Risk Factors for Chronic Abdominal Pain After RYGB: Are Patients Adequately Selected Beforehand?

PURPOSE: Chronic abdominal pain after RYGB is a known issue. Identifying the potential patient-related and modifiable risk factors might contribute to diminish the risk for this undesirable outcome. METHODS: A single-center retrospective cohort study with prospective data collection was conducted with inclusion of all patients who underwent RYGB surgery between 2015 and 2021. Data from the NBSR and medical records were used. Patients with chronic abdominal pain were defined when pain lasting or recurring for more than 3 to 6 months. RESULTS: Six hundred sixty-four patients who underwent RYGB surgery were included with a median follow-up of 60.5 months. Forty-nine patients (7.3%) presented with chronic abdominal pain. Postoperative complications (OR 13.376, p = 0.020) and diagnosis of depression (OR 1.971, p = 0.037) were associated with developing abdominal pain. On the other hand, ex-smokers (OR 0.222, p = 0.040) and older age (0.959, p = 0.004) presented as protective factors. CONCLUSION: Postoperative complications and diagnosis of depression are risk factors for chronic pain after RYGB. The role of the bariatric MDT remains crucial to select these patients adequately beforehand.

Multi-tissue profiling of oxylipins reveal a conserved up-regulation of epoxide:diol ratio that associates with white adipose tissue inflammation and liver steatosis in obesity.

BACKGROUND: Obesity drives maladaptive changes in the white adipose tissue (WAT) which can progressively cause insulin resistance, type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated liver disease (MASLD). Obesity-mediated loss of WAT homeostasis can trigger liver steatosis through dysregulated lipid pathways such as those related to polyunsaturated fatty acid (PUFA)-derived oxylipins. However, the exact relationship between oxylipins and metabolic syndrome remains elusive and cross-tissue dynamics of oxylipins are ill-defined. METHODS: We quantified PUFA-related oxylipin species in the omental WAT, liver biopsies and plasma of 88 patients undergoing bariatric surgery (female N = 79) and 9 patients (female N = 4) undergoing upper gastrointestinal surgery, using UPLC-MS/MS. We integrated oxylipin abundance with WAT phenotypes (adipogenesis, adipocyte hypertrophy, macrophage infiltration, type I and VI collagen remodelling) and the severity of MASLD (steatosis, inflammation, fibrosis) quantified in each biopsy. The integrative analysis was subjected to (i) adjustment for known risk factors and, (ii) control for potential drug-effects through UPLC-MS/MS analysis of metformin-treated fat explants ex vivo. FINDINGS: We reveal a generalized down-regulation of cytochrome P450 (CYP)-derived diols during obesity conserved between the WAT and plasma. Notably, epoxide:diol ratio, indicative of soluble epoxide hydrolyse (sEH) activity, increases with WAT inflammation/fibrosis, hepatic steatosis and T2DM. Increased 12,13-EpOME:DiHOME in WAT and liver is a marker of worsening metabolic syndrome in patients with obesity. INTERPRETATION: These findings suggest a dampened sEH activity and a possible role of fatty acid diols during metabolic syndrome in major metabolic organs such as WAT and liver. They also have implications in view of the clinical trials based on sEH inhibition for metabolic syndrome. FUNDING: Wellcome Trust (PS3431_WMIH); Duke-NUS (Intramural Goh Cardiovascular Research Award (Duke-NUS-GCR/2022/0020); National Medical Research Council (OFLCG22may-0011); National Institute of Environmental