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Alterations in Serum Zinc and Polyunsaturated Fatty Acid Concentrations in Treatment-Naive HIV-Diagnosed Alcohol-Dependent Subjects with Liver Injury

Year: 2018
Type: article
Study design: Observational Study
Abstract: Heavy alcohol drinking causes alterations in the metabolism of fatty acids and zinc that participate in inflammation and liver injury. HIV infection has been reported to cause dysregulated polyunsaturated fatty acid (PUFA) and zinc metabolism. In this pilot study, we examined the role of dysregulated PUFA metabolism and zinc deficiency in the liver injury occurring in heavy drinkers with early-stage HIV diagnosis. Fourteen heavy drinking alcohol-dependent (AD) patients [seven with treatment-naive HIV diagnosis (AD+HIV) and seven without HIV infection (AD)] participated in this study. Liver injury, serum zinc, PUFAs, viral load, CD4+ count, and drinking measures using lifetime drinking history (LTDH), and timeline follow-back past 90 days (TLFB90) were evaluated. Liver injury was also assessed in seven age- and gender-matched socially drinking HIV treatment-naive patients who served as disease controls. HIV viral load by itself did not show any correlation with liver injury. Liver enzymes were significantly elevated in both AD+HIV and AD patients, and AD+HIV patients had significantly higher alanine aminotransferase (ALT) levels than did AD patients, even with lower drinking. Serum zinc was significantly lower in AD+HIV patients. Only AD+HIV patients showed a significant elevation in linoleic acid (LA) and alpha-linoleic acid (ALA) levels. Serum zinc and ALT, LA and ALT, and ALA and ALT were significantly associated only in AD+HIV patients. The association between LA and ALT showed a higher effect than did the ALA and ALT association in the AD+HIV patients. Interestingly, AD+HIV subjects (who drank less), nevertheless, showed more liver injury compared with AD patients, who reported heavier drinking. We speculate that the underlying proinflammatory response resulting from zinc deficiency and an elevation in serum LA likely contributed to liver injury in AD+HIV patients, even with a comparatively lower degree of heavy drinking.
DOI: 10.1089/aid.2018.0124
Authors: Vatsalya Vatsalya, Matthew C. Cave, Rajarshi Kumar, Shweta Srivastava, Sujita Khanal, Alfred B. Jenson, Melanie L. Schwandt, Shirish S. Barve, Vijay A. Ramchandani, Craig J. McClain
Institutions: National Institutes of Health, University of Louisville, Louisville VA Medical Center, National Institute on Alcohol Abuse and Alcoholism, Calcutta National Medical College and Hospital, West Bengal University of Health Sciences
Language: English
Field: Medicine
Open Access status: green
Funders: U.S. Department of Veterans Affairs, University of Louisville, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, National Institute on Aging, National Institute of General Medical Sciences
Awards: 2/2 Alcohol associated Comorbidities and Microbiome Evaluation in HIV (ACME HIV), G1486559928, G1997962874, Role of Gut Microbial Dysbiosis and Aging on HIV-associated neurocognitive and brain dysfunction, Novel Therapies for Alcoholic Hepatitis, Mechanisms for alcohol induced gut barrier dysfunction in ALD, Novel therapies in alcoholic hepatitis University of Louisville, G5032143250, Alcohol Pharmacokinetics and Pharmacodynamics in Humans, 1/2 Alcohol Associated Comorbidities and Microbiome Evaluation in HIV (ACME HIV), Oxidized Metabolites of Linoleic Acid in Alcohol-induced Liver Injury, Role of Gut Microbiome and DHA Deficiency in Alcohol Induced Neuroinflammation, SAM Deficiency Mediated Epigenetic Mechanisms in Alcohol induced Immunosuppression, The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ Injury, Hepatobiology and Toxicology COBRE
OpenAlex ID: W2895440914
FWCI: 0.571
Cites: 37
Cited by: 5
Related to: 10