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Vitamin E and liver damage in MZ heterozygous infants with alpha 1-antitrypsin deficiency
1Department of Pediatrics, Regional Hospital, Bolzano/Bozen, Italy.
Insights
Vitamin E supplementation reduced liver dysfunction in infants with alpha-1-antitrypsin deficiency (PiMZ carriers) at two months. This highlights the role of oxidative stress in infant liver damage and the protective potential of antioxidants.
Area of Science:
- Pediatric Hepatology
- Biochemistry
- Nutritional Science
Background:
- Alpha-1-antitrypsin deficiency (AATD) predisposes infants to liver disease.
- PiMZ carriers may experience subclinical liver issues due to unchecked protease activity and oxidative stress.
- Hepatic damage in infants can be severe, impairing liver function.
Purpose of the Study:
- To investigate the impact of vitamin E on liver dysfunction in PiMZ carriers.
- To explore the role of oxidative free radicals in infant liver damage.
- To assess the relationship between plasma alpha-tocopherol levels and liver damage.
Main Methods:
- Observational study of PiMZ carriers.
- Assessment of liver dysfunction at two and five months of age.
- Measurement of plasma alpha-tocopherol levels.
Main Results:
- Vitamin E reduced liver dysfunction frequency in PiMZ carriers at two months.
- This protective effect was not observed at five months.
- Liver damage correlated with low plasma alpha-tocopherol levels.
Conclusions:
- Oxidative free radicals contribute to liver damage in infants with AATD.
- Vitamin E demonstrates a protective role against early-onset liver dysfunction.
- Further research is needed on vitamin E's interaction with other antioxidants in AATD.
Abstract:
Low levels of alpha 1-antitrypsin can predispose affected infants to develop a wide spectrum of liver diseases. Heterozygous PiMZ carriers can be affected by a subclinical liver involvement in the first six months of life. The liver damage appears to be mediated by the activity of toxic oxygen waste products originating from partially unchecked proteases which can cause enough damage to impair hepatic function significantly. In the present study it was found that the antioxidant properties of vitamin E were able to reduce the frequency of liver dysfunction in PiMZ carriers at two but not at five months of age. Liver damage is highly related to low levels of alpha-tocopherol in the plasma. These findings show that oxidative free radicals can promote liver damage in inadequately protected young infants, such as those affected by alpha 1-antitrypsin deficiency. The protective role of vitamin E in relation to the developmental expression of other antioxidant scavengers is discussed.
