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Influence of protein intake and liver function on acid base balance in premature infants
Insights
Late metabolic acidosis (LMA) in infants is linked to impaired liver function, particularly after formula feeding. Higher serum bile acid levels and altered stool characteristics indicate this condition, suggesting liver function checks before high protein intake.
Area of Science:
- Neonatal Medicine
- Pediatric Gastroenterology
- Biochemistry
Background:
- Late metabolic acidosis (LMA) is a concern in infants.
- Factors contributing to LMA require further investigation, especially in formula-fed infants.
Purpose of the Study:
- To investigate the factors promoting late metabolic acidosis (LMA) in infants.
- To identify potential markers for LMA and understand its pathogenesis.
Main Methods:
- Study included 43 patients with LMA.
- Compared renal function, serum bile acid concentration, stool volume, and fecal fat excretion between acidotic and non-acidotic infants.
- Investigated the impact of postnatal adaptation and formula feeding.
Main Results:
- No significant differences in renal function (urine volume, molar excretion) between groups.
- Significantly higher serum bile acid concentrations in LMA patients.
- Increased fractional stool volume and higher fecal fat excretion observed in LMA patients.
- Acidosis often developed after introduction of formula feeding.
Conclusions:
- Impaired postnatal liver function development, potentially due to severe postnatal adaptation disturbances (e.g., respiratory distress, sepsis), is a key factor in LMA pathogenesis.
- Serum bile acid concentration is a reliable marker for LMA.
- Liver function should be assessed before introducing protein intake exceeding that of breastfed infants.
Abstract:
In 43 patients with late metabolic acidosis (LMA) the factors promoting LMA were investigated. Postnatal adaptation was distributed in all cases, in 35 patients acidosis developed after introduction of formula feeding. Whereas no differences were observed in renal function (urine volume and renal molar excretion) between acidotic and non-acidotic patients, there was a significantly higher concentration of bile acids in serum (26.1 +/- 9.6 vs 98.6 +/- 21.6 mumol/l), a significantly increased fractional volume of stools (8.2 +/- 1.3 vs 11.4 +/- 1.9% of intake, and higher faecal fat excretion (26.5 +/- 5.2 vs 39.1 +/- 6.6% of faecal weight) in LMA patients than non-acidotic formula-fed infants. It is suggested that impaired postnatal development of liver function caused by severe disturbances of postnatal adaptation (respiratory distress, persistent fetal circulation, sepsis) is one of the most important factors in the pathogenesis of LMA. Thus, liver function should be checked before a protein intake surpassing that of a breastfed infant is introduced. Concentration of the serum bile acid level seems a reliable marker of LMA.