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Inicio Annals of Hepatology IL-10 Y TNF-α IN SERUM OF PATIENTS WITH CHRONIC HEPATITIS C AND HEPATIC DAMAGE ...
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Vol. 27. Núm. S2.
Oral presentations at the XVI National Congress of the Mexican Association of Hepatology
(enero 2021)
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Vol. 27. Núm. S2.
Oral presentations at the XVI National Congress of the Mexican Association of Hepatology
(enero 2021)
Open Access
IL-10 Y TNF-α IN SERUM OF PATIENTS WITH CHRONIC HEPATITIS C AND HEPATIC DAMAGE CHRONIC AND ACUTE FOR ALCOHOL CONSUMPTION
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M. Hernandez-Santillan1, M. Martínez-Castillo1, D. Santana-Vargas1, Z. Medina-Avila1, A. Hernández-Barragan1, J. Limón-Castillo1, J.L. Pérez-Hernández2, F. Higuera-De la Tijera2, P. Cordero-Pérez3, L. Muñoz-Espinoza3, J. Córdova-Gallardo4, D. Kershenobich1,5, G. Gutiérrez-Reyes1
1 Laboratorio de Hígado, Páncreas y Motilidad (HIPAM). Unidad de Medicina Experimental, UNAM. Ciudad de México, México
2 Hospital General de México “Dr. Eduardo Liceaga”. Ciudad de México, México
3 Hospital Universitario, Facultad de Medicina, UANL. Nuevo León, México
4 Hospital General Dr. Manuel Gea González. Ciudad de México, México
5 Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán”. Ciudad de México, México
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Vol. 27. Núm S2

Oral presentations at the XVI National Congress of the Mexican Association of Hepatology

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Introduction and Objectives

The virus of hepatitis C (HCV) and alcoholic liver disease (ALD), are of the main causes of liver disease mortality. There is a need to determine biomarkers, serum cytokines are candidates since they participate in the immunopathogenesis of these diseases by activating the inflammatory process. Increased serum levels of IL-10 and TNF-α have been reported in cirrhosis and have been associated with progression to hepatocellular carcinoma. While TNF-α has become a key factor in the inflammatory process with high circulating levels in alcoholic hepatitis (HA). The objective of this work is to evaluate the serum levels of IL-10 and TNF-α in patients with chronic hepatitis C and ALD.

Materials and methods

A cross-sectional and multicenter study. Patients with chronic Hepatitis C (CHC) and CiOH (cirrhotic by alcohol) and alcoholic hepatitis (HA) with criteria for alcoholism (WHO) were included, personalized survey, clinical and biochemical evidence of ALD was recorder. The groups were compared with subjects with a negative viral panel obtained from the CT blood bank (controls). IL-10 and TNF-α from serum was quantified using the multiple suspension arrangement method (Milliplex®-MERCK ©). Statistical analysis was performed using SPSS software version 22 using Mann Whitney U test. It was considered statistically significant p <0.05; values ​​expressed as median (Q3, Q1).

Results

A total of 110 subjects were included, 25 for CHC, 25 CiOH, 10 HA and 50 CT. We observed a significant increase on bilirubin, mainly in HA vs CT (p≤0.001), also AST and GGT was overproduced in CHC, CiOH and HA vs CT (p≤0.001). IL-10 was found elevated in CHC vs CT (p≤0.0001) and in CiOH vs CT (p≤0.05), which confirms that this anti-inflammatory cytokine increases in accordance with liver disease progresses. TNF-α was found to be increased in CiOH vs CHC (p≤0.05), increased levels in HA vs three study groups CHC, CiOH and CT (p≤0.001).

Discussion

Overproduction of IL-10 in CHC and CiOH support that this anti-inflammatory cytokine increases as liver disease progresses, possibly due to its role as a regulator in inflammation. Has been reported the increment of IL-10 and TNF-α in patients with HA, it is related to the severity of HA and mortality1. Also, there are reports about high levels of TNF-α in patients with CHC2, that contrast with our data, this may be because TNF-α acts differently in a chronic stage. The low concentration of TNF-α in HCc may reflect the regulatory mechanisms of the virus.

Conclusions

This study confirms the participation of IL-10 as a cytokine present in stages of chronic liver damage, elevated serum levels of TNF-α in HA compared to CiOH indicates that the inflammatory process actively participates in the acute damage induced by excessive alcohol consumption.

The authors declare that there is no conflict of interest.

This work was partially financed by CONACyT SALUD-2016-272579 (GRG) and PAPIIT- UNAM TA200515 (GRG)

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