Immune Function and Drug Treatment in Anti-Retrovirus Negative Intravenous Drug Users

Abstract

A recent cross-sectional study by Klimas, et al., (1) showed that a clinically significant degree of immune impairment exists in methadone treated intravenous drug users (IVDUs) in the absence of human T cell lymphotropic virus, subtypes I or II (HTLV) or human immunodeficiency virus (HIV-1) infection or use of street drugs. The methadone-treated group exhibited significant differences in lymphocyte phenotype with elevations in the numbers of CD4+CD29 + (T helper), CD8 + (T suppressor/cytotoxic), CD8+I2+ cells (activated T suppressor/cytotoxic), and CD2+CD29+ (activated total T) lymphocytes. Despite these increases in lymphocyte numbers, lymphocyte function was suppressed in the methadone group, with poor response to phytohemagglutinin (PHA) and pokeweed mitogen (PWM) in culture, except for the subset of subjects who were HTLV positive. Moreover, natural killer (NK) cell cytotoxicity was significantly reduced in the methadone group. These findings could not be ascribed to psychoimmunologic interactions, to concomitant use of street drug or alcohol (2). Other investigators have reported, in studies of peripheral blood mononuclear cells from patients on methadone, a significant impairment of the ability to generate Superoxide anion (3). Morphine, and to a lesser extent, methadone reduced phagocytosis, intracellular killing and Superoxide production in polymorphonuclear leukocytes and in monocytes (4). In heroin addicts, both before and after methadone treatment, skin test anergy to seven recall antigens was common (3). Other types of immunomodulation by methadone have been reported. Kreek (5) noted persistence of lymphocytosis in patients maintained on methadone for three or more years.