Abstract
Alcohol use disorder (AUD) patients comorbid with hepatitis C virus (HCV) infection (HCV + AUD) could have progressively severe clinical sequels of liver injury and inflammation. Serum zinc and several polyunsaturated fatty acids (PUFAs) get dysregulated in AUD as well as HCV. However, the extent of dysregulation of PUFAs and zinc deficiency and their interaction in HCV + AUD as a comorbid pathology has not been studied. We examined the role of dysregulation of FAs and low zinc in HCV + AUD patients. 138 male and female participants aged 21–67 years were grouped as HCV-only (Gr. 1; n = 13), HCV + AUD (Gr. 2; n = 25), AUD without liver injury (Gr. 3; n = 37), AUD with liver injury (Gr. 4; n = 51), and healthy volunteers (Gr. 5 or HV; n = 12). Drinking history, individual demographic measures, fasting fatty acids, liver function, and zinc were measured and analyzed. HCV + AUD patients showed the highest ALT level compared to the rest of the groups. Serum zinc concentrations were the lowest, and the proinflammatory shift was the highest (characterized by ω6 : ω3 ratio) in the HCV + AUD patients. Total ω3, eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) were the lowest in HCV + AUD patients. Total ω3, α-linoleic acid (α-LA) along with covariable number of drinking days past 90 days (NDD90), eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) independently showed significant association with low zinc in the HCV + AUD patients. Heavy drinking pattern showed that NDD90 has a significant mediating role in the representation of the relationship between candidate ω3 PUFAs and zinc uniquely in the HCV + AUD patients. Low serum zinc showed a distinctively stronger association with total and candidate ω3s in the HCV + AUD patients compared to the patients with HCV or AUD alone, supporting dual mechanism involved in the exacerbation of the proinflammatory response in this comorbid cohort. This trial is registered with NCT#00001673.
Highlights
Hepatitis C virus (HCV) is the most common chronic bloodborne infection, affects 5 million Americans, and causes very high morbidity and mortality [1]
We evaluated the association of HCV-viral load and serum zinc and polyunsaturated fatty acids (PUFAs) in HCV patients with or without Alcohol use disorder (AUD) to show the extent of linked response in this comorbid patient cohort
Alanine Aminotransferase (ALT) level was used as a reference to assess liver injury (Medline Plus-National Institutes of Health, 2014); 40 IU/L for ALT was used as the upper limit of normal, and values ≥41 IU/L indicated liver injury as per the guideline that existed till 2014. e standard lower limit of normal for serum zinc was 71 mcg/dL in this study. e comprehensive fatty acid panel measured specific and total ω3 and ω6 FA levels using gas chromatography/mass spectrometry. e screening was performed to identify patients with HCV, which was conducted with COBAS Ampliprep/COBAS Taqman HCV test methodology; HCV diagnosis was a firsttime report in Gr. 1 and Gr. 2
Summary
Hepatitis C virus (HCV) is the most common chronic bloodborne infection, affects 5 million Americans, and causes very high morbidity and mortality [1]. Hepatitis C virus (HCV) has lasting morbidity and lasting effect on the liver and overall health [2]. Alcohol use disorder (AUD) is known to be consequential in alcoholic liver disease (ALD) [3]. ALD is a major form of liver disease that is responsible for the mortality and morbidity in the USA and worldwide [4]. AUD diagnosed individuals with HCV infection (HCV + AUD) have reported a propensity for liver injury compared with AUD patients, with a prevalence of HCV and AUD comorbidity being 16.3% [6]
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