Background Hospital discharges against medical advice (AMA) is associated with negative health outcomes and re-admissions. Patients with substance use disorders (SUD) are up to three times more likely to be discharged AMA as compared to those without SUD. Studies suggest that undertreated withdrawal and a perception of stigma may increase the risk, however, to date, there are no published qualitative studies exploring the specific reasons why patients with SUD leave prematurely. Methods Semi-structured interviews with patients ( n = 15) with SUD with documented AMA discharges from our hospital between 9/2017 and 9/2018. Maximum variation sampling was employed to display diversity across gender, race, age, and type of substance use disorder (alcohol vs opioids). Patients were interviewed until no new concepts emerged from additional interviews. Two coders separately coded all transcripts and reconciled code assignments. Results Four core issues were identified as patients’ reasons for leaving the hospital prematurely: undertreated withdrawal and ongoing craving to use drugs, uncontrolled acute and chronic pain, stigma and discrimination by hospital staff about their SUD, and hospital restrictions, including not being allowed to intermittently leave the hospital floor. For patients with histories of criminal involvement, being hospitalized reminded them of being incarcerated. Conclusion These findings shed light on the reasons patients with SUD are discharged from the hospital AMA, an event that is associated with increased thirty-day mortality and hospital re-admission. AMA discharges represent missed opportunities for the health care system to engage with patients struggling with a SUD. Our findings support the need for inpatient addiction treatment, particularly for management of withdrawal and co-occurring pain, and the need to address health care provider associated stigma surrounding addiction.

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The capacity of immune complexes to augment antibody (Ab) responses is well established. The enhancing effects of immune complexes have been attributed mainly to Fc-mediated adjuvant activity, while the ability of Abs to induce antigenic alterations of specific epitopes as a result of immune complex formation have been less well studied. Previously we have shown that the interaction of anti-CD4-binding site (CD4bs) Abs with HIV-1 gp120 induces conformation changes that lead to enhanced antigenicity and immunogenicity of neutralizing epitopes in the V3 loop. The present study shows that significant increases in the antigenicity of the V3 and C1 regions of gp120 were attained for several subtype B gp120s and a subtype C gp120 upon immune complex formation with the anti-CD4bs monoclonal Ab (mAb) 654-D. Such enhancement was observed with immune complexes made with other anti-CD4bs mAbs and anti-V2 mAbs, but not with anti-C2 mAbs, indicating this activity is determined by antigen specificity of the mAb that formed the immune complex. When immune complexes of gp120LAI/654-D and gp120JRFL/654-D were tested as immunogens in mice, serum Abs to gp120 and V3 were generated at significantly higher titers than those induced by the respective uncomplexed gp120s. Notably, the anti-V3 Ab responses had distinct fine specificities; gp120JRFL/654-D stimulated more cross-reactive anti-V3 Abs than gp120LAI/654-D. Neutralizing activities against viruses with heterologous envelope were also detected in sera of mice immunized with gp120JRFL/654-D, although the neutralization breadth was still limited. Overall this study shows the potential use of gp120/Ab complexes to augment the immunogenicity of HIV-1 envelope gp120, but further improvements are needed to elicit virus-neutralizing Ab responses with higher potency and breadth.

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