naloxone and Hepatitis

HIV/AIDS rates are higher in the Southern United States compared to other regions of the country. Reasons for disparities include poverty, health care access, and racism. People who inject drugs (PWID) account for 8% of HIV/AIDS incidence rates. Harm reduction can connect PWID to needed resources. AIDS United Southern REACH grantees developed the Southern Harm Reduction Coalition (SHRC) as a means to decrease HIV/AIDS and viral hepatitis rates, criminalization of drug users and sex workers, and drug overdose.. Investigators used an intrinsic case study design to examine the context of harm reduction in the Southern United States, successful strategies, and outcomes. Data collection included key informant interviews and coalition documents. The community coalition action theory was used to examine the data.. The SHRC initiated regional conferences and customized trainings. Strengths-based language and utilization of diverse strengths among coalition members were used to effect change. Coalition outcomes included syringe decriminalization legislation, syringe exchange, naloxone access, naloxone funding legislation, and 911 Good Samaritan laws, along with expanded support for PWID.. Advocacy successes can be applied to similar organizations in the Southern United States to promote harm reduction and potentially decrease HIV/AIDS burden, viral hepatitis, criminalization, and overdose.

Topics: Acquired Immunodeficiency Syndrome; Adult; Community Participation; Drug Overdose; Female; Harm Reduction; Health Services Accessibility; Health Status Disparities; Hepatitis; HIV Infections; Humans; Naloxone; Needle-Exchange Programs; Public Health; United States

Fas (CD95)-induced hepatocyte apoptosis and cytotoxic activity of neutrophils infiltrating the injured liver are two major events leading to hepatitis. Because it has been reported that opioids, via a direct interaction, sensitize splenocytes to Fas-mediated apoptosis by upregulating Fas messenger RNA (mRNA) and modulated neutrophil activity, we assumed that opioids may participate in the pathophysiology of hepatitis. Using the hepatitis model induced by agonistic anti-Fas antibody in mice, we showed that opioid receptor blockade reduced liver damage and consequently increased the survival rate of animals when the antagonist naltrexone was injected simultaneously or prior to antibody administration. Treatment of mice with morphine enhanced mortality. Naloxone methiodide-a selective peripheral opioid antagonist-had a protective effect, but the absence of opioid receptors in the liver, together with lack of morphine effect in Fas-induced apoptosis of primary cultured hepatocytes, ruled out a direct effect of opioids on hepatocytes. In addition, the neutralization of opioid activity by naltrexone did not modify Fas mRNA expression in the liver as assessed with real-time quantitative polymerase chain reaction. Injured livers were infiltrated by neutrophils, but granulocyte-depleted mice were not protected against the enhancing apoptotic effect of morphine. In conclusion, opioid receptor blockade improves the resistance of mice to Fas-induced hepatitis via a peripheral mechanism that does not involve a down-modulation of Fas mRNA in hepatocytes nor a decrease in proinflammatory activity of neutrophils.

Topics: Animals; Antibodies; Cells, Cultured; fas Receptor; Female; Hepatitis; Liver; Mice; Mice, Inbred BALB C; Morphine; Naloxone; Narcotic Antagonists; Narcotics; Quaternary Ammonium Compounds; RNA, Messenger