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Alcohol use disorder in HCV increases depression, inflammatory response

Hepatitis C with comorbid alcohol use disorder correlated with increased depression and anxiety, dysregulated cytokine expression, and compromised blood-brain barrier function, according to a recently published study.

“Like HCV infection, chronic alcohol use induces inflammatory responses that contribute to its adverse [central nervous system] and neuropsychiatric effects,” Jennifer M. Loftis, PhD, from the VA Portland Health Care System in Oregon, and colleagues wrote. “The aim of this study was to investigate how comorbid [alcohol use disorder (AUD)] contributes to abnormalities in inflammatory mediators and psychiatric impairments in Veterans with HCV.”

Loftis and colleagues enrolled 55 veteran patients with HCV, 42 of whom had AUD. The researchers evaluated the patients at three time points over 12 weeks to assess changes in alcohol use and inflammatory changes.

HCV viral load was not significantly different between those with and without AUD.

Comorbid AUD correlated significantly with elevated alanine aminotransferase (P = .03) and aspartate aminotransferase levels (P = .01), symptoms of depression based on the Beck Depression Inventory Second Edition (P = .003), and symptoms of posttraumatic stress disorder based on the PTSD Checklist-Civilian Version (P = .008) compared with patients without AUD.

Comorbid AUD also correlated with altered expression of inflammatory factors in plasma, including IL-8 (P = .006), IL-10 (P = .03) and S100B (P = .048). Increased expression of all three factors persisted over time despite self-reported reductions in alcohol consumption among patients with AUD.

Additionally, a follow-up analysis showed that patients with circulating S100B higher than 12 pg/mL reported a higher average consumption of alcohol compared with patients with lower levels of circulating S100B.

“Higher levels of S100B may be indicative of CNS injury in individuals with HCV and AUD,” the researchers wrote. “Our initial findings suggest a predictive value of S100B and its inflammatory signaling effects in the neuropathological consequences of comorbid HCV and AUD; however, follow-up mechanistic studies are necessary to corroborate these observations.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.