In:
Lipids, Wiley, Vol. 37, No. 10 ( 2002-10), p. 953-957
Abstract:
Long‐chain PUFA (LCP) deficiency is a frequent complication in cholestatic infants. We investigated the effects of LCP‐supplemented formula on EFA status in infants with cholestasis. Twenty‐three infants with cholestasis (biliary atresia after surgery, 8; intrahepatic cholestasis, 15) aged 1.9 to 4.9 mon (median 3.1 mon) were randomized to receive commercial infant formulas either without LCP or with LCP from egg phospholipids for 1 mon. Liver tests, nutrient intakes, and plasma phospholipid FA (%w/w) were determined at baseline and after intervention. At baseline, patients had high serum direct bilirubin levels (5.9 ± 3.0 mg/dL; mean ± SD), they were malnourished (body fat mass: 40 ± 13% of normal) and presented with PUFA deficiency [plasma phospholipid PUFA: 28.43%w/w (26.56–30.53) in patients vs. 37.02%w/w (34.53–39.58) in controls; median (1st–3rd quartile)] with elevated Mead acid and palmitoleic acid. LCP‐supplemented ( n =11 and‐nonsupplemented groups ( n =12) did not differ in age, indicators of liver function, and EFA status at baseline. After the intervention, LCP‐supplemented infants had higher levels of arachidonic acid [7.2 (5.9–8.8) vs. 4.2 (3.0–5.3) %w/w; P 〈 0.001] and DHA [2.8 (2.2–3.2) vs. 1.6 (1.0–2.1) %w/w; P 〈 0.05], accompanied by increased [BARS concentration: 1.9 (1.4–2.2) vs. 1.3 (1.1–1.6) nmol/mL; P 〈 0.05]. We concluded that LCP‐supplemented formulae improve LCP status of infants with severe cholestasis but may enhance lipid peroxidation.
Type of Medium:
Online Resource
ISSN:
0024-4201
,
1558-9307
DOI:
10.1007/s11745-006-0986-z
Language:
English
Publisher:
Wiley
Publication Date:
2002
detail.hit.zdb_id:
2030265-4
SSG:
12
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