During the final prenatal period of fetal lung development in humans, important maturational processes occur, including the production of surfactant necessary to decrease surface tension at the air-liquid interface of the alveoli. During early gestation, the glucocorticoid receptor is expressed in the fetal lung, and glucocorticoids stimulate the production of surfactant-associated proteins and increase phospholipid synthesis by enhancing the activity of phosphatidylcholine. Other glucocorticoid-induced effects may include stimulation of cell maturation and differentiation, inhibition of DNA synthesis, changes in interstitial tissue components, stimulation of antioxidant enzymes, and regulation of pulmonary fluid metabolism. Recently, it was suggested that glucocorticoids are also important in postnatal pulmonary development, and may be related to the development of neonatal lung disease in preterm infants. Surfactant deficiency that can be prevented by antenatal corticosteroid treatment causes infant respiratory distress syndrome and requires mechanical ventilation. Ventilation by itself or in combination with high levels of oxygen, fluid overload, pulmonary infections, sepsis, and air leak syndrome causes an acute pulmonary inflammatory reaction that may result in chronic lung disease or bronchopulmonary dysplasia. Glucocorticoids are effective in the treatment of chronic lung disease of prematurity and regulate the inflammatory response by the interaction with transcription factors such as nuclear factor kappaB and activated protein 1. Indeed, inflammatory cells and the levels of chemokines and cytokines in bronchoalveolar fluid decrease after dexamethasone treatment. However, treatment of fetuses and preterm infants with repeated and/or high doses of corticosteroids may have considerable long-term side effects on somatic, brain, and lung growth. The difficult balance between short-term gain and the possible long-term side effects of glucocorticoids in preterms remains a difficult issue.

To study the maturity of the adrenal cortex in preterms born before 33 wk of gestation, basal levels of cortisol and cortisone and the cortisol and 17-hydroxyprogesterone (17-OHP) response to 1 microg/kg adrenocorticotropic hormone stimulation were measured in 24 appropriate-for-gestational age preterm infants (26-33 wk; 690-1985 g). Gestational age influenced the response of cortisol, 17-OHP, and the ratio between cortisol/17-OHP in the studied infants. In preterms born <30 wk of gestation, levels of cortisol, and the ratio between cortisol/17-OHP were lower compared with preterms born between 30 and 33 wk. Levels of cortisone were higher in preterms born <30 wk, suggesting a lower activity of 11 beta-hydroxysteroid dehydrogenase that may be related to maturity as well. These findings indicate that the adrenal cortex function in preterm infants is closely related to the duration of gestation and may be important in neonatal morbidity.

The development of the hypothalamic-pituitary-adrenal (HPA) axis in the human fetus is a complex process. The feto-placental unit may be responsible for important maturational processes in vital organ systems in the fetus. A late gestational cortisol surge may be important in fetal maturation, particularly maturation of the lungs. Several striking differences exist between the function of the HPA axis in the fetus and in adults, such as a relative deficiency of 3beta-hydroxysteroid dehydrogenase in the fetal adrenal cortex. With the transition from intrauterine to extra-uterine life several changes occur in the function of the HPA axis. In infants born before term, the function of the HPA axis may still be immature at both the central and adrenal level. This immaturity of the HPA axis may be important in the development of neonatal morbidity. The present review describes the development of the HPA axis in the fetus and in preterm infants and discusses the possible role of HPA immaturity in the development of neonatal morbidity.

Renal abscesses are infrequently encountered in children. We describe a girl diagnosed with bilateral renal abscess. Although ultrasonography and computerised tomography are used to establish the diagnosis, in our case magnetic resonance imaging proved to be a useful additional diagnostic method. Using percutaneous aspiration, we were able to establish the correct diagnosis and identify the causative micro-organism. The patient was successfully treated with a combined intravenous and oral course of antibiotics. In conclusion, renal abscesses can occur in children without a history of reflux or urinary tract infection; this should be kept in mind when evaluating a child with fever. In addition, full recovery can be achieved solely with antibiotics.

Small for gestational age preterm infants have a higher risk of neonatal morbidity compared to appropriate for gestational age preterm infants. A diminished adrenal response to stress may be involved in the higher postnatal morbidity. The adrenal cortex response in relation to fetal growth was studied by ACTH stimulation tests in 43 preterm infants (born < or = 32 wk). The cortisol and 17-hydroxyprogesterone (17-OHP) responses to 1 microg/kg ACTH were analyzed in relation to birth weight SD scores (BW-SDS) corrected for gestational age, gender, and parity. BW-SDS was significantly associated with the cortisol and 17-OHP response. Infants with the lowest BW-SDS had the lowest cortisol levels after stimulation. No effect of size at birth was found on the ratio between cortisol and 17-OHP. In addition, basal cortisone levels in a single blood sample were higher in infants with the lowest BW-SDS than in infants with higher BW-SDS, but the ratio between cortisol and cortisone was comparable in the two groups. We conclude that the response of cortisol and 17-OHP to ACTH stimulation in preterm infants is related to fetal growth. The lack of influence of fetal growth on the ratio between cortisol and 17-OHP after ACTH stimulation suggests that the activities of 21- and 11 beta-hydroxylase are not affected. The lower adrenal response to stimulation may be important in neonatal morbidity and possibly the development of disease in later life in growth-restricted preterm infants.