Páginas: 9 (2092 palabras) Publicado: 27 de abril de 2010
To the Editor: We read with interest the article by
Clifford et al.,1 who conducted a retrospective study
of neurocognitive deficits and peripheral neuropathy
in subjects with stable, treated HIV infection and
active hepatitis C infection (HCV).
The authors compared the subjectsusing the
Trail-Making A and B tests and the Wechsler
Adult Intelligence Scale–Revised (WAIS-R) digit
symbol test. No significant differences between
groups were observed, which led authors to conclude
that active HCV infection does not affect
neurocognitive function in subjects with optimally
controlled HIV infection. However, additional
factors may have influenced results.
Evaluatingneurocognitive dysfunction in chronic
HCV is challenging and the assessment tools used by
Clifford et al. may have been suboptimal. Studies
that have demonstrated cognitive differences between
viremic HCV-positive and HCV-negative individuals
have utilized extensive batteries of cognitive
tests that have assessed performance of cognitive domains
individually and with high precision.2,3
It hasbeen shown that there is executive function
impairment in HCV-positive individuals with minimal
or absent HCV-related liver disease.2,3 Using less
detailed tools may lead to inadequate findings. Co´rdoba
et al.4 concluded that their use of noncomputerized
assessments with inferior sensitivity may have
contributed to their inability to demonstrate neurocognitive
differences betweenindividuals with
chronic HCV and healthy controls.
Clifford et al.1 also acknowledge the absence of
information on hepatic function and complications
of chronic liver disease—including hepatic encephalopathy—
which may have affected cognitive performance,
potentially confounding results. All cases of
HCV were viremic but the severity of liver dysfunction
was unknown. Even in minimal hepaticencephalopathy
or in HCV-infected individuals without
significant liver disease, cognitive deficits can be
The use of additional, sophisticated, psychometric
tests and group stratification for underlying hepatic
function may have illuminated differences
between the authors’ study groups. The impact of
HIV infection and HCV infection on the CNS is of
great interest and furtherstudies are needed to understand
this complex field of cerebral dysfunction.
L.J. Garvey, H. Pflugrad, A. Thiyagarajan, V.P.B.
Grover, S.D. Taylor-Robinson, A. Winston, London, UK
Disclosure: Dr. Winston has received honoraria or research grants
or been a consultant or investigator in clinical trials sponsored by
Abbott, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead
Sciences,GlaxoSmithKline, Janssen Cilag, Roche, and Pfizer.
Dr. Garvey, Dr. Pflugrad, Dr. Thiyagarajan, Dr. Grover, and
Dr. Taylor-Robinson report no disclosures.
Reply from the Authors: We appreciate Garvey et
al.’s interest in our recent report.1 We noted the limitations
of our test battery and agree that more detailed
testing may uncover statistical differences in
our populations. Poorly tested domains inour battery
may remain problematic. These deficits may
elude quantitative testing in a large population yet it
is unlikely that patients themselves are greatly affected.
We regret not having more information on
liver function and alcohol use, yet this shortfall
would have been far more important had we observed
impairment. Like Garvey et al., we assumed
that liver disease would makeneurologic function
worse. We also assumed that HCV—prone to affect
the liver—would make the HCV-positive population
more likely to have liver disease. We believe it is unlikely
that either undetected liver disease or alcohol
abuse (with subsequent liver or brain disease) would
improve the performance of coinfected patients obscuring
an otherwise important clinical deficit in the
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