Characterization of the inflammatory profile in patients with compensated and decompensated liver cirrhosis through cytosines determined by spectroscopy.

Introduction and Objectives

Inflammatory cytokines influence the progression of cirrhosis and decompensation. The study aims to characterize the inflammatory response of patients with compensated and decompensated liver cirrhosis through inflammatory cytokines and evaluate the state of the disease, type of decompensation, severity and the development of acute on chronic liver failure.

Materials and Patients

Hospitalized patients with a diagnosis of compensated and decompensated liver cirrhosis were included. Upon admission, saliva samples were collected in microcentrifuge tubes to measure cytosines (IL-6, IL-1β, IL-10, ILF-γ and TNF), lipids and immunoglobulins: A, M and G using Fourier transform infrared spectroscopy (FTIR). Clinical and biochemical variables (complete blood count, blood chemistry, liver biochemistry, serum electrolytes, lipid profile and C-reactive protein), MELD 3.0 and Child Pugh scales were included. The statistical analysis was used the SPSS V24 program for continuous quantitative variables expressed in measures of central tendency and dispersion according to the normality of the data, the ordinal quantitative variables were expressed in frequencies and percentages, Spearman correlation analysis and a linear regression analysis were performed, from which a ROC curve and the Youden's J statistic and its sensitivity and specificity were determined, with a statistically significant p <0.05.

Results

It was included 40 patients: 19 compensated and 21 decompensated. The most common decompensation was hepatic encephalopathy. (20%) (MELD 3.0 12.5 ± 3.59 vs 21.61 ±7.47, p<0.000). Statistical significance was found in leukocytes, neutrophils and INR as well as differences in the levels of IgG, IgM, IL-6, IL1β, IFN-γ and IL-10 between the causes of decompensation (Figure 1) and decreased IgM levels. And IFN-γ in decompensated patients compared to compensated patients. A negative correlation was found between neutrophil levels and IgM, IL6, IL1β, IL10 and IFN-γ levels. The linear regression analysis gave the following formula m= 2.648+ (-0.267*infection) + (-0.926*abs1) + (0.084*abs2) + (0.442*abs3) + (-0.051*abs12) + (0.005*IgM) + (-0.064*IFNγ) + (-0.2*Leukocytes) + (0.223*Neutrophils) + (0.006*Urea), R=0.623. With the same formula, AUROC: 0.877 and p value <0.0001, Youden's J statistic cutoff of 1.3913, obtaining sensitivity of 92.1%, and specificity of 78.9%. The correlation with Child-Pugh is negative with IgM levels, while it was no association between the presence of infection and decompensation (X²= 0.053, p= 0.818), an association was indeed observed between Child-Pugh and the presence of infection (X²= 15.126, p= 0.001).

Conclusions

No correlation was found between levels of IgG, IL-6, IL1β, IFN-γ and IL-10 and the MELD 3.0 and Child Pugh scales, there is only a correlation between the Child Pugh clinical stage and IgM. Low levels of IgM and IFN-γ could be markers in patients with decompensated cirrhosis.