February 9, 2004
One of the unresolved issues of hepatitis C (HCV) infection is the potential role of this virus with regard to neurocognitive dysfunction. Some patients with HCV infection report "brain fog" and it has been debated whether this symptom is more frequent in HCV-infected patients, and if so, what causes it.
Previous studies have shown that HCV is able to replicate in the brain (Laskus, 9th CROI, Abstract 649). Patients with viremic HCV infection have been shown to have a higher rate of impairment in neurocognitive tasks together with abnormalities on cerebral proton magnetic resonance spectroscopy compared with successfully treated HCV-infected patients (Forton, Hepatology, 2002).
This present study was a sub-study of ACTG 5095 and focused on 235 treatment-naive HIV-infected patients, of whom 25 were co-infected with HCV antibody positive. All patients had neuropsychological performance testing at study entry which consisted of the Trailmaking Test (parts A and B), the WAIS Digit Symbol task, and the Center for Epidemiologic Studies-Depression Scale (CES-D).
With regard to baseline characteristics, the HCV-infected patients were similar to the un-infected patients. Differences included a lower educational level among the HCV-positive group (mean of 11.8 years) versus the HCV-negative group (mean 13.8 years), and a higher prevalence of intravenous drug use in the HCV-positive group.
The results of testing showed that HCV-positive patients had poorer overall neuropsychological performance. They also performed less well on the Digit Symbol task and these differences persisted after controlling for confounding variables with multivariate regression analysis.
Significant depression was noted in 52% of the HCV-positive patients compared with 33% in HCV-negative patients (p=0.055). Utilizing subscales of depression, most of the differences were related to the "somatic complaint" portion of the CES-D scale.
The authors concluded that this data was consistent with the hypothesis that HCV has a negative impact on neurocognitive function. They did concede however, that this study was limited by the potential influence of multiple potential confounding factors.
Following presentation of the data, a comment from the audience raised the point that the poorer neuropsychological performance might be partly related to cerebral damage from intravenous drug use which was more prevalent in HCV-positive patients.
Another member of the audience pointed out that no data was presented regarding hepatic synthetic function in the two groups. The implication of this comment was that some of the HCV-positive patients may have had cirrhosis and varying degrees of hepatic encephalopathy which may have skewed the results.
The most significant limitation of the study seems to have been the relatively small number of HCV-positive patients. There are challenges associated with the use of multivariate regression in small data sets which restricts the ability to control for potential confounders. For example, just a few patients with hepatic encephalopathy could have influenced the results of the HCV-positive group.
In summary, this interesting study adds to the growing body of information that suggests HCV may negatively impact neurocognitive function.
Abstract: Hepatitis C and Neuropsychological Function in Treatment Naive HIV-1-Infected Subjects -- A5097s Baseline Analysis (Oral 26)
Authored by: Y. Yang, S. Evans, R. Gulick, D. Clifford, AIDS Clinical Trials Group A5097s Team
Affiliations: Harvard Sch. of Publ. Hlth., Boston, MA; Weill Med. Coll. of Cornell Univ., New York, NY; Washington Univ. Sch. of Med., St. Louis, MO
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