The substantial improvement in survival in France for newborns born at 25 through 31 weeks' gestation was accompanied by an important reduction in severe morbidity, but survival remained rare before 25 weeks. Although improvement in survival at extremely low gestational age may be possible, its effect on long-term outcomes requires further studies. The long-term results of the EPIPAGE-2 study will be informative in this regard.
This study confirms that the currently recommended dose regimen (10-5-5 mg/kg) of IBU is associated with a high closure rate (80%) and few adverse effects in premature infants with a PMA of 27-29 weeks. The failure rate was much higher below 27 weeks. A higher dose regimen (20-10-10 mg/kg) might achieve a higher closure rate. However, tolerability and safety of this dose regimen should be assessed in a larger population before considering the use of these doses for ductus arteriosus closure.
ArticlesTranslational Investigation nature publishing group
INTRODUCTION:To implement neuroprotective strategies in newborns, sensitive and specific biomarkers are needed for identifying those who are at risk for brain damage. We evaluated the effectiveness of matrix metalloproteinases (MMPs) and their naturally occurring tissue inhibitors of metalloproteinases (TIMPs) in predicting neonatal encephalopathy (Ne) damage in newborns. RESULTS: Plasma MMP-9 and TIMP-1 levels were upregulated as early as 1 h after the hI insult but not did not show such elevations after other types of injury (ibotenate-induced excitotoxicity, hypoxia, lipopolysaccharide-induced inflammation), and brain levels reflected this increase soon thereafter. We confirmed these results by carrying out plasma MMP-9 and TIMP-1 measurements in human newborns with Ne. In these infants, protein levels of MMP-9 and TIMP-1 were found to be elevated during a short window up to 6 h after birth. DISCUSSION: This feature is particularly useful in identifying newborns in need of neuroprotection. a second peak observed 72 h after birth is possibly related to the second phase of energy failure after a hI insult. Our data, although preliminary, support the use of MMP-9 and TIMP-1 as early biomarkers for the presence and extent of perinatal brain injury in human term newborns. METHODS: We first used a mouse model of neonatal hI injury to explore mechanistic aspects such as the time course of these markers after the hypoxia-ischemia event, and the correlation between the levels of these candidate markers in brain and plasma.T he major perinatal brain lesions associated with cerebral palsy and cognitive impairment are periventricular white matter damage and cortical-subcortical lesions, observed mainly in preterm and term infants, respectively (1,2). A crucial step for the implementation of neuroprotective therapies is the rapid detection of neonates at risk. Despite this urgent need, no appropriate and easily detectable biomarkers for perinatal injury are currently available.Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are involved in multiple processes during development and in adulthood (3-5), including perinatal hypoxia-ischemia (HI) and white matter damage in human neonates. Recent studies in adult MMP-9 knockout mice have demonstrated the key role played by this metalloproteinase in the pathophysiology of traumatic and hypoxic-ischemic (HI) brain injury (6). Concordantly, MMP-9 has been shown to have deleterious effects in the immature brain after HI injury (7). Several of these studies demonstrated a significant increase in MMP-9 expression in the central nervous system within the first 24 h after the insult. MMP-9 also has long-term beneficial effects on neurovascular remodeling and behavioral recovery after stroke in adult rats (8,9). In the adult rat central nervous system, elevated TIMP-1 expression levels may play a neuroprotective role after kainate-induced excitotoxic seizures (10), and gene transfer of TIMP-...
The aim of this study was to define the current demographic, clinical and prognostic characteristics of acute post-streptococcal glomerulonephritis (APSGN) in French Polynesia and to compare these features with those of other populations. Fifty children, all of whom were <15 years old and had been admitted to the Territorial Hospital of Papeete for APSGN between January 2005 and December 2007, were retrospectively enrolled in the study. Diagnostic criteria were microscopic or macroscopic haematuria, decreased C3 fraction of the complement and evidence of recent streptococcal infection. The annual incidence was 18 cases per 100,000 children <15 years of age in 2007. Most of the children (98%) enrolled in the study were of Polynesian ethnic origin, 27 were male (54%), and the average age at presentation was 6.7 years. Signs of previous respiratory infections were clearly evident in 40% of the children. Most of the patients presented during the rainy season, correlating with the relatively high incidence of skin infections at this time. The majority of patients had proteinuria (98%), with 25% having proteinuria in the nephrotic range (proteinuria/urinary creatinine >3 g/g). The presentation was severe in 22% of the children (congestive cardiac failure, severe hypertension and/or encephalopathy), and renal failure was an initial presenting symptom in 43.7%. The C3 fraction was lower in severe presentations, but the type of haematuria, level of proteinuria and inflammatory syndrome were not correlated with immediate severe forms or with initial renal failure. Haematuria resolved in a mean of 7.7 months and proteinuria in a mean of 3.9 months. None of the children had hypocomplementemia for more than 8 weeks. Acute post-streptococcal glomerulonephritis is endemic among French Polynesians, and they can be considered to be a high-risk population. Despite a high incidence of skin infections, however, the predominance of respiratory infections potentially indicates that French Polynesia is on the way to become a low-incidence area. Systematic detection and treatment of group A Streptococcus should be intensified.
Cerebellum injury is a severe and underestimated complication in very low birth-weight infants. Six cases of extreme premature babies are reported: 3 of them died during the neonatal period; the other 3 survived with severe neurological disabilities. Microcephaly, strabismus, and severe developmental delay without major motor handicap are very peculiar for the preterm in the long-term outcome. Easy diagnosis is possible by specific ultrasound windows and early diagnosis is required regarding the possible severe prognosis and to organize precisely the follow-up.
Localized skin necrosis with deeper soft tissue injury at birth is unusual and has been rarely reported in association with cerebral infarction. Two cases with forearm necrotic skin associated with injured deeper soft tissue are described in which brachial artery thrombosis was documented. Considering the possibility of disseminated thrombosis, cerebral ultrasound showed brain infarction due to unilateral middle cerebral artery thrombosis on Doppler. The origin of the embolism was identified in the inferior vena cava and umbilical and portal vein. No thrombophilia or other risk factors were identified. The various causes of the cutaneous lesions pointed to an antenatal process whose etiology and mechanisms are discussed. Localized necrotic skin lesions must be considered as part of a systemic embolic process and can lead to extensive especially cerebral ultrasound exploration.
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