The caudal deficiency and asplenia anomalies have been described separately in children. Two sibs with these two entities are described. Only another similar case, with caudal deficiency and polysplenia anomalies was found in the literature. It is possible that this association could be a new syndromic entity. An autosomal recessive mode of inheritance is suggested.

We report on a monozygotic twin with sirenomelia and anencephaly. This association seems to have been observed only twice before. In addition to these anomalies the patient had cleft palate, rachischisis, and segmentation vertebral anomalies affecting the cervical and the upper thoracic spine. The second twin was a liveborn female infant with a large cystic paraovarian teratoma, and duplication of internal genitalia.

This work is based on the follow-up evaluation of 67 moderate (MD) or severe gastric dysplasias (SD) diagnosed by endoscopic biopsy. Forty-one patients had moderate gastric dysplasia, 22 (53.65%) had regression of MD, 14 patients (34.4%) had persistence, three (7.31%) had progression to SD, and two (4.87%) had transformation in gastric adenocarcinoma. Twenty-six patients were diagnosed with severe gastric dysplasia: in 12 patients (46.15%) gastric lesions regressed to normality (five cases), mild (six cases) or moderate dysplasia (one case); six patients (23.07%) showed persistent histologic changes of SD in the subsequent biopsy specimens; eight patients (30.7%) presented progression of lesions to gastric adenocarcinoma after 1 to 79 months of follow-up evaluation. The authors conclude that moderate and severe gastric dysplasias are preneoplastic lesions and a valuable marker of gastric cancer risk; the risk of gastric cancer after moderate or severe dysplasia is of 9.52%, excluding those cases with short follow-up. The authors claim that these patients may receive a conservative clinical treatment with frequent endoscopic studies until the appearance of either early carcinoma to indicate gastrectomy, or no dysplasia at all or mild dysplasia in specimens from at least two consecutive biopsies.

Our series, which is the largest prospective cohort of FDRs published, reports an elevated incidence of SP in FDRs, thus supporting the need for screening colonoscopy in FDR and its inclusion in the guidelines.

The development of the normal human upper tibial growth plate was studied at autopsy in 46 stillborns and 79 newborns of 20-41 weeks gestational age. During this time period, the histology of this plate evolves from a highly cellular structure with relatively poor columnar organization and matrix development to the well known structure seen later in postnatal life. The thickness of the growth plate, assessed in the area surrounding the longitudinal tibial axis, decreases continuously from 1.15 mm on the 20th week to 0.6 mm on the 38th week. This decrease results from losses of both matrix and cellular components, mostly of the latter. However, the relative fraction of area occupied by the matrix significantly increased (12%) and matrix area per cell increased 1.5 times over the last half of gestation, indicating a maturation process of the plate towards a more matrix-oriented structure with age. In this maturation process the number of cells per unit area does not change and the average size of the cells appears to decrease. Plate thickness does not decrease further in the final 3 weeks of pregnancy and increases in early neonatal life; this has no apparent influence on the tibial growth rate. In the period under study the relative anatomical participation of the upper tibial growth plate decreases from approximately 4% of the radiographic length of the tibia on the 20th week to less than 1% at term. Present data will provide fetal and neonatal growth plate standards needed to obtain a better understanding of this structure during both normal and abnormal conditions.