Introduction - It is known that preeclampsia causes uteroplacental insufficiency, which then causes hypoxia in the fetus and its organs. As a result of placental insufficiency, fetal stagnation develops with complications in the form of intrapartum hypoxia of the fetus, perinatal morbidity, asphyxia of the fetus, as well as other postnatal complications.
The aim of the paper - is to analyze the importance of determining the length of the right lobe of the fetal liver and lactate-dehydrogenase in the serum of the fetus in pregnant women with preeclampsia in predicting fetal growth retardation as well as the risk of fetal well-being in pregnancy.
Material and methods - 120 pregnant women were included in the research, of which 60 pregnant women are with physiological pregnancy and 60 pregnant women with preeclamptic pregnancy with IUGR. In pregnant women with a physiological pregnancy, the pregnancy develops in a physiological way, with the birth of a child with a normal weight corresponding to the gestational age, normal development of the placenta, normal development of the umbilical cord and amniotic fluid. In pregnant women with preeclampsia, preeclampsia developed with the presentation of atrial pressure higher than TA = 140/90mmHg, with the presence of proteinuria higher than 0.5gr/l, as well as the determination of IUGR using the Hadlock formula. The results are calculated with these statistical methods. Examination of the normality of the distribution of continuous numerical changes was performed by inspection of histograms, quantile plots, and formal testing using the Kolgomorov-Smirnov test. Analysis of variables was performed using Pearson's x2 test or Fisher's exact probability test. Analysis of features of normally distributed continuous ratio was performed using independent simple T test for independent samples, while non-parametric distributed numerical variables were analyzed using Mann-Whitney U test for independent samples. Pearson and Spearman correlation coefficients were used according to data type and normality of distribution.
Results - Our study with the help of the correlation coefficient according to Sperman has revealed that there is no significant difference in the linear correlation between the week of gestation and LDH values in the ser Our study by means of the correlation coefficient according to Spearman has found that there is a statistically significant difference of the positive linear correlation between the week of gestation and LDH values of the fetus/newborn with growth retardation IUGR (rs=0.274; p> 0.05). Mann Whitney analysis found that fetuses/newborns with growth retardation (IUGR) have higher serum LDH values [Me=795.00 to 1490.00] compared to fetuses/newborns with normal growth and development [Me =587.00 U/L (IQR=376.00 to 783.00)]. There is a significant statistical difference with the mean values of LDH in serum between fetuses with growth retardation (IUGR) and fetuses with normal growth and development [U=1203.000, z=-3.135, p=0.002]. Statistical data using the Mann Whitney test in our research showed that in fetuses with growth retardation (IUGR) the median length of the fetal liver is lower [Me=0.05 (IQR=0.03 to 0.08)] compared to fetuses with normal growth and development [Me=0.09 (IQR=0.06 to 0.12)]. There is a statistically significant difference between the median fetal liver length ratio and serum LDH between fetuses with growth retardation (IUGR) and fetuses with normal growth and development [U=973.000, z=-4.341, p< 0.001].
Discussion - There is a significant statistical difference with the mean values of LDH in serum between fetuses with growth retardation (IUGR) and fetuses with normal growth and development [U=1203.000, z=-3.135, p=0.002]. The increase in the level of lactate dehydrogenase enzymatic activity in fetuses with growth retardation is explained in this way. In fetuses with growth retardation (IUGR), the increase in the level of enzymatic activity of lactate dehydrogenase, which follows and is caused by hypoxia in the cells of the liver, transverse muscles and kidneys. Due to hypoxia, the permeability of the cell membrane is disturbed, as LDH molecules are transferred from the tissues to the plasma.
The authors' studies (10) have found that in preeclampsia there is an increased level of lactate dehydrogenase and aspartate aminotransferase, which is consistent with our results. Our results have shown that there is an increase in the level of LDH in preeclampsia, which are consistent with the results of the authors (1, 2).
The clarification of the achieved results is based on these data that the growth retardation of the fetus due to hypoxia, which develops into preeclampsia, increases the activity of lactate dehydrogenase, which affects the glycolytic process of the breakdown of carbohydrates. In the conditions of hypoxia, damage to the liver cells follows, as well as the disorder of the permeability of the cell membrane, in some cases, the transfer of lactate dehydrogenase from the cell to the serum follows, as well as the increase in the level in the blood. The other mechanism is explained by the fact that the increase in the level of LDH follows due to stress and hypoxia of the fetus as well as due to the increase in fetal cortisol from the adrenal gland. It is assumed that the high level of fetal prolactin stimulates the synthesis of lactate dehydrogenase in the fetal liver.
There is a statistically significant difference between the median fetal liver length ratio and serum LDH between fetuses with growth retardation (IUGR) and fetuses with normal growth and development [U=973.000, z=-4.341, p< 0.001]. These data are explained by the fact that the length of the right lobe of the fetal liver (FLL- Fetal Liver Length) in fetuses with growth retardation is smaller than the length of the left lobe, and on the other side of preeclampsia with fetal growth retardation, there is the phenomenon of blood redistribution so that the amount of blood supplying the right lobe is much lower. In addition, the right lobe of the liver is strengthened with deoxygenated blood because over 60% of the oxygenated blood does not pass to the liver due to the presence of the Ductus Arantii, which exceeds the liver and flows into the inferior vena cava. In adult humans, the ratio between the right lobe of the liver and the left lobe is 6:1. Due to these morphological changes (the presence of the ductus Aranti) and physiological changes (the phenomenon of blood circulation distribution that exists in IUGR) of the fetus, the amount of oxygenated blood passing through the right lobe of the liver is much lower in relation to the left lobe of the liver, for this reason there is stagnation in the growth of the right lobe of the liver.
Conclusion - Research has shown that the FLL/LDH ratio values in fetuses with preeclampsia are lower compared to fetuses with normal development. Research has shown that the FLL/LDH ratio values in fetuses with preeclampsia are lower compared to fetuses with normal development. These data show that the length of the right lobe of the fetal liver in preeclampsia with IUGR is lower compared to the values of the length of the liver in fetuses with normal growth and development. As well as the LDH values of fetuses with growth retardation are higher compared to the LDH values of fetuses with normal growth and development. So the ratio FLL/LDH mathematically ( ) it is lower in fetuses with growth retardation compared to fetuses with normal growth. At the same time, these parameters result in significant values in the prediction of growth retardation and fetal well-being during intrauterine life. Based on the purpose of the work, the methodology and the results, we find that the ratio between the length of the fetal liver and LDH are significant indicators for the prediction of growth retardation in the fetus with preeclampsia.
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