Prematurity and Low Birth Weight and Their Impact on Childhood Growth Patterns and the Risk of Long-Term Cardiovascular Sequelae.

Preterm birth (before 37 completed weeks of gestation) is a global health problem, remaining the main reason for neonatal mortality and morbidity. Improvements in perinatal and neonatal care in recent decades have been associated with a higher survival rate of extremely preterm infants, leading to a higher risk of long-term sequelae in this population throughout life. Numerous surveillance programs for formerly premature infants continue to focus on neurodevelopmental disorders, while long-term assessment of the impact of preterm birth and low birth weight on child growth and the associated risk of cardiovascular disease in young adults is equally necessary. This review will discuss the influence of prematurity and low birth weight on childhood growth and cardiovascular risk in children, adolescents and young adults. The risk of cardiovascular and metabolic disorders is increased in adult preterm survivors. In early childhood, preterm infants may show elevated blood pressure, weakened vascular growth, augmented peripheral vascular resistance and cardiomyocyte remodeling. Increased weight gain during the early postnatal period may influence later body composition, promote obesity and impair cardiovascular results. These adverse metabolic alterations contribute to an increased risk of cardiovascular incidents, adult hypertension and diabetes. Preterm-born children and those with fetal growth restriction (FGR) who demonstrate rapid changes in their weight percentile should remain under surveillance with blood pressure monitoring. A better understanding of lifelong health outcomes of preterm-born individuals is crucial for developing strategies to prevent cardiovascular sequelae and may be the basis for future research to provide effective interventions.

Children with corpus callosum anomalies: clinical characteristics and developmental outcomes.

INTRODUCTION: Corpus callosum abnormalities are complex, aetiologically diverse, and clinically heterogeneous conditions. Counselling parents regarding their causes and associated syndromes, and predicting the neurodevelopmental and seizure risk prognosis, is challenging. MATERIAL AND METHODS: We describe the clinical characteristics, associated anomalies, and neurodevelopmental outcomes of children with agenesis of corpus callosum (ACC). Fifty-one neonates with ACC/hypoplasia of the corpus callosum were identified over a 17-year period, and their medical records were retrospectively reviewed. RESULTS: Patients were classified into two groups depending on the presence or absence of associated abnormalities. The first group (17 patients, 33.4%) presented with isolated callosal anomalies. The second group included 34 patients (66.6%) with associated cerebral and extracerebral anomalies. We achieved an identifiable genetic aetiology in 23.5% of our cohort. Magnetic resonance imaging was performed in 28 patients (55%), and of these 39.3% had additional brain anomalies. During the study period, five patients died early in the neonatal period and four were lost to follow up. Of the 42 followed patients, 13 (31%) showed normal neurodevelopment, 13 (31%) showed mild delay, and 16 (38%) had a severe delay. Fifteen (35.7%) had epilepsy. CONCLUSIONS AND CLINICAL IMPLICATIONS: We have confirmed that callosal defects are frequently accompanied by brain and somatic anomalies. Additional abnormalities were shown to be significantly associated with developmental delay and increased risk of epilepsy. We have highlighted essential clinical features that may provide diagnostic clues to physicians and we have given examples of underlying genetic disorders. We have provided recommendations about extended neuroimaging diagnostics and widespread genetic testing that may impact upon daily clinical practice. Paediatric neurologists may therefore use our findings to help base their decisions regarding this matter.

Fetal alcohol spectrum disorders - diagnostic difficulties in the neonatal period and new diagnostic approaches.

Fetal alcohol spectrum disorders (FASD) is a group of disorders that can occur in children whose mothers consumed alcohol in pregnancy. Diagnosis of fetal alcohol syndrome is based on the appearance of growth deficiency, the presence of the three key features of facial dysmorphism (short palpebral fissures, thin upper lip, smooth or flattend philtrum) and/or disorders in the central nervous system (minimum 3) and prenatal exposure to alcohol (confirmed if possible). Early diagnosis of fetal alcohol syndrome - after birth or in infancy - is very often impossible or very difficult due to the incomplete manifestation of the key dysmorphic features. The latest reports offer the chance of diagnosing children in the neonatal period. The research focuses on the analysis of ethanol metabolites in the biological tissues in pregnant women or newborns. These unique ethanol metabolites include: fatty acid ethyl esters (FAEE) present in the meconium, blood, hair of the mother and the newborn, ethyl glucuronide in the placenta and meconium, urine, nails and hair, and phosphatidylethanol (PEth) found in the infant blood. The presence of fatty acid ethyl esters in the meconium could be a non-invasive and cost-effective method of early detection of disorders associated with prenatal alcohol exposure.