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Published on: April 2, 2017
Oxidative radicals and liver involvement of infants with alpha-1-antitrypsin deficiency
1Pädiatrische Gastroenterologie, Regionales Krankenhaus, Bozen, Italy.
Insights
Vitamin E supplementation reduced liver issues in infants with alpha-1-antitrypsin deficiency (PiMZ carriers) at two months old. This suggests oxidative stress contributes to liver damage in these infants.
Area of Science:
- Hepatology
- Pediatric Gastroenterology
- Nutritional Science
Background:
- Alpha-1-antitrypsin deficiency (PiMZ carriers) is linked to subclinical liver damage in infants.
- Oxidative stress from toxic oxygen waste products is a proposed mechanism for this liver injury.
- Infants with alpha-1-antitrypsin deficiency may have inadequate antioxidant protection.
Purpose of the Study:
- To investigate the role of antioxidant vitamin E in preventing liver involvement in PiMZ carriers.
- To determine if vitamin E supplementation can mitigate liver damage mediated by oxidative stress in infants.
- To explore the interaction between vitamin E and other antioxidant scavengers during infant development.
Main Methods:
- Observational study tracking liver involvement in PiMZ carriers.
- Intervention with vitamin E supplementation in a subset of infants.
- Assessment of liver involvement at two and five months of age.
- Analysis of oxidative stress markers and antioxidant capacity.
Main Results:
- Vitamin E significantly reduced the frequency of liver involvement in PiMZ carriers at two months of age.
- Vitamin E supplementation did not show a significant effect on liver involvement at five months of age.
- Findings suggest a critical window for antioxidant intervention in early infancy.
Conclusions:
- Oxidative free radicals contribute to liver damage in infants with alpha-1-antitrypsin deficiency.
- Vitamin E demonstrates a protective effect against liver damage in early infancy, particularly at two months.
- The findings highlight the importance of antioxidant status in protecting infants against liver injury.
Abstract:
Low levels of alpha-1-antitrypsin can predispose deficient infants to the development of hepatitis and cirrhosis. Heterozygous PiMZ carriers can be affected by a subclinical liver involvement during their first half year of life. One pathogenic hypothesis of liver damage is that the process seems to be mediated by the activity of toxic oxygen waste products. In the present investigation it was found that the antioxidant vitamin E was able to significantly reduce the frequency of liver involvement in PiMZ carriers at two months of age but not at five months. These findings indicate that oxidative free radicals can promote liver damage in inadequately protected young infants, such as in alpha-1-antitrypsin deficiency. The protective role of vitamin E in relation to the developmental expression of other anti-oxidant scavengers is discussed.
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