PREVALENCE OF COMBINED LIVER DAMAGE IN MEXICAN POPULATION

Introduction and Objectives: Metabolic syndrome and alcohol consumption are the two main causes of liver steatosis. Often, one of them predominates for its development and the other acts as a cofactor. The impact of these entities separately and their damage in synergy in the Mexican population is currently unknown. Our objective is to determine the prevalence of non-alcoholic liver steatosis, alcoholic liver steatosis, and dual damage in donors from the blood bank of the Hospital General de México “Dr. Eduardo Liceaga” (HGMEL) using transient elastography (TE). Materials and Methods: Pilot study. prospective, transversal, descriptive, and analytical. Healthy donors from the HGMEL blood bank who attended from June 8 to 29 2021 ≥18 years old, of any gender, will be included with a body mass index (BMI) ≥18.5. Donors with liver disease of any etiology and liver malignancy will be excluded. Donors who did not attend TE will be eliminated. The equipment used for TE was FibroScan® 502 Touch. Descriptive statistics will be used with measures of central tendency and dispersion. Results: 30 donors were recruited, four were eliminated for not having performed TE. The age of the subjects was 36.53 ± 12.13 years. There were 13 female subjects and 13 males. Seven (26.92%) donors were classified with non-alcoholic fatty liver disease (NAFLD), 2 (7.69%) with alcoholic fatty liver disease (ALD), and 1 (3.84%) subject with liver steatosis due to combined damage; the 16 (61.55%) remaining subjects corresponded to a healthy population. From the NAFLD group, S1 steatosis was documented in 1 subject (14.28%), S2 in 2 (28.56%), and S3 in 4 (57.16%); F0-F1 liver stiffness was found in 6 (85.72%) subjects, and F4 in 1 (14.28%); Of this group, 3 (42.86%) subjects were classified as overweight, 3 (42.86%) with grade 2 obesity, and 1 (14.28%) with grade 3 obesity. On the other hand, from the ALD group, one donor was found with steatosis S1, and 1 with S2; one of them had liver stiffness F0-F1 with an AUDIT score of 17 and a risk pattern for excessive alcohol consumption (117 g 2 to 4 times a month), while the other subject had F4 fibrosis with an AUDIT score of 7 and a pattern risk of excessive consumption (208 g 2 to 4 times per month), both consume beer. Finally, one donor had liver steatosis due to combined damage, with S3 for steatosis and F4 liver stiffness (27.4 kPa, the highest record in the study); He has grade 3 obesity (BMI 44.41), an AUDIT score of 4, and a pattern of excessive consumption (78 g 2 to 4 times a month) of distillates. Discussion: What is relevant about this work is that it studies an apparently healthy population and, according to our results, 38.45% (10) of the subjects already have a degree of liver steatosis and even 11.53% (3) showed advanced fibrosis. Our findings are similar to others about the prevalence of nonalcoholic liver steatosis, such as the work of the López-Velázquez group (26%) in 2014. Our study is novel in the investigation of alcoholic liver steatosis and the combined damage. Those issues are scarce addressed in our country. We also collect additional information, such as the identification of the consumption pattern of people with risky alcohol intake and the type of drink they consume. Conclusions: Our study shows that liver steatosis in this sample of the Mexican population is predominantly non-alcoholic; all subjects within this group have high BMI. Excessive risk consumption is prevalent in subjects with alcohol-related steatosis, and beer is the most frequent drink. In combined damage, obesity and excessive consumption of distillates seem to be the cause of severe steatosis. The only patient in this group already shows advanced fibrosis, which makes us suspect that dual damage accelerates the rate of fibrosis progression.The authors declare that there is no conflict of interest.