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Inicio Annals of Hepatology DETERMINATION OF LEUKOCYTE PROFILE IN CHRONIC ALCOHOL CONSUMPTION
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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
DETERMINATION OF LEUKOCYTE PROFILE IN CHRONIC ALCOHOL CONSUMPTION
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E.A. Alamo-Capula1, M. Hernandez Santillan1, A. Hernandez-Barragan1, S. Sánchez-Valle1, I. Altamirano-Mendoza1, Z. Medina-Avila1, M. Martínez-Castillo1, D. Santana-Vargas1, Y. Bejar2, F. Higuera de la Tijera2, J.L. Pérez-Hernández2, D. Kershenobich1, G. Gutiérrez-Reyes1
1 Laboratorio Hígado, Páncreas y Motilidad (HIPAM). Unidad de Investigación en Medicina Experimental, UNAM. Ciudad de México, México
2 Hospital General de México “Dr. Eduardo Liceaga". Ciudad de México, México
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Table 1. Leukocyte profile of patients with different types of alcohol-related liver damage
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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 objective

Chronic alcohol consumption can induce Alcoholic Liver Disease (ALD) promoting biological alterations and liver damage; however, the immunological changes usually are underestimated. It has been reported, the increase of leucocytes in alcoholic hepatitis patients1, but the regulation of other cell lineages has not fully evaluated.

Objective

To evaluate the leukocyte profile in patients with liver damage induces by chronic and acute alcohol consumption.

Material and methods

A Cross-sectional study. Patients were classified as follow: (1) Controls with alcohol consumption <10g/day, AUDIT <8 (CT); (2) Chronic alcohol consumption AUDIT> 8, without clinical or biochemical data of liver damage (OH, alcoholism); (3) Cirrhotic patients due to alcohol (CiOH) and (4) Patients with alcoholic hepatitis (AH). Leukocytes, lymphocytes, monocytes, neutrophils, eosinophils, and basophils were determined by hematic biometry. U-Mann Whitney was used for statistical analysis, p <0.05 was considered significant.

Results

570 patients were included. The mean in age was: 29.5±10.8 for CT; 31±12.6 for OH; 47.6±7.7 for CiOH and 41.2±9.2 years old (p<0.001). Alcohol consumption was higher in CiOH 240 (320, 120; p<0.001) and AH 320 (480, 160; p<0.05). Albumin decreases in CiOH 2.9 (3.5, 2.2; p<0.001) and AH 1.9 (2.3, 1.6; p<0.001). On the other hand, AST, ALT and GGT increase in CiOH and AH, 49.5 (75.3, 38; p<0.001), 155 (177, 121; p<0.001) for AST, 32.5 (47.3, 24; p<0.001), 49 (75, 35.3; p<0.001) for ALT and 91.5 (191.8, 48; p<0.001), 224 (525.5, 104; p<0.001) for GGT. There was no a significant difference in eosinophils and basophils. The statistical number of leukocyte profile is described in Table 1.

Data is expressed as the median with interquartile values (Q3-Q1). a) Differences between Alcoholism and Controls; b) Cirrhosis and Controls; c) Alcoholic Hepatitis and Controls; d) Alcoholism and Cirrhosis; e) Alcoholism and Alcoholic Hepatitis; f) Cirrhosis and Alcoholic Hepatitis. €p<0.05; +p<0.01; *p<0.001.

Discussion

During alcoholism, lymphocytes decrease, whereas neutrophils increase; this could be related to a susceptibility to recurrent respiratory and gastrointestinal infections. Lymphocytes and neutrophils decrease in CiOH; the reduction in neutrophils could be explained because the stimuli in CiOH decrease. In patients with AH, monocytes and neutrophils increase, that in a consequence increases the inflammatory state, promoting liver fibrosis and mortality.

Conclusion

Chronic alcohol consumption, liver cirrhosis and alcoholic hepatitis promote cellular alterations, this phenomenon is more evident in AH. Our findings can be used to design novel detection strategies for the treatments of chronic and acute alcohol consumption.

Conflict of interest: The authors declare that there is no conflict of interest.

This work was partially financed by CONACyT SALUD-2016-272579 y PAPIIT-UNAM TA200515

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