Neuropsychiatric symptoms associated with hepatitis C virus (HCV)

Infectious Disease Advisor Contributing Writer 

September 12, 2018 

HCV Neuropsychiatric Symptoms Likely Linked to Virus' Effects on Brain Function

The neuropsychiatric symptoms associated with hepatitis C virus (HCV) infection are likely caused by the body's response to the virus' effects on brain function, according to a study recently published in the Journal of Viral Hepatitis. This neuro-inflammatory and systemic response is akin to that observed in patients with autoimmune diseases of the liver.

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Reference 

Dirks M, Haag K, Pflugrad H, et al. 

Neuropsychiatric symptoms in hepatitis C patients resemble those of patients with autoimmune liver disease but are different from those in hepatitis B patients 

[published online August 18, 2018]. J Viral Hepat. doi: 10.1111/jvh.12979

Abstract 

Chronic fatigue, mood alterations and cognitive impairment are frequent accessory symptoms of HCV‐infection. Fatigue and mood alterations have also been observed in autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC), but not in hepatitis B virus (HBV)‐infection, thus indicating an autoimmune response as possible cause of HCV‐infection associated encephalopathy. Data, however, are sparse. This study aims to prove that HCV patients feature similar to those with autoimmune liver disease but contrary to HBV patients regarding neuropsychiatric symptoms.

132 non‐cirrhotic patients (HCV: 46, HBV: 22, AIH: 27, PBC: 29, AIH/PBC: 8) completed questionnaires addressing the domains mentioned above. Eighty‐eight underwent a comprehensive neuropsychological assessment. Patient groups were compared among each other and to 33 healthy controls.

Fatigue, anxiety and depression scores were significantly increased, and the SF‐36 mental score significantly decreased in all patient groups compared to controls. Fatigue was significantly more pronounced in HCV than in HBV patients. HCV patients scored significantly worse than HBV patients but not AIH and PBC patients in the SF‐36. HCV, AIH and PBC but not HBV patients did significantly worse than controls in word learning. Recognition of words was impaired in HCV, AIH and PBC patients and recognition of figures in HCV patients, exclusively (p≤0.002). HCV patients did also worse than controls and HBV patients concerning alertness and working memory (p≤ 0.001).

The neuropsychiatric profiles of HCV patients are similar to those of AIH and PBC patients but differ from those of HBV patients, suggesting an autoimmune response as a possible cause for these differences.