Background and Aims Opioid use disorder (OUD) has led to not only increases in overdose deaths, but also increases in endocarditis and osteomyelitis secondary to injection drug use (IDU). We studied the association between initiation of medications for opioid use disorder (MOUD) and treatment outcomes for people with infectious sequelae of IDU and OUD. Design and setting This is a retrospective cohort study reviewing encounters at 143 HCA Healthcare hospitals across 21 states of the United States from 2014 to 2018. Participants Adults aged 18–65 with the ICD diagnosis code for OUD and endocarditis or osteomyelitis (n = 1407). Measurements Main exposure was the initiation of MOUD, defined as either methadone or buprenorphine at any dosage started during hospitalization. Primary outcomes were defined as patient‐directed discharge (PDD), 30‐day re‐admission and days of intravenous antibiotic treatment. Covariates included biological sex, age, ethnicity, other co‐occurring substance use disorders, and insurance status. Findings MOUD was initiated among 269 (19.1%) patients during hospitalization. Initiation of MOUD was not associated with decreased odds of PDD. Initiation of MOUD did not impact 30‐day re‐admission. Patients who received MOUD, on average, had 5.7 additional days of gold‐standard intravenous antibiotic treatment compared with those who did not [β = 5.678, 95% confidence interval (CI) = 3.563, 7.794), P < 0.05]. Conclusion For people with opioid use disorder hospitalized with endocarditis or osteomyelitis, initiation of methadone or buprenorphine appears to be associated with improved receipt of gold‐standard therapy, as quantified by increased days on intravenous antibiotic treatment.

Methionine is a key nutrient required for the synthesis of S‐adenosylmethionine (SAM). SAM is the universal methyl group donor. Methionine gamma lyase deaminase (Mgld) is an enzyme that degrades methionine into alpha‐ketobutyrate and methylthiol. In this study, the Mgld gene was cloned into vectors that expressed Mgld, either in the cytosol or in the nucleus. The prostate cancer cell line, PC3 (ATCC‐CRL1435) was transfected with vectors containing Mgld. The PC3 cells experience cell death when Mgld is expressed in the cytosol or nucleus. In the presence of Proparglycine (PGLY), a Mgld inhibitor, the cells proliferate to a moderate degree. Co‐treatment of the PGLY with the nuclear Mgld caused a slight decrease of cells whereas with cytoplasmic Mgld caused a slight increase. In the cytoplasm, methionine is required for forming cysteine; cysteine in turn is required for glutathione (cells redox agent). Both cysteine and methionine are required for protein synthesis. Therefore, cytosolic dwindling of methionine will hamper protein synthesis and it should, in general, affect the growth of Mgld treated cells when compared to controlled cells. The addition of PGLY alone or in combination with the cytosolic vector increased proliferation, while the addition of PGLY to the nuclear vector caused modest cell death. We conclude that the methylation status of PC3 might be different and it affects the growth in varying degrees depending on the location of the Mgld expression. We speculate that PGLY might affect expressed Mgld and endogenous cytosolic cystathione beta‐synthase activity, resulting in complex cell fate, a hypothesis that needs to be tested further.Support or Funding InformationNSU Internal grantThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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