Introduction: Patients with opioid use disorder (OUD) who receive medication for opioid use disorder (MOUD), either buprenorphine or methadone, have decreased all-cause and overdose mortality. Although in patients with congestive heart failure, OUD is associated with a greater number of heart failure hospitalizations (HFH), no studies were conducted on the outcomes of MOUD in this population. Hypothesis: We hypothesized that in patients with OUD and congestive heart failure, MOUD is associated with a decreased number of HFH. Methods: We retrospectively reviewed records of patients treated at the Rutgers NJMS Ambulatory Care Center, diagnosed with both heart failure and opioid use disorder between 2016 and 2018. We conducted multivariate linear regression to identify predictors of HFH. Results: Among 91 included patients, 60% were male, mean age was 58 ± 7 years old. The majority (75%) of patients were of African American ethnicity. Mean left ventricular ejection fraction (LVEF) was 41 ± 18%; 32% patients had preserved, 22% had mid-range and 46% had reduced LVEF. Over the 2-year period, 57% of patients were treated with buprenorphine, and 76% with methadone - a total of 87% of all patients were on MOUD. Less than half (37%) of the patients had medical insurance. Median number of HFH was 2.0 (IQR 0.0 - 8.5). In multivariate analysis ( table ), number of HFH correlated positively with the presence of insurance (β = 4.02 [95% CI 1.06 to 6.98], p = 0.008) and number of missed appointments (β = 0.33 [95% CI 0.11 to 0.55], p = 0.003), and negatively with MOUD (β = –5.41 [95% CI -9.52 to -1.31], p = 0.01). HFH were not associated with LVEF (p = 0.746), diastolic dysfunction (p = 0.855) or age and gender. Conclusions: In patients with OUD and congestive heart failure, MOUD is independently associated with less HFH and is one of its strongest predictors. Expanding access to methadone and buprenorphine appears to be critical in improving the quality of care of this vulnerable and underserved population.
Tumour-induced osteomalacia (TIO) is a rare paraneoplastic syndrome. The constellation of findings of unprovoked fractures, hypophosphataemia, urinary phosphate wasting and a negative genetic evaluation suggest a TIO diagnosis. Tumours leading to TIO are often small and difficult to localise using standard imaging studies. The68Ga-DOTATATE CT/positron emission tomography, a somatostatin receptor imaging modality, is the radiographical study of choice for localisation. It is highly sensitive and specific since tumours that cause oncogenic osteomalacia have been shown to express somatostatin receptors. Complete surgical resection is the treatment of choice; however, it may not always be feasible. Burosumab, a human anti-fibroblast growth factor-23 monoclonal antibody, is a therapeutic option in cases of unresectable TIO to normalise phosphorus levels and improve fracture healing. Our patient was initiated on burosumab, which led to healing of his fractures and profound symptomatic improvement of his pain. TIO is often undiagnosed for many years, leading to significant patient morbidity.
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