A Longitudinal Hepatitis B Vaccine Cohort Demonstrates Long-lasting Hepatitis B Virus (HBV) Cellular Immunity Despite Loss of Antibody Against HBV Surface Antigen.

BACKGROUND: Long-lasting protection resulting from hepatitis B vaccine, despite loss of antibody against hepatitis B virus (HBV) surface antigen (anti-HBs), is undetermined. METHODS: We recruited persons from a cohort vaccinated with plasma-derived hepatitis B vaccine in 1981 who have been followed periodically since. We performed serological testing for anti-HBs and microRNA-155 and assessed HBV-specific T-cell responses by enzyme-linked immunospot and cytometric bead array. Study subgroups were defined 32 years after vaccination as having an anti-HBs level of either ≥10 mIU/mL (group 1; n = 13) or <10 mIU/mL (group 2; n = 31). RESULTS: All 44 participants, regardless of anti-HBs level, tested positive for tumor necrosis factor α, interleukin 10, or interleukin 6 production by HBV surface antigen-specific T cells. The frequency of natural killer T cells correlated with the level of anti-HBs (P = .008). The proportion of participants who demonstrated T-cell responses to HBV core antigen varied among the cytokines measured, suggesting some natural exposure to HBV in the study group. No participant had evidence of breakthrough HBV infection. CONCLUSIONS: Evidence of long-lasting cellular immunity, regardless of anti-HBs level, suggests that protection afforded by primary immunization with plasma-derived hepatitis B vaccine during childhood and adulthood lasts at least 32 years.

A Case of Potential Pharmacokinetic Kratom-drug Interactions Resulting in Toxicity and Subsequent Treatment of Kratom Use Disorder With Buprenorphine/Naloxone.

The botanical product kratom produces opioid-like effects at high doses and is sometimes used for opioid replacement by individuals with opioid use disorder. Mitragynine, a major alkaloid contained in kratom leaves, has been shown to inhibit multiple cytochromes P450 (CYPs) in vitro, including CYP2D6 and CYP3A. As such, kratom may precipitate pharmacokinetic drug interactions when co-consumed with certain medications. We present a case of a patient taking 150 mg venlafaxine (CYP2D6/3A substrate), 300 mg quetiapine (CYP3A substrate), and a high amount of kratom (~90 g) daily. The patient presented to the emergency department with serotonin syndrome and corrected electrocardiogram abnormalities that may have been secondary to supratherapeutic exposure to venlafaxine and/or quetiapine. The patient's symptoms resolved after discontinuation of venlafaxine and quetiapine. He was amenable to medication therapy for kratom discontinuation and successfully completed an at-home induction with buprenorphine/naloxone. This case report adds to the literature about potential pharmacokinetic kratom-drug interactions and suggests that buprenorphine/naloxone can facilitate recovery from kratom use disorder.

Rapid Transition to Buprenorphine in a Patient With Methadone-Related QTc Interval Prolongation.

BACKGROUND: Patients with opioid use disorder (OUD) who are managed on methadone often require transition to buprenorphine therapy. Current recommendations require months to gradually taper off of methadone; however, in some cases, the need to transition is urgent. Only a few rapid methadone-to-buprenorphine transitions have been reported and there are no established protocols to guide clinicians in these cases. CASE PRESENTATION: A 43-year-old man on 95 mg methadone for opioid use disorder experienced cardiac arrest attributable to ventricular fibrillation caused by QTc interval prolongation from methadone. In the hospital, a gradual taper of methadone was initiated but proved intolerable; the patient requested to restart his home dose of methadone and leave against medical advice. A rapid transition was initiated instead. Naltrexone (25 mg) was used to precipitate acute withdrawal followed 1 hour later by a "rescue" with buprenorphine/naloxone (16 mg/4 mg). The Clinical Opiate Withdrawal Score (COWS) peaked at 21 post-naltrexone and fell quickly to 15 within a half-hour of buprenorphine/naloxone administration. The patient was maintained on a total daily dose of 16 mg/4 mg buprenorphine/naloxone through the time of discharge. CONCLUSIONS: A patient requiring an urgent taper off of methadone due to adverse cardiac effects successfully transitioned to buprenorphine/naloxone within 2 hours by using naltrexone to precipitate withdrawal followed by a "rescue" with buprenorphine/naloxone. A relatively high dose of 16 mg/4 mg buprenorphine/naloxone successfully arrested withdrawal symptoms. With further refinement, this protocol may be an important technique for urgent methadone-to-buprenorphine transitions in the inpatient setting.