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Hepatitis C Seropositivity Is Not a Risk Factor for Sensory Neuropathy in Patients with HIV Infection
Catherine Cherry*1,2,3, J McArthur4, J Affandi5, E Yunihastuti6, S Vanar7, A Kamarulzaman7, D Imran6, D Hooker1, S Wesselingh1,2,3, and P Price8
1Macfarlane Burnet Inst, Melbourne, Australia; 2Monash Univ, Melbourne, Australia; 3Alfred Hosp, Melbourne, Australia; 4Johns Hopkins Univ, Baltimore, MD, US; 5Murdoch Univ, Perth, Australia; 6Pokdisus HIV Care Clinic, Jakarta, Indonesia; 7Univ of Malaya, Kuala Lumpur, Malaysia; and 8Univ of Western Australia, Perth
Background: Sensory neuropathy (SN) remains one of
the commonest neurological problems seen in HIV patients. Co-infection with hepatitis
C (HCV) is often cited as a risk factor for SN in HIV, but epidemiologic data
to support this association are lacking. This collaboration aimed to determine
whether HCV co-infection is associated with increased SN risk among ambulatory
patients with HIV.
Methods: Patients were assessed for SN in HIV care
clinics in Melbourne, Jakarta, Kuala Lumpur, and Baltimore. SN was defined by
the presence of both supportive symptoms and signs. ART history and medical
data including HCV antibody status, were collected on all patients. HCV
serostatus was assessed as an SN risk factor using a c2 test and multivariate analyses using logistic
regression modelling in Stata 9.2 (StataCorp) were undertaken to correct for
treatment exposures and demographics.
Results: We assessed 503 patients (206 in Melbourne [83% Caucasian], 98 in Jakarta [66% Malay], 97 in Kuala Lumpur [86% Chinese],
and 104 in Baltimore [88% African American]). HCV seroprevalence was 31%
overall, but varied by site (61% in Baltimore, 51% in Jakarta, 16% in Melbourne, and 10% in Kuala Lumpur). On univariate analysis, HCV serostatus was not
associated with SN among patients at any non-Australian site (p >0.2
for all). In Melbourne the presence of HCV antibodies associated with a reduced
risk of SN (p = 0.003). When all cohorts were combined, there was no
association between HCV serostatus and symptomatic SN (p = 0.8). After correcting
for exposure to stavudine (a known neurotoxin) HCV antibodies associated with reduced
SN risk among patients in Melbourne (p = 0.007) and in Baltimore (p
= 0.08), but remained unrelated to SN status in the combined data set (p
= 0.75).
Conclusions: HCV co-infection was not associated
with increased SN risk among HIV patients attending any of the clinics studied.
These data represent patients of African American, Asian, and Caucasian descent
with varying HCV rates and ART exposure. We did not assess HCV RNA or liver
damage in this study. However, the apparent “protective” effect of HCV in some
centers is not explained by differential uptake of stavudine-based ART by
co-infected patients (often intravenous drug users). We conclude that HCV
co-infection is not a major contributing factor to the continued high rates of
SN observed among HIV patients globally.
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