Association of serum zinc with markers of liver injury in very heavy drinking alcohol-dependent patients |
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| Affiliation: | 1. Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Louisville, Louisville, KY;2. Section on Human Psychopharmacology, LCTS DICBR NIAAA National Institutes of Health, Bethesda, MD;3. Robley Rex Veterans Medical Center, Louisville, KY;4. University of Louisville Alcohol Research Center, Louisville, KY;5. Hepatobiology & Toxicology COBRE, University of Louisville, Louisville, KY;6. Department of Biostatistics and Bioinformatics, School of Public Health and Information Sciences, University of Louisville, Louisville, KY;7. Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY;8. Office of Clinical Director, NIAAA National Institutes of Health, Bethesda, MD;1. Department of Physiology & Pharmacology, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, USA;2. Department of Pharmacology Toxicology and Therapeutic Chemistry, School of Pharmacy and Food Sciences, University of Barcelona;3. IBUB (Institute of Biomedicine, University of Barcelona);4. CIBERobn (Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y Nutrición);1. Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, 316C Leverton Hall, Lincoln, NE 68583-0806, USA;2. School of Veterinary Medicine and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska-Lincoln, Ken Morrison Life Sciences Research Center, Rm 139, 4240 Fair Street, Lincoln, NE 68583-0900, USA |
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| Abstract: | Zinc deficiency is a frequent complication of alcohol abuse for multiple reasons including poor intake, increased excretion, internal redistribution and altered transporters. Zinc deficiency has been postulated to play a role in the development/progression of alcoholic liver disease (ALD). This study aimed to relate serum zinc levels with alcohol intake, serum albumin concentration and markers of inflammation and liver injury. One hundred and eight male and female very heavy drinking (≥10 drinks/day) individuals without clinical evidence of ALD were grouped by serum zinc concentration: normal-zinc group (zinc level≥71 μg/dl) included 67 patients, and low-zinc group (zinc level<71 μg/dl) included 41 patients. Data were collected on demographics, drinking history in last 90 days (heavy drinking days, HDD90 and total drinks, TD90), lifetime drinking history (LTDH) and clinical/ laboratory assessments. Our data show that in a very well-characterized, chronically heavy-drinking population without clinical evidence of liver disease, about 40% of subjects had low serum zinc levels. Frequency of heavy drinking days (HDD90) was significantly higher in the low-zinc group. Total drinks in past 90 days, LTDH and HDD90 showed significant associations with low zinc levels. The group with the low serum zinc had a higher aspartate aminotransferase/alanine aminotransferase ratio (good marker of alcoholic liver disease). Those in the low-zinc group had the lower albumin levels, a marker of hepatic synthetic function, and the highest C-reactive protein level, a biomarker of inflammation. |
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