Investigating health-related quality of life, mood and neuropsychological test performance in a homogeneous cohort of Irish female hepatitis C patients.

Neurocognitive dysfunction has been reported in individuals with chronic hepatitis C (CHC) infection, but HCV populations investigated have often included participants with numerous potential confounding comorbidities. This pilot study sought to investigate functional capacity and neurocognitive function in a homogeneous state-infected HCV population with histologically defined mild liver disease, free from the comorbid factors typically associated with HCV populations. A further aim was to examine cognitive function in a treatment naive population with a similar history of iatrogenic HCV exposure and spontaneous viral clearance. A convenience sample of 29 women, all of whom were carefully screened to exclude relevant comorbidities, was recruited to the study. Twenty women with a history of iatrogenic HCV exposure were recruited from prospective specialist tertiary care liver clinics. A comparison group of healthy controls (n = 9) was also assessed. Study participants underwent mood, health-related quality of life and neuropsychological assessment. CHC patients reported significantly higher levels of cognitive fatigue than healthy controls (F = 3.4, P = 0.04). On cognitive testing, CHC patients showed impairments compared with healthy controls on estimates of general memory [F(2,25) = 4.1, P = 0.03, partial eta squared = 0.25], delayed auditory recognition [F(2,25) = 4.2, P = 0.03, partial eta squared= 0.22] and sustained attention [F(2,25) = 3.6, P = 0.04, partial eta squared = 0.22]. Increased cognitive fatigue only correlated with delayed auditory memory recall ability (r = 0.724, P = 0.006). In conclusion, these findings appear to support the presence of neurocognitive abnormalities in an iatrogenically infected, homogeneous female HCV population who were carefully screened to eliminate other factors affecting neurocognitive test performance and may indicate underlying neurophysiological causative mechanisms.