Vagal system impairment in human immunodeficiency virus-positive patients with chronic hepatitis C: does hepatic glutathione deficiency have a pathogenetic role?

• Published in: Scandinavian journal of gastroenterology Vol. 32; no. 12; p. 1261
• Main Authors: Barbaro, G, Di Lorenzo, G, Soldini, M, Bellomo, G, Belloni, G, Grisorio, B, Barbarini, G
• Format: Journal Article
• Language: English
• Published: England 1997
• Subjects: Adult; Electrocardiography; Erythrocytes - chemistry; Erythrocytes - metabolism; Female; Glutathione - deficiency; Hepatitis C - complications; Hepatitis, Chronic - complications; HIV Infections - complications; Humans; Leukocytes, Mononuclear - metabolism; Liver - metabolism; Male; Malondialdehyde - analysis; Neural Conduction - physiology; Peripheral Nervous System Diseases - etiology; Vagus Nerve - physiopathology
• ISSN: 0036-5521; 1502-7708
• DOI: 10.3109/00365529709028157

Both an autonomic impairment and a systemic depletion of reduced glutathione (GSH) may be documented in patients with chronic liver diseases and in human immunodeficiency virus (HIV)-positive patients. The coefficients of electrocardiographic R-R interval variation (CVc) were assessed in 125 patients with chronic hepatitis C (CHC) (65 HIV-positive and 60 HIV-negative) and in 61 healthy controls. The CVc values were correlated with hepatic (H-GSH), plasmatic (P-GSH), lymphocyte (L-GSH), and erythrocyte (E-GSH) concentrations of GSH and with erythrocyte malonyldialdehyde (MDA) levels. Compared with healthy controls, in CHC patients the concentrations of H-GSH, P-GSH, L-GSH, and E-GSH were reduced, whereas MDA levels were increased with a statistically significant difference (P < 0.001). CVc was significantly reduced in patients with CHC (especially in those who were HIV-positive) and correlated significantly with the values of H-GSH, P-GSH, L-GSH, E-GSH, and MDA (P < 0.001). A dysfunction of the cardiac vagal system may be detected in patients with CHC (especially in those who are HIV-positive); this abnormality may be related to a reduced response to oxidative stress because of a systemic depletion of GSH.