group (62.9 vs. 8.3%; p < 0.001). Seventeen of 35 patients in the MIFD group had no clinical complications. MIFD itself was thought to be the main cause of IUGR in these patients. 78.4% of multiparae in the MIFD group gave unsuccessful obstetrical histories such as intrauterine fetal death and fetal growth retardation. Four of 6 patients with a history of MIFD and SFD delivery in a previous pregnancy repeated the same episode. These data indicate the MIFD recurrence rate in subsequent pregnancies must be high. Patients with a history of both SFD delivery and MIFD in previous pregnancies were defined as high-risk patients and they were given orally 30 mg of aspirin and 150 mg of dipyridamole daily and/or daily intravenous injection of 10,000 IU heparin during pregnancy. As a result, MIFD did not recur in all cases of the treated group and 87.5% (7/8) of the treated group could deliver approximate-for-date infants compared with 33.3% (2/6) of the untreated group (p < 0.05). These results indicate that anticoagulant and antiplatelet therapies are extremely effective for prevention of MIFD and IUGR due to MIFD.
We report a hitherto unknown, lethal osteochondrodysplasia in two Japanese siblings born to consanguineous parents. The skeletal abnormalities are characterised by mesomelic brachymelia with bowed forearms, a round pelvis with shortened greater sciatic notches, an ossification defect of the pubic bones, and absence of ossification centers in the cervical vertebral bodies. The associated visceral anomalies comprised periportal fibrosis and cystic dysplasia of the intrahepatic bile ducts, pancreatic ductal ectasia, a simple renal cyst, microcephaly with multifocal laminar necrosis and ectopic gray matter, dysplastic tracheobronchial cartilage, abnormal lobulation of the lung, diaphragmatic hernia, and stenotic pulmonary valve. Thrombocytopenia was present but megakaryocytes were slightly increased in the bone marrow. The patients showed various dysmorphic features including aniridia, a long palpebral fissure, prominent nasal bridge, beaked nose, flat philtrum, low-set fleshy ears, micrognathia with submucosal cleft palate, and multiple joint contractures.
We present a case of pemphigus vulgaris which developed during pregnancy. The newborn infant was normal. Bullous lesions were successfully treated by pulse therapy with high-dose corticosteroids. This is, to our knowledge, the first report in English from Japan describing pemphigus vulgaris associated with pregnancy.
The relationship between maternal plasma levels of beta-endorphin (beta-Ep) during labor and various obstetrical factors was investigated in 115 healthy pregnant women. beta-Ep was determined by radioimmunoassay using double-antibody RIA kit (INCSTAR Corporation, Stillwater, M'S.). The results were as follows: (1) The primiparous women showed a significant increase of maternal plasma levels of beta-Ep at delivery compared with the multiparous women. In addition, the group of women whose Bishop's score at the onset of labor was 5 points or less showed a significant increase of maternal plasma levels of beta-Ep at delivery compared with that in the group of women whose Bishop's score was 6 points or more. (2) The increase in maternal plasma levels of beta-Ep during the first and the second stage of labor was significantly higher in obese women (pre-pregnancy BMI > or = 24) than in normal weight women (pre-pregnancy BMI < 24). In normal weight women in pre-pregnancy, the group of women whose weight gain during pregnancy was 11kg or more showed a significantly higher increase of beta-Ep compared with that in the group of women whose weight gain was less than 11 kg. These results suggest that a stressful delivery caused a significant increase of maternal plasma levels of beta-Ep during labor. Moreover, obesity and marked weight gain during pregnancy caused a remarkable increase in beta-Ep probably due to latent dystocia.
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