The Effect of Probiotic Supplement on Urinary D-lactic Acid Level in Newborns
The Effect of Probiotic Supplement on Urinary D-lactic Acid Level in Newborns
It is thought that prophylactic enteral probiotics in newborns may play a role in the
 prevention of infection and NEC-related morbidity by preventing bacterial migration in the
 mucosa, reducing their number by competing with pathogenic bacteria, providing microbial
 balance, and increasing intestinal immunity.

 In our study, it was determined to detect normal D-lactic acid levels in urine in late
 premature (babies born after 34 weeks of gestation) and term babies, to show the negative
 effect of antibiotic treatment on the intestinal flora indirectly by measuring urinary
 D-lactic acid, and the probiotic support in babies using antibiotics was disrupted. We aim to
 investigate our hypothesis that it will have a corrective effect on the intestinal flora by
 comparing urinary D-lactic acid levels.
Lactic acid exists as two optical isomers, L-lactic acid and D-lactic acid. These isomers are
 metabolized to or synthesized from pyruvate by the action of isomer-specific enzymes
 (L-lactate dehydrogenase and D-lactate dehydrogenase). Mammals, including humans, do not
 possess D-lactate dehydrogenase, and therefore D-lactate production in human tissue is very
 limited. The endogenous single D-lactate synthesis known in man is carried out by glyoxalase.
 In this pathway, methylglyoxal is converted into D-lactate by the enzymes glyoxalase-1 and
 glyoxalase-2. Due to this restricted production, the blood D-lactate level in healthy people
 is so low that L-lactate is the major physiological enantiomer of lactate in the human body.

 The bacterial flora in the human gastrointestinal tract has the ability to produce L and / or
 D-lactate depending on the amount of L-LDH and D-LDH present. Some strains of bacteria have
 the enzyme DL-lactate racemase to convert one isomer to another. Therefore, racemization
 reactions can further increase the amount of D-lactate isomers present in the column.
 Although there is no D-lactate dehydrogenase enzyme in humans, D-Lactate is metabolized into
 pyruvate by the enzyme D-2-hydroxy acid dehydrogenase (D-2-HDH), an intramitochondrial
 flavoprotein with high activity in the liver and renal cortex. The kidney's threshold for
 D-lactate is much lower than L-lactate and is efficiently excreted in urine as well as
 metabolic clearance. Thus, under normal conditions, D-lactate produced by tissue metabolism
 or bacterial fermentation in the gut; It does not cause a clinically significant increase in
 lactate in blood, urine or feces.

 D-lactic acidosis is a well-defined complication of short bowel syndrome due to the
 combination of altered gastrointestinal tract anatomy and abnormal bacterial flora. Many case
 reports reported in the literature are associated with short bowel syndrome secondary to
 various causes. There are studies investigating the effects of fermented formulas and
 probiotics on D-lactic acid in healthy babies. In these studies, no increased risk for
 D-lactic acidosis was found in healthy infants fed with probiotic supplemented formulas.

 Considering the studies on newborns; In babies with necrotizing enterocolit, it has been
 shown that urinary D-lactate excretion increased as a result of increased enteric bacterial
 activity. In another study, plasma D-lactic acid level was found to be high in premature
 babies with necrotizing enterocolitis. However, more detailed studies on newborns are needed.
Inclusion Criteria:

 -  Late preterm and term babies

 -  Babies who are fed only breast milk and / or formula with breast milk

 -  Babies who have to be given formula support in the early period because they cannot
 receive breast milk or are not sufficient in the neonatal period, therefore probiotic
 support is started and continues

 -  Babies whose antibiotic treatment is started in the neonatal period

 -  Babies whose parents consent to participate in the study

 Exclusion Criteria:

 -  Hypoxic ischemic encephalopathy

 -  Babies with urinary tract infections

 -  Babies with a history of premature rupture of membranes

 -  Chromosomal abnormality

 -  Those with major congenital anomaly, gastrointestinal system anomaly

 -  Presence of any known immunodeficiency,