Changes of autonomic and sensory function during 24 weeks of antiviral treatment in patients with chronic HCV infection

Background and aim: Neurological complications of chronic Hepatitis C virus (HCV) infection are known predominantly in the peripheral nervous system. Symptoms of sensomotor neuropathies mainly change for the better during anti-HCV treatment, but they can worsen, as well. It is not known, how autonomic function changes during inteferon+ribavirin treatment.

Methods: 24 HCV PCR positive, treatment-naive patients were enrolled in the study (age=46.5±10.6 years). Cardiovagal autonomic function was assessed by determining heart rate variability (HRV) and spontaneous baroreflex sensitivity (BRS) indices. Heart rate was derived from ECG, continuous radial artery pressure was measured simultaneously by applanation tonometry. Peripheral sensory nerve function on median and peroneal nerves was characterized by current perception thresholds, measured by neuroselective diagnostic stimulator. Laboratory assays for liver transaminases, albumin, glucose, mixed cryoglobulin, and serum HCV-level were made. 180µg peginterferon alfa-2a weekly and 1000mg ribavirin daily was given. Measurements were made 1 day before first dose, then on 12th week and on 24th week of antiviral therapy.

Results: HRV low-frequency domain (LF) and BRS sequence (BRSseq) indices decreased after 12 weeks of therapy compared to the initial values; than increased significantly again for the 24th week. (211±163ms at week 0 vs. 99±66ms at week 12 vs. 180±184ms at week 24 for LF; 8.4±4.3 vs. 5.5±2.2 vs. 8.1±3.9ms/mmHg for BRSseq [mean±SEM]; p<0.05). This trend was found in all examined autonomic indices, both in subgroups of patients with and without early viral response, and with and without mixed cryoglobulinemia, respectively. Sensory function did not change during 24 weeks of therapy.

Conclusion: The short term and reversible deterioration of autonomic function at the beginning of anti-HCV therapy may reflect the changes of immune-system caused by the immune-mediator interferon. To evaluate further tendencies, we continue the follow-up examinations.