Background: Hypoxic-ischaemic encephalopathy is a major cause of neurologic impairment and mortality in neonates. Early knowledge of brain injury is important to guide therapeutic decisions and reliably inform the parents. Increased secretoneurin levels have been detected in adult patients suffering from brain injury and it has also been shown to be a promising early serum biomarker of unfavourable neurological outcome. However, no data are available in neonates. Objective: The aim of this study was to obtain reference values for secretoneurin in healthy term neonates and then to assess the potential of this neuropeptide as a biomarker in the context of hypoxic-ischaemic encephalopathy in asphyxiated term neonates. Methods: A total number of 139 term neonates, of which 7 were asphyxiated and 132 were healthy, were prospectively enrolled. Secretoneurin serum concentrations were assessed by radioimmunoassay. Results: In healthy controls, secretoneurin serum concentrations were influenced by the mode of delivery (highest in infants born per vacuum extraction and lowest in infants born per caesarean section) and abnormal cardiotocography. In asphyxiated term neonates, secretoneurin concentrations were higher in umbilical cord blood and significantly lower 48 h after birth in comparison to healthy controls. Conclusion: Secretoneurin levels are elevated in cord blood in infants suffering from hypoxic-ischaemic encephalopathy following perinatal asphyxia. The potential of secretoneurin as a marker of neonatal hypoxic-ischaemic brain injury should be further evaluated in larger trials.
The prevalence of gallbladder polyps reported in the present study (6.1 %) is higher than figures previously published for populations in Germany or Europe. The majority of polyps were pedunculate and solitary. A typical risk factor profile for gallbladder polyps could not be identified in the present population sample.
The case demonstrates the difficulties in the diagnosis of tuberculosis in patients with signs and symptoms similar for those caused by other multisystemic diseases. When tuberculous meningitis is considered, therapy should be initiated even in cases with negative microbiological tests because of severe consequences when treatment is delayed.
Background
Hypoxic-ischaemic encephalopathy (HIE) is a major cause of neurologic impairment and mortality in neonates suffering from perinatal asphyxia. Early information on prognosis is of great importance to guide therapeutic decisions and to inform the parents. The neuropeptide secretoneurin (SN) was shown to be a promising early serum biomarker of an unfavourable neurological outcome in adult patients after cardiopulmonary resuscitation. Currently, there are no studies on SN levels in neonates available.
Aim
To determine physiological SN levels in healthy term neonates and to assess its potential as a biomarker for HIE in newborn infants.
Methods
At present this study prospectively enrolled 46 healthy term born neonates (29 male) and four term born neonates with moderate to severe HIE. SN levels were assessed by radioimmunoassay in cord blood.
Results
In healthy newborn infants mean SN serum levels in cord blood were 126.33 ± 87.47 fmol/ml. In the four patients diagnosed with moderate to severe HIE, SN levels in cord blood were significantly higher compared to healthy controls (253.48 ± 102.55 fmol/ml, p < 0.05).
Conclusion
SN serum levels in healthy neonates contained on average 126 fmol/ml, which is in accordance with elevated SN serum levels observed in children compared to adults in a previous study. In patients with moderate to severe HIE SN serum levels were significantly increased compared to healthy controls. We are currently enrolling further patients to investigate a possible association with the neurological outcome.
Background
Preterm brain injury causes neurodevelopmental disability. Excitotoxicity plays an important role in the pathogenesis of preterm brain injury. The neuropeptide secretoneurin (SN) was shown to enhance angiogenesis and neurogenesis in a rodent model of adult ischaemic brain damage. SN might be considered a promising substance in newborn brain injury.
Aim
To evaluate the effect of SN as a therapeutic strategy in an established
in vivo
model of excitotoxic newborn brain injury.
Methods
Five-day-old mice pups were subjected to an intracranial injection of ibotenic acid into the right brain hemisphere. After recovery for one hour, animals were randomly treated with an intraperitoneal injection of i) vehicle, ii) SN 0.25 µg/g body weight (bw) or iii) SN 2.5 µg/g bw. Brains were harvested 24 and 120 h after the insult and processed for histological analysis. As a primary outcome parameter lesion size in cortical grey and white matter was evaluated.
Results
SN administration had no significant effect on lesion size 120 h after the insult. When evaluated 24 h after the excitotoxic insult, SN showed a marked, but non-significant trend towards a decreased lesion size in white matter (SN 0.25 µg/g 323.33 ± 128.82, SN 2.5 µg/g bw 298.46 ± 137.46, vehicle 440.00 ± 227.81, n = 13–19, p = 0.06). SN had no effect on lesion size in grey matter.
Conclusion
This study shows a trend towards a reduced injury in white matter in an
in vivo
model of neonatal brain injury. We are currently performing immunohistochemical analysis to evaluate underlying mechanisms that could result in long-term protection.
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