Early high C-reactive protein in infants with open abdominal wall defects does not predict sepsis or adverse outcome.

AIM: To study CRP values and relate it to outcome in infants with antenatal diagnosis of gastroschisis, exomphalos and other surgical conditions. METHODS: Over five years, infants admitted to our neonatal unit with gastroschisis, exomphalos and other surgical diagnoses were identified. Serum CRP measurements in first 5 days were studied. Group one included 33 gastroschisis patients, group two, 18 exomphalos patients, and group three, 38 patients with other surgical diagnoses. Outcome measures included TPN days, time to full feeds and duration of hospitalization. RESULTS: Infants with gastroschisis were more premature (36.9 vs 38.1 weeks) with lower birth weights (2515 vs 3078 g), than infants with exomphalos. CRP values on admission in gastroschisis group were significantly higher than exomphalos and other diagnoses groups (33.7 +/- 6.4 vs 8.8 +/- 6.0 vs 5.7 +/- 2.0, respectively, p < 0.05). All blood cultures were sterile. There was no relationship between high CRP and death or adverse outcome (TPN days, time to full feeds or duration of hospitalization) in the gastroschisis group. CONCLUSION: Infants with gastroschisis exhibit high early CRP, which may not indicate sepsis or adverse outcome. This increase can complicate the assessment of these infants. Clinicians should be aware of this finding as it could inform management decisions in this group.

Detection of meticillin-resistant staphylococcus aureus (MRSA) colonization in newborn infants using real-time polymerase chain reaction (PCR).

OBJECTIVE: Meticillin-resistant staphylococcus aureus (MRSA) colonization on neonatal units is a common and important clinical problem. Effectiveness of polymerase chain reaction (PCR) for detecting MRSA nasal colonization of infants was evaluated and compared to culture-based methods. The effect of skin decolonization in affected infants was studied. METHODS: Paired nasal swabs were collected from infants in our neonatal unit over a 12-month period (September 2007-2008). Colonization with MRSA was determined with a commercially available PCR method and compared to culture. RESULTS: A total of 696 paired nasal swabs were taken. Three infants were colonized at the beginning and were included. There were positive PCRs in 12 infants. Five infants cultured MRSA from a nasal swab at the same time. No infants were culture-positive when PCR was negative (sensitivity 100%, specificity 99% compared to culture). PCR results were available within 24 h. Five infants were PCR+ and isolated meticillin-sensitive Staphylococcus aureus. This organism gave a false-positive PCR result. Two infants transferred in on broad-spectrum antibiotics were PCR+ and negative by culture. Decolonization led to negative nasal PCR and culture in 4/5 infants to discharge. CONCLUSIONS: PCR methods are sensitive and specific for detection of MRSA colonization in newborn infants of all gestations with results 1-2 days before culture.

Maternal origin of inflammatory leukocytes in preterm fetal membranes, shown by fluorescence in situ hybridisation.

The aim of this study was to determine the maternal or fetal origin of inflammatory leukocytes in fetal membranes from cases of chorioamnionitis. Fetal membranes were collected from male preterm infants and chorioamnionitis was diagnosed histologically. Fluorescence in situ hybridisation for X and Y chromosomes was used to determine the gender of infiltrating leukocytes in the chorion and amnion. Leukocytes, trophoblast and mesenchymal cells were identified using immunohistochemistry for CD45, cytokeratin-7 and vimentin, respectively. Leukocytes present in the chorion and amnion were labelled XX, indicating maternal origin, and these cells were immunoreactive for the leukocyte marker CD45 but not for vimentin or cytokeratin-7. All other cells in the chorion and amnion were labelled XY and of fetal origin. The results indicated that maternal leukocytes invade the amnion and chorion in chorioamnionitis and we suggest that this is part of the maternal inflammatory response to intrauterine infection.

Beckwith-Wiedemann syndrome associated with congenital hypothyroidism in a preterm neonate: a case report and literature review.

This report describes for the first time the association of Beckwith-Wiedemann syndrome (BWS) and hypothyroidism in a 25 weeks preterm neonate. Antenatal diagnosis of exomphalos in association with postnatal transient hypoglycemia and macroglossia formed the basis of the diagnosis of BWS. Primary hypothyroidism was detected on routine Guthrie card examination. Molecular DNA analysis demonstrated biparental inheritance of chromosome 11p15.5. Dosage analysis of differently methylated region showed evidence of loss of maternal methylation at KvDMR1.

Fetal and neonatal gene therapy: benefits and pitfalls.

The current approaches to gene therapy of monogenetic diseases into mature organisms are confronted with several problems including the following: (1) the underlying genetic defect may have already caused irreversible pathological changes; (2) the level of sufficient protein expression to ameliorate or prevent the disease requires prohibitively large amounts of gene delivery vector; (3) adult tissues may be poorly infected by conventional vector systems dependent upon cellular proliferation for optimal infection, for example, oncoretrovirus vectors; (4) immune responses, either pre-existing or developing following vector delivery, may rapidly eliminate transgenic protein expression and prevent future effective intervention. Early gene transfer, in the neonatal or even fetal period, may overcome some or all of these obstacles. The mammalian fetus enjoys a uniquely protected environment in the womb, bathed in a biochemically and physically supportive fluid devoid of myriad extra-uterine pathogens. Strong physical and chemical barriers to infection might, perhaps, impede the frenetic cell division. The physical support and the biochemical support provided by the fetal-maternal placental interface may, therefore, minimize the onset of genetic diseases manifest early in life. The fetal organism must prepare itself for birth, but lacking a mature adaptive immune system may depend upon more primordial immune defences. It is the nature of these defences, and the vulnerabilities they protect, that are poorly understood in the context of gene therapy and might provide useful information for approaches to gene therapy in the young, as well as perhaps the mature organism.