1988-LB: Effects of Alcohol Consumption among Patients with Hepatic Steatosis and Prediabetes or Diabetes

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In December of 2023, a multisociety Delphi consensus on fatty liver disease nomenclature was published renaming nonalcoholic fatty liver disease (NAFLD) to metabolic dysfunction-associated steatotic liver disease (MASLD) and introduced the term MetALD, which identifies patients with MASLD, who also are moderate consumers of alcohol. However, the effects of moderate alcohol consumption among patients with hepatic steatosis and prediabetes/diabetes are not well known.In order to better understand the effects of alcohol consumption in these patients, we analyzed data from NHANES 2017-2020 including self-report alcohol intake, and transient elastography (TE). Hepatic steatosis was defined based on controlled attenuation parameter ≥ 288 dB/m.A total of 1,757 patients with diabetes (47%) or prediabetes (53%) were included in the study (age: 55 ± 15 years; Sex: 44% female; BMI: 34.0 ± 7.0 kg/m2; A1c: 6.5 ± 1.4%). Based on self-reporting, patients were divided in 7 groups according to alcohol grams consumed per week (no alcohol consumption, 0-10, 10-50, 50-100, 100-200, 200-500, >500). Increasing alcohol consumption was associated with decreased insulin resistance by HOMA-IR (from 6.9 ± 6.0 to 3.7 ± 1.9, p=0.042) and A1c (from 6.7 ± 1.5 to 5.7 ± 0.5%, p<0.001), but increased BP (SBP: from 129 ± 19 to 137 ± 17 mmHg, p=0.006; DBP: from 76 ± 12 to 85 ± 11 mmHg, p<0.001), TG (from 153 ± 118 to 209 ± 193 mg/dL, p=0.056), and HDL-C (from 47 ± 11 to 57 ± 18 mg/dL, p<0.001). Alcohol consumption was associated with worse liver enzymes (AST, ALT, and GGT, all p<0.001) without concomitant changes in hepatic steatosis or fibrosis by imaging.In patients with hepatic steatosis and prediabetes or diabetes, moderate alcohol consumption was associated with improvement in insulin sensitivity, but worsening of other cardiometabolic risk factors (i.e., blood pressure and triglycerides). This can result in an overclassification of patients with MetALD, even in patients where alcohol may be the only driver of the disease. Disclosure S.S. Bantu: None. E. Petrie: None. M. Gray: Consultant; Novo Nordisk. F. Bril: Consultant; Novo Nordisk.

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