No abstract

No abstract

Summary Ten placentae with massive subchorionic thrombohaematomas are reported. This lesion, which is composed of maternal clotted blood, separates the chorionic plate of the placenta from the villous chorion and is traversed by the main cotyledonary branches of the fetal circulation. In some instances it dissects into the layers of the chorionic plate. In anatomical terms it is identical to the lesion which has been described in early pregnancy under the title of Breus’ mole. Previous reports suggested that the lesion was confined to early pregnancies and was a consequence of fetal death. In our series all ten placentae were from pregnancies of at least 25 weeks' maturity and six were more than 30 weeks. Seven infants were liveborn and three survived the neonatal period. Differential diagnosis is discussed along with aetiology, which is still obscure although earlier theories implicating fetal death may be discounted.

No abstract

No abstract

Standards for human fetal intestinal length are not well established but have important implications for the care of the preterm and intrauterine growth-retarded (IUGR) infant. Our purpose was to examine the relationship between intrauterine growth and intestinal length in the human fetus. One hundred infants were studied. Birth weight and gestational age ranged from 76 to 4,385 g and from 12 to 42 weeks, respectively. Twenty-one infants were noted to be IUGR. Intestinal length (total, small, large) increased (p < 0.0001) with birth weight, gestational age, and crownheel length but was reduced in IUGR infants. The ratio of body weight to intestinal length increased with gestation but was also reduced in IUGR infants. In conclusion, a reduced functional mass, as suggested by decreased intestinal length or body weight:intestinal length ratio, may contribute to the poor weight sometimes seen in the very-low-birth weight or IUGR infant.

Mice homozygous for the autosomal-recessive gene hypothyroid (hyt) had congenital hypothyroidism of fetal onset after 15 days postconception. Neonatal hyt/hyt mice had reduced serum thyroxine ranging from 1/5 to 1/6 of normal as well as significantly delayed somatic and behavioral development. Delayed somatic development included retarded eye opening and ear raising, and reduced body length and body weight. The hyt/hyt animals compared to their normal littermates demonstrated delayed reflexive behavior and abnormal motor and adaptive behavior. The somatic and behavioral measures clearly distinguished hyt/hyt animals from their normal littermates even without T4 determination. The somatic and reflexive behavioral abnormalities in the hyt/hyt mouse were similar to other rodent models of human congenital hypothyroidism. The hyt/hyt mouse provided an ideal model for exploring the effect of severe primary inherited hypothyroidism related to deficient autonomous fetal thyroid function and was consistent with the hypothesis that thyroid hormone deficit in utero and in the early neonatal period significantly altered functional development.

The hyt/hyt mouse (BALB/cBY-hyt, C.hytRF) provides a useful model for exploring the effect of inherited severe primary hypothyroidism. Studies were undertaken to try to define the basis of the primary hypothyroidism in mice homozygous for the autosomal recessive gene, hyt. These mice had congenital hypothyroidism of fetal onset after 15 days post conception. Through their lifetime, the hyt/hyt mice had reduced serum thyroxine (T₄), triiodothyronine (T₃), reduced thyroid gland intralumenal colloid on electron microscopy and a 100-fold elevation of TSH-like activity compared to hyt/+ littermates. Thyroglobulin made in hyt/hyt animals was similar in size to normal thyroglobulin which was inconsistent with a major structural thyroglobulin gene defect. The thyroglobulin was iodinated. Marked, erratic dilation of rough endoplasmic reticulum (RER) was noted in hyt/hyt mouse follicular cells. Despite these ultrastructural findings, pulse chase and immunoprecipitation studies with isolated hyt/hyt and normal thyroid glands indicated that normal thyroglobulin processing occurred in the RER and Golgi of the hyt/hyt mice. The hyt/hyt thyroid glands were hypoplastic compared to hyt/ + littermates. Histologically, the hyt/hyt thyroid glands demonstrated an increase in smaller follicular cells, and greater variability in follicular size compared to hyt/ + littermates. Histological and ultrastructural abnormalities in the gland were similar to those seen in certain cases of human congenital hypothyroidism with TSH receptor insensitivity of the thyroid gland. These findings along with the significant TSH elevation, the reduction in colloid and in serum T₃ and T₄, the efficacy of the hypothalamo-pituitary-thyroid feedback system, and previous observations of reduced iodine uptake and intrathyroidal T4 [3], suggested that primary hypothyroidism in the hyt/hyt mouse might be due to a defect in TSH responsivity of the thyroid gland.