Background: Steatotic liver disease (SLD) encompasses metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (AALD) at extremes as well as an overlap group termed MASLD with increased alcohol intake (MetALD). The Alcoholic Liver Disease/Nonalcoholic Fatty Liver Disease Index (ANI) was proposed to differentiate ALD from nonalcoholic fatty liver disease (NAFLD). We analysed the performance of the ANI in differentiating within the SLD spectrum. Methods: In a cross-sectional study at a tertiary care center, 202 adults (>18 years) who were prospectively diagnosed with SLD defined by magnetic resonance imaging-proton density fat fraction >6.4% were enrolled.Alcohol consumption (AC) was recorded according to thresholds for significant AC: 140–350 g/week (or 20– 50 g/day) for females and 210–420 g/week (or 30–60 g/day) for males. The ANI was calculated, and area under the receiver operating characteristic curve (AUROC) was generated. Results: Of 202 patients (47 years [interquartile range, IQR, 38 to 55], 23.75% females, 77% obese, 42.1% with diabetes, 38.1% hypertensive, 28.7% statin use), 40.5% were ever-alcohol consumers; 120 (59%), 50 (24.7%), and 32 (15.8%) were MASLD (ANI, –3.7 [IQR, –7 to –1.6]; MetALD, – 1.45 [IQR, –2.4 to 0.28]; and AALD, 0.71 [IQR, –1.3 to 4.8], respectively; P<0.05 for all). The AUROC of the ANI for MASLD and AALD was 0.79 (IQR, 0.72 to 0.84; cut-off <–3.5) and 0.80 (IQR, 0.74 to 0.86; cut-off >–1.49), respectively. The ANI outperformed aspartate transaminase/alanine transaminase (AST/ALT) ratio (AUROC=0.75 [IQR, 0.69 to 0.81]) and gamma glutamyl transpeptidase (GGT) (AUROC=0.74 [IQR, 0.67 to 0.80]). Addition of GGT did not improve model performance (AUCdiff = 0.004; P= 0.33). Conclusion AC is common in MASLD. The ANI distinguishes MASLD and AALD, with individual cut-offs within the intermediate zone indicating MetALD. ANI also outperforms AST/ALT ratio or GGT.

Background: Steatotic liver disease (SLD) encompasses metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (AALD) at extremes as well as an overlap group termed MASLD with increased alcohol intake (MetALD). The Alcoholic Liver Disease/Nonalcoholic Fatty Liver Disease Index (ANI) was proposed to differentiate ALD from nonalcoholic fatty liver disease (NAFLD). We analysed the performance of the ANI in differentiating within the SLD spectrum. Methods: In a cross-sectional study at a tertiary care center, 202 adults (>18 years) who were prospectively diagnosed with SLD defined by magnetic resonance imaging-proton density fat fraction >6.4% were enrolled.Alcohol consumption (AC) was recorded according to thresholds for significant AC: 140–350 g/week (or 20– 50 g/day) for females and 210–420 g/week (or 30–60 g/day) for males. The ANI was calculated, and area under the receiver operating characteristic curve (AUROC) was generated. Results: Of 202 patients (47 years [interquartile range, IQR, 38 to 55], 23.75% females, 77% obese, 42.1% with diabetes, 38.1% hypertensive, 28.7% statin use), 40.5% were ever-alcohol consumers; 120 (59%), 50 (24.7%), and 32 (15.8%) were MASLD (ANI, –3.7 [IQR, –7 to –1.6]; MetALD, – 1.45 [IQR, –2.4 to 0.28]; and AALD, 0.71 [IQR, –1.3 to 4.8], respectively; P<0.05 for all). The AUROC of the ANI for MASLD and AALD was 0.79 (IQR, 0.72 to 0.84; cut-off <–3.5) and 0.80 (IQR, 0.74 to 0.86; cut-off >–1.49), respectively. The ANI outperformed aspartate transaminase/alanine transaminase (AST/ALT) ratio (AUROC=0.75 [IQR, 0.69 to 0.81]) and gamma glutamyl transpeptidase (GGT) (AUROC=0.74 [IQR, 0.67 to 0.80]). Addition of GGT did not improve model performance (AUCdiff = 0.004; P= 0.33). Conclusion AC is common in MASLD. The ANI distinguishes MASLD and AALD, with individual cut-offs within the intermediate zone indicating MetALD. ANI also outperforms AST/ALT ratio or GGT.

