Increased docosahexaenoic acid and n-3 polyunsaturated fatty acids in milk from mothers of small for gestational age preterm infants.

The study aimed to test whether or not milk fatty acid composition in mothers of small for gestational age (SGA) infants is similar to that in mothers of adequate for gestational age (AGA) infants. Thirty three mothers of SGA preterm infants and 66 mothers of AGA preterm infants were included. Milk and plasma fatty acids were analyzed using capillary gas chromatography. Milk DHA (0.68 ±â€¯0.37 vs. 0.44 ±â€¯0.24; p < 0.01) was higher and n-6:n-3 PUFA ratio (12.0 ±â€¯4.64 vs. 16.0 ±â€¯6.32; p < 0.05) was lower in mothers of SGA infants. Plasma ARA and DHA were increased in mothers of SGA infants and decreased in their infants. Milk ARA or DHA was positively related to the correspondent fatty acid in plasma (r = 0.374, p = 0.010 for ARA and r = 0.690, p < 0.001 for DHA). Breast milk in mothers of preterm infants born SGA is enriched in DHA and n-3 PUFA. Breastfeeding SGA preterm infant with own mother's milk is recommended.

Postnatal RBC arachidonic and docosahexaenoic acids deficiencies are associated with higher risk of neonatal morbidities and mortality in preterm infants.

Arachidonic (AA) and docosahexaenoic (DHA) acids are essential for the health and development of the neonate. Red blood cell (RBC) fatty acids were analyzed in 583 very low birth weight (VLBW) infants and 274 term infants using capillary gas chromatography. VLBW infants exhibited significantly lower RBC AA (13.0 ± 0.89 vs. 13.5 ± 0.98) and DHA (3.77 ± 0.60 vs. 3.80 ± 0.62), but higher n6:n3 ratio (3.97 ± 0.46 vs. 3.63 ± 0.37) than term infants. In VLBW infants, DHA was lower in those born with small for gestational age (3.69 ± 0.57 vs. 3.86 ± 0.58) and those who suffered from neonatal sepsis (3.73 ± 0.60 vs. 3.86 ± 0.55). Both AA and DHA were significantly lower in infants who developed respiratory distress syndrome or intraventricular hemorrhage, and those who died during the hospital stay. VLBW infants had lower postnatal RBC AA and DHA levels than term infants did. These deficits are associated with higher risk of neonatal morbidities and mortality.

Unbalanced bone remodeling in Tunisian patients with inflammatory bowel diseases.

BACKGROUND: Bone loss is an ignored complication in inflammatory bowel diseases. Its underling mechanisms are not fully elucidated. OBJECTIVES: To investigate bone turnover in patients with inflammatory bowel diseases. METHODS: The study included 67 patients with inflammatory bowel diseases and 54 age- and sex-matched healthy subjects. Urinary degradation products of C-terminal telopeptide of type I collagen, serum osteocalcin, parathyroid hormone, 25 hydroxy vitamin D and interleukin-6 were assessed. Bone mineral density was measured by dual energy-X-ray absorptiometry and osteoporosis was defined as T score < -2.5 SD. RESULTS: Patients showed significantly higher levels of C-terminal telopeptide of type I collagen and interleukin-6 and lower levels of 25 hydroxy vitamin D. Serum osteocalcin and parathyroid hormone were in normal range. In multivariate analysis, urinary degradation products of C-terminal telopeptide of type I collagen were associated with disease activity (p=0.04) and osteocalcin was associated with parathyroid hormone (p=0.04). Urinary degradation products of Cterminal telopeptide of type I collagen and interleukin-6 were significantly increased in inflammatory bowel disease patients with osteoporosis. No association was found between osteoporosis and serum osteocalcin, parathyroid hormone and 25 hydroxy vitamin D. CONCLUSION: Bone resorption rate is increased and is associated with osteoporosis in inflammatory bowel disease patients. Inflammation, malnutrition, and hypovitaminosis D may contribute to the bone loss.