EBV can indefinitely proliferate target lymphocytes and the characteristics of latent activation, which proved to be the source of infectious mononucleosis (IM) in 1968.EBV mainly invades pharyngeal epithelial cellsand then targets B lymphocytes. It uses the molecular mechanism of B lymphocytes to replicate the viral genome and produce memory B lymphocytes. The latter enters the circulatory system, or remains inactive until triggered to reactivate [4,5], and further induces T cells to transform into cytotoxic effector cells, namely atypical lymphocytes, leading to a series of immune damages[4,5,16].
EBV-IM can cause multiple system damages, leading to some complications, such as liver damage, pneumonia, acute nephritis, meningitis, peripheral neuropathy, hepatitis, ruptured spleen, skin ulcers, hemophagocytic syndrome, etc., among which liver injury is the most common [10-12,17,18],which is mainly manifested as elevated transaminase. The mechanism of liver damage caused by EBV-IM is still unclear. Relevant research showed that EBV does not directly infect hepatocytes, bile duct epithelium or vascular endothelium, but causes cytotoxic CD3+ and CD8+ T lymphocyte infiltration, which leads to liver cell damage；Other research showed that the level of inflammatory cytokines in the serum of EBV-IM patients is increased, and the level of interferon-gamma (IFN-γ) and its breakdown products can cause liver dysfunction.Thepresent study found that the incidence of elevated transaminase in EBV-IM accounted for 80.3%, which is similar to foreign literature reports.[20,21]
The present study conducted a monfactor analysis of possible influencing variables and further logistic regression analysis. The results found that for EBV-IM with elevated ALT, GGT, ALB, Age, and ALYM were risk factors, and fever is the protective factor; for EBV-IM complicated with elevated AST, GGT and MPV/PLT% were risk factors.
The ALT in the liver is mainly found in the liver cytoplasm, and its intracellular concentration is 1000-3000 times higher than that in the serum. When the liver cells are slightly damaged, due to the degeneration and necrosis of the liver cells, the permeability of the liver cell membranes increases, etc., ALT penetrates the blood in a large amount, which makes the serum ALT content significantly increase, and the sensitivity is strong.In addition, liver enzymes also include AST and GGT. AST is mainly found in the mitochondria of the liver cytoplasm and is distributed in other parts of the human body, such as the myocardium and skeletal muscle cells. Therefore, it is less sensitive than ALT in terms of responding to liver function. ; GGT mainly exists on liver cell membranes and microsomes. Therefore, when ALT and AST increase, GGT may also increase. This study shows that when GGT>26.05U/L, there may be an increase in ALT and AST.
There was a correlation between elevated transaminases in children with EBV-IM and age[23-26],It was considered that as age increases, the immune system gradually improves, which leads to the damage of liver cells. EBV causes a strong CD4+ and CD8+ T cell response during the pathogenic process. Mature single CD4+ and CD8+ T cells are first detected in the thymus at the 15th week, and they appear in large numbers in the periphery before birth. But it is significantly different from adult T cells in that it responds poorly to foreign antigens. As the age increases, the immune system of children is gradually improved, and the immune defense response becomes stronger.This study included 533 children with EBV-IM, a total of 277 cases (52.0%) with elevated ALT, and the incidence of liver damage in the 3 to the 6-year-old group was 35.7% (95/277), which was higher than that in other age groups. Factors and multivariate analysis suggest that age is an independent risk factor for elevated ALT, and when the age is greater than 5.26 years, it is necessary to be alert to the possibility of abnormalities. This conclusion is consistent with the results of Zhang et al.,so the treatment process children pay attention and follow up. When EBVinfection occurs, a series of immune reactions occur in the body, which can induce T cells to transform into cytotoxic effector cells, that is, atypical lymphocytes. The latter may cause damage to liver cells and trigger the increase of transaminase. The liver is the main source of ALB production. In the setting, when liver cell injury cannot be compensated, it can cause albumin content to decrease. This study suggested that when ALYM>11.9%, ALB<43.5g/L, EBV-IM children may have ALT abnormalities.
Fever is the most common symptom of EBV-IM, which easily attracts parents' attention. The protection mechanism is not clear at present. The possible reason is that the interval between treatment after onset is longer than that in children with fever. The interval between the non-fever group is 5(4,7) , And the fever group interval is 4(3,6). According to Mann-Whitney U test, Z=-2.632, P=0.008; Related studies suggest that MPV/PLT% may be a new diagnostic indicator of EBV-IM in children, and indirectly to predict liver injury,this study shows that MPV/PLT% is a risk factor for EBV-IM with elevated AST. When MPV/PLT%>4.67, AST may be increased concurrently.
In the context of liver disease, such as alcoholic cirrhosis, RDW was higher in patients than in normal controls[29,30]. Research suggested that RDW can be used as an index to predict liver damage in children with EBV-IM[31,32], RDW-CV is often used instead of RDW in clinical practice. The present study showed that there is no significant difference in the distribution of RDW-CV in the non-liver damage group and the liver damage group of children with EBV-IM, and the difference is not statistically significant (P>0.05), the possible reason is that EBV-IM is mostly acute onset after occult infection, lasting for several weeks, while RDW-CV is more used to respond to chronic damage.