The American journal of gastroenterology · 2004
Cognitive lifetime drinking history in nonalcoholic fatty liver disease: some cases may be alcohol related.
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Hayashi Paul H, Harrison Stephen A, Torgerson Sigurd, Perez Tammy A, Nochajski Thomas, Russell Marcia
Аннотация
OBJECTIVES: We aimed to determine the prevalence of significant alcohol intake in previously diagnosed nonalcoholic fatty liver (NAFL) patients.
METHODS: We measured current and total lifetime alcohol intake (TLAI) in biopsy-proven NAFL patients using the cognitive lifetime drinking history (CLDH), a computerized questionnaire. One nurse administered the CLDH without physician presence. Physicians took alcohol histories prior to any knowledge of this study. Advanced and nonadvanced fibrosis patients were tested. A single pathologist (ST) scored all biopsies (inflammation 0-6; fibrosis 0-4).
RESULTS: Twenty-three patients (11 men) were studied. Thirteen had bridging fibrosis or cirrhosis. [mean age: 52.3 yr (range 28-69); mean body mass index (BMI): 37 kg/m2 (range 27-48.6)]. All but three had hyperlipidemia, diabetes, and/or hypertension. Mean TLAI was 60.2 kg (range 0.17-471.7), but three patients were above 100 kg (threshold for cirrhosis risk) at 305.5, 336.7, and 471.7. These three had inflammation/fibrosis scores of 3/3, 3/0, and 5/2, respectively. Those with >100 kg tended to have higher serum AST and inflammation score. Prior physician-obtained alcohol history determined <or=20 g/day for all patients and did not mention TLAI in any. CLDH confirmed <or=20 g/day current alcohol intake in 21 of 23 patients, but intakes were 30.2 g/day and 41.2 g/day in two.
CONCLUSIONS: Some NAFL patients may have alcohol fatty liver disease instead. Routine physician interviews obtain less accurate alcohol histories compared to CLDH. The clinical significance of past alcohol intake and methods of measuring alcohol ingestion in fatty liver patients deserves further investigation.
METHODS: We measured current and total lifetime alcohol intake (TLAI) in biopsy-proven NAFL patients using the cognitive lifetime drinking history (CLDH), a computerized questionnaire. One nurse administered the CLDH without physician presence. Physicians took alcohol histories prior to any knowledge of this study. Advanced and nonadvanced fibrosis patients were tested. A single pathologist (ST) scored all biopsies (inflammation 0-6; fibrosis 0-4).
RESULTS: Twenty-three patients (11 men) were studied. Thirteen had bridging fibrosis or cirrhosis. [mean age: 52.3 yr (range 28-69); mean body mass index (BMI): 37 kg/m2 (range 27-48.6)]. All but three had hyperlipidemia, diabetes, and/or hypertension. Mean TLAI was 60.2 kg (range 0.17-471.7), but three patients were above 100 kg (threshold for cirrhosis risk) at 305.5, 336.7, and 471.7. These three had inflammation/fibrosis scores of 3/3, 3/0, and 5/2, respectively. Those with >100 kg tended to have higher serum AST and inflammation score. Prior physician-obtained alcohol history determined <or=20 g/day for all patients and did not mention TLAI in any. CLDH confirmed <or=20 g/day current alcohol intake in 21 of 23 patients, but intakes were 30.2 g/day and 41.2 g/day in two.
CONCLUSIONS: Some NAFL patients may have alcohol fatty liver disease instead. Routine physician interviews obtain less accurate alcohol histories compared to CLDH. The clinical significance of past alcohol intake and methods of measuring alcohol ingestion in fatty liver patients deserves further investigation.