Brown, Brooke

INTRODUCTION: Ongoing surveillance after successful endoscopic eradication therapy for Barrett's esophagus (BE)-related neoplasia is essential to detect and manage recurrence. Despite established surveillance interval recommendations after complete eradication of intestinal metaplasia (CE-IM), patient compliance with repeat endoscopy is frequently suboptimal. Understanding patient drivers to adherence is essential to inform interventions that address the high rates of overdue surveillance and loss to follow-up. METHODS: Patients with BE-related neoplasia who achieved CE-IM were eligible for inclusion and classified as delayed or on-time for endoscopic surveillance. Patients were prospectively enrolled and participated in structured virtual interviews designed to explore barriers and facilitators to on-time care. A rapid qualitative analysis approach was applied, continuing until thematic saturation was reached. RESULTS: Thirty-nine patients were interviewed: 22 (56.4%) were delayed, and 17 (43.6%) were on-time for surveillance. Patients in the delayed group had longer mean BE segment lengths and a higher prevalence of tobacco use. Geographic distance from the treatment center was the most frequently cited barrier to follow-up (n = 17; 43.5%). Other common barriers were access limitations, financial concerns, misunderstanding of disease course, and test-related anxiety. DISCUSSION: Patient-related drivers of delay in postendoscopic eradication therapy surveillance are largely logistical, socioeconomical, and psychological in nature. Solutions to reduce the significant burden on the patient and achieve timely surveillance may include transitioning patients back to their local endoscopists after CE-IM or incorporating nonendoscopic surveillance methods through patient centered approaches.

AbstractWe investigated how obesity impacts the response of circulating insulin‐like growth factor‐1 (IGF‐1) to a single bout of endurance exercise in humans with and without obesity. Blood samples were collected before exercise, at 15 and 40 min during a 45‐min cycling session at 65% of heart rate reserve, and 15 min post‐exercise. Serum levels of total IGF‐1, free IGF‐1, IGF binding proteins 1 (IGFBP‐1) and 3 (IGFBP‐3), growth hormone, and insulin were measured. Both total IGF‐1 and IGFBP‐3 serum concentrations increased significantly (p < 0.05) during exercise in the study participants without obesity but not in those with obesity, returning to basal levels immediately after exercise. There was a statistically significant main effect on the growth hormone response, with circulating levels being higher in participants without obesity (p < 0.05). No significant effects were observed for either free IGF‐1 or IGFBP‐1 serum concentrations in response to exercise in either group (p > 0.05). We conclude that humans with obesity have blunted serum total IGF‐1 response during exercise. However, a concurrent attenuation in serum IGFBP‐3 response, which regulates free (i.e., biologically active) IGF‐1 in circulation, results in no change in circulating free IGF‐1 levels during endurance exercise in individuals with obesity.