Julia Casado-Carbajo

BACKGROUND Buprenorphine is an effective and safe medication for opioid use disorder that can be delivered in office-based addiction treatment (OBAT). Yet, over half of people who initiate buprenorphine disengage and return to unhealthy opioid use. Accordingly, it is critical to improve OBAT retention. Mobile applications using embodied conversational agents (ECA) have improved care in other chronic diseases and may increase OBAT retention. OBJECTIVE To explore patient perspectives on how an ECA can support retention in OBAT programs. METHODS We conducted a series of 6 focus groups with a single cohort of 8 patients receiving treatment with buprenorphine within an OBAT program. Focus group topics included experiences with treatment initiation and retention, beliefs about barriers to retention, understanding participants’ perspectives for how an application with an ECA could support retention for new patients, and feedback on ECA prototypes. A socioecological model guided our deductive and inductive thematic analyses. RESULTS Participants had been engaged in care for 4-18 years. They identified how an ECA could address barriers to retention across four levels of the socioecological model. At the society level, the application could provide information about basic needs including housing and food access. At the community level, participants expressed unclarity about buprenorphine and wanted information about dose, side effects and discontinuation strategies that had been verified by their healthcare provider. At the interpersonal level, they endorsed the application’s ability to function as peer-support. They recommended that the agent embodied a peer in recovery and that storytelling related to lived experience would be a constructive tool. CONCLUSIONS An ECA was perceived as a helpful tool to support retention in OBAT by addressing fundamental socioecological needs and by providing information and linkage to resources. Implementation of an ECA system based on these findings should be evaluated in a clinical trial to improve retention in OBAT programs.

Background: Vitamin D deficiency is a risk factor for liver disease, insulin resistance, and beta cell dysfunction. Individuals with alcohol use disorder (AUD) have many comorbidities, with a heavy burden of liver disease and metabolic complications, including type 2 diabetes mellitus (T2DM). Objective: We aimed to analyze the prevalence and associations of vitamin D deficiency in patients admitted for in-hospital treatment of AUD. Methods: A cross-sectional study was conducted in patients consecutively admitted for the treatment of AUD between January 2017 and October 2023. Sociodemographic data, substance use characteristics, and blood parameters were available at admission. Vitamin D status was assessed through the serum concentrations of 25-hydroxyvitamin D [25(OH)D] levels using a direct competitive chemiluminescent immunoassay method. Deficiency of vitamin D was defined as a concentration less than 20 ng/mL; impaired fasting glucose (IFG) was defined by fasting blood glucose >100 mg/dL (5.6 mmol/L), and advanced liver fibrosis by an FIB-4 index >3.25. Results: Two hundred and forty-three patients were included (75% male) with a mean age of 49 ± 10 years, mean BMI of 26.4 ± 7.3, mean alcohol consumption of 163 ± 81 g/day, and a mean duration of AUD of 18.1 ± 11.2 years. Mean 25(OH)D, fasting blood glucose, AST, ALT, and platelets were 14.4 ± 10.2 ng/mL, 103.4 ± 40.9 mg/dL, 55.1 ± 75.8 U/L, 44.8 ± 76.6 U/L, and 206.3 ± 84.8 × 10⁹/L, respectively. The prevalence of vitamin D deficiency was 80.6%, and 41.1% of patients had levels less than 10 ng/mL. IFG was present in 32.3% of patients, and 20.5% had FIB-4 values >3.25. In the multivariable analysis, IFG (OR, 2.51; 95% CI: 1.02–6.17, p = 0.04) and advanced liver fibrosis (OR, 4.27; 95% CI: 1.21–15.0, p = 0.02) were the only factors associated with vitamin D deficiency. Conclusions: Vitamin D deficiency was very prevalent in this series of patients with AUD and was associated with impaired fasting glucose and advanced liver fibrosis.