To determine whether early and prolonged supply of ARA and DHA improves quality of growth and clinical outcomes in extreme premature infants as compared to our present nutrient supply. By closely assessing nutritional intake, anthropometric measures, clinical outcomes and several biomarkers of inflammation and metabolism, we hope to elucidate mechanisms of inflammation and metabolic mediated damage to major organs such as brain, lung, eye and cardiovascular system of extremely premature infants.
Conditions
Interventions
Trade Name: Clinoleic
Pharmaceutical Form: Emulsion for infusion
Trade Name: Omegaven
Pharmaceutical Form: Emulsion for infusion
Sponsors
Oslo University Hospital
Eligibility
Sex/Gender
All
Inclusion criteria
Inclusion criteria: All extremely preterm infants born at OUH between 01.09.17 and 31.12.19 with GA=65 years) no F.1.3.1 Number of subjects for this age range
Exclusion criteria
Exclusion criteria: congenital malformations, chromosomal abnormalities and critical illness with short life expectancy
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Main Objective: To assess the effects of an early nutritional intervention on clinical outcomes and quality of growth in extreme premature infants (gestational age < 29 weeks). Main hypothesis: Early, enhanced supply of the essential FAs DHA and ARA will improve brain growth and maturation, as compared to standard nutrient supply. ;Secondary Objective: To explore potential differences in inflammatory and metabolic pathway responses related to nutrient supply, age, sex, comorbidities, as well as pre- and postnatal growth. Secondary hypotheses: Early, enhanced supply of the essential FAs DHA and ARA will improve quality of growth and cognitive development and it will reduce the frequency of inflammation-related neonatal comorbidities and long-term cardiovascular disease risk. ;Primary end point(s): Brain maturation assessed by MRI with spectroscopy (MRS) and diffusion tensor imaging (DTI) ;Timepoint(s) of evaluation of this end point: Term equivalent age (+/- 2 weeks). | — |
Secondary
| Measure | Time frame |
|---|---|
| Secondary end point(s): 1) Nutritional intakes 2) Anthropometric measurements: Weight nadir, time to regain birth weight, change in weight, length and HC (absolute and z-scores), and growth velocity from birth to 28 days and 36 weeks postmenstrual age (PMA), and at 3, 6, 12 and 24 months as well as 8 years CA. 3) Body composition 4) The cumulative incidence of neonatal morbidities associated with inflammation (BPD, ROP, NEC, WMI, and late onset septicemia). The frequency of persistent ductus arteriosus, postnatal growth restriction, hyperglycemia and hypotension. 5) Inflammatory, metabolic and nutrient markers in blood, urine and feces. 6) Neurodevelopment assessed by neurological and neuropsychological examinations as well as sophisticated neuroimaging modalities and neurophysiological tests. 7) Cardiovascular health assessed by echocardiography (both structural and functional) and with blood pressure (BP) measurements. 8) Lung function ;Timepoint(s) of evaluation of this end point: 1) daily during neonatal hospitalization 2) during neonatal hospitalization: weight daily, HC/lenght weekly; thereafter as given above. 3) at 36 weeks PMA, 6 months, and 8 years CA 4) short-time clinical outcomes will be registrered during neonatal hospitalization 5) days 0,1,2,3,5,7,14,21,28, and at 32 and 36 weeks PMA as well as at 3, 6, 12, and 2 and 8 years CA. 6) cerebral ultrasound and EEG at days 0,1,2 and at 32 and 36 weeks PMA. EEG also at 24 months CA. Standardized neurological examination and neuropsychological test (Bayley III) at 2 years CA. MRI at 8 years CA. 7) Echocardiography at days 0,1,2 and at 36 weeks PMA as well as at 2 and 8 years CA 8) Lung function at 36 weeks PMA and at 2 and 8 years CA | — |
Countries
Norway
Contacts
Public ContactDepartment of Neonatal Medicine
Oslo University Hospital
Outcome results
None listed