Background: Steatotic liver disease (SLD) encompasses metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (AALD) at extremes as well as an overlap group termed MASLD with increased alcohol intake (MetALD). The Alcoholic Liver Disease/Nonalcoholic Fatty Liver Disease Index (ANI) was proposed to differentiate ALD from nonalcoholic fatty liver disease (NAFLD). We analysed the performance of the ANI in differentiating within the SLD spectrum. Methods: In a cross-sectional study at a tertiary care center, 202 adults (>18 years) who were prospectively diagnosed with SLD defined by magnetic resonance imaging-proton density fat fraction >6.4% were enrolled.Alcohol consumption (AC) was recorded according to thresholds for significant AC: 140–350 g/week (or 20– 50 g/day) for females and 210–420 g/week (or 30–60 g/day) for males. The ANI was calculated, and area under the receiver operating characteristic curve (AUROC) was generated. Results: Of 202 patients (47 years [interquartile range, IQR, 38 to 55], 23.75% females, 77% obese, 42.1% with diabetes, 38.1% hypertensive, 28.7% statin use), 40.5% were ever-alcohol consumers; 120 (59%), 50 (24.7%), and 32 (15.8%) were MASLD (ANI, –3.7 [IQR, –7 to –1.6]; MetALD, – 1.45 [IQR, –2.4 to 0.28]; and AALD, 0.71 [IQR, –1.3 to 4.8], respectively; P<0.05 for all). The AUROC of the ANI for MASLD and AALD was 0.79 (IQR, 0.72 to 0.84; cut-off <–3.5) and 0.80 (IQR, 0.74 to 0.86; cut-off >–1.49), respectively. The ANI outperformed aspartate transaminase/alanine transaminase (AST/ALT) ratio (AUROC=0.75 [IQR, 0.69 to 0.81]) and gamma glutamyl transpeptidase (GGT) (AUROC=0.74 [IQR, 0.67 to 0.80]). Addition of GGT did not improve model performance (AUCdiff = 0.004; P= 0.33). Conclusion AC is common in MASLD. The ANI distinguishes MASLD and AALD, with individual cut-offs within the intermediate zone indicating MetALD. ANI also outperforms AST/ALT ratio or GGT.

Background/Aims: Gastric dysrhythmias, loss of normal 3 cycles per minute (CPM) gastric myoelectrical activity (GMA), and variable loss of interstitial cells of Cajal are reported both in gastroparesis (GP) and functional dyspepsia (FD). We hypothesize that the patients with GP, and FD with normal gastric emptying (NGE) and delayed gastric emptying (DGE) may vary in symptom severity, and GMA profiles. Methods: Symptoms and their severity were evaluated by gastroparesis cardinal symptom index (GCSI), Abell scoring, short-form Nepean dyspepsia index (SF-NDI), the World Health Organization quality of life, and Rome IV subtyping for FD. Solid-meal gastric emptying was assessed by nuclear scintigraphy. Water load satiety test (WLST)-based electrogastrography determined GMA. Results: Patients with GP (n = 40) had higher GCSI than those with FD (n = 39; [12 DGE, 27 NGE] (2.79 [2.17-3.33] vs 1.67 [0.83-2.61] vs 0.83 [0.55-1.93]; P < 0.001, in GP vs FD-NGE vs FD-DGE, respectively), severe Abell grade (Grade III in 17 [43%] vs 0% vs 0%, in GP vs FD-NGE vs FD-DGE, respectively), severe SF-NDI (80.5 [63.5-102.5] vs 50 [27-91] vs 30 [21.25-45.5]); and poor QOL. Sixteen (40%) GP had impaired gastric accommodation (< 238 mL). Post-WLST 3 CPM normal/hypernormal GMA was observed in 17 (42%), 18 (67%), and 5 (42%) patients with GP, FD (NGE), and FD (DGE), respectively; and 3 CPM hyponormal in remaining patients in each group.Post-WLST dysrhythmia was comparable. Conclusions WLST-electrogastrography coupled with GE study may distinguish between normal/dysrhythmic GMA revealing pathophysiologicalphenotypes of GP and FD. Analysing extent of power change in normogastric, and dysrhythmic frequencies may comprehensively elucidate disease severity.

Background/Aims: Gastric dysrhythmias, loss of normal 3 cycles per minute (CPM) gastric myoelectrical activity (GMA), and variable loss of interstitial cells of Cajal are reported both in gastroparesis (GP) and functional dyspepsia (FD). We hypothesize that the patients with GP, and FD with normal gastric emptying (NGE) and delayed gastric emptying (DGE) may vary in symptom severity, and GMA profiles. Methods: Symptoms and their severity were evaluated by gastroparesis cardinal symptom index (GCSI), Abell scoring, short-form Nepean dyspepsia index (SF-NDI), the World Health Organization quality of life, and Rome IV subtyping for FD. Solid-meal gastric emptying was assessed by nuclear scintigraphy. Water load satiety test (WLST)-based electrogastrography determined GMA. Results: Patients with GP (n = 40) had higher GCSI than those with FD (n = 39; [12 DGE, 27 NGE] (2.79 [2.17-3.33] vs 1.67 [0.83-2.61] vs 0.83 [0.55-1.93]; P < 0.001, in GP vs FD-NGE vs FD-DGE, respectively), severe Abell grade (Grade III in 17 [43%] vs 0% vs 0%, in GP vs FD-NGE vs FD-DGE, respectively), severe SF-NDI (80.5 [63.5-102.5] vs 50 [27-91] vs 30 [21.25-45.5]); and poor QOL. Sixteen (40%) GP had impaired gastric accommodation (< 238 mL). Post-WLST 3 CPM normal/hypernormal GMA was observed in 17 (42%), 18 (67%), and 5 (42%) patients with GP, FD (NGE), and FD (DGE), respectively; and 3 CPM hyponormal in remaining patients in each group.Post-WLST dysrhythmia was comparable. Conclusions WLST-electrogastrography coupled with GE study may distinguish between normal/dysrhythmic GMA revealing pathophysiologicalphenotypes of GP and FD. Analysing extent of power change in normogastric, and dysrhythmic frequencies may comprehensively elucidate disease severity.

Background/Aims: Gastric dysrhythmias, loss of normal 3 cycles per minute (CPM) gastric myoelectrical activity (GMA), and variable loss of interstitial cells of Cajal are reported both in gastroparesis (GP) and functional dyspepsia (FD). We hypothesize that the patients with GP, and FD with normal gastric emptying (NGE) and delayed gastric emptying (DGE) may vary in symptom severity, and GMA profiles. Methods: Symptoms and their severity were evaluated by gastroparesis cardinal symptom index (GCSI), Abell scoring, short-form Nepean dyspepsia index (SF-NDI), the World Health Organization quality of life, and Rome IV subtyping for FD. Solid-meal gastric emptying was assessed by nuclear scintigraphy. Water load satiety test (WLST)-based electrogastrography determined GMA. Results: Patients with GP (n = 40) had higher GCSI than those with FD (n = 39; [12 DGE, 27 NGE] (2.79 [2.17-3.33] vs 1.67 [0.83-2.61] vs 0.83 [0.55-1.93]; P < 0.001, in GP vs FD-NGE vs FD-DGE, respectively), severe Abell grade (Grade III in 17 [43%] vs 0% vs 0%, in GP vs FD-NGE vs FD-DGE, respectively), severe SF-NDI (80.5 [63.5-102.5] vs 50 [27-91] vs 30 [21.25-45.5]); and poor QOL. Sixteen (40%) GP had impaired gastric accommodation (< 238 mL). Post-WLST 3 CPM normal/hypernormal GMA was observed in 17 (42%), 18 (67%), and 5 (42%) patients with GP, FD (NGE), and FD (DGE), respectively; and 3 CPM hyponormal in remaining patients in each group.Post-WLST dysrhythmia was comparable. Conclusions WLST-electrogastrography coupled with GE study may distinguish between normal/dysrhythmic GMA revealing pathophysiologicalphenotypes of GP and FD. Analysing extent of power change in normogastric, and dysrhythmic frequencies may comprehensively elucidate disease severity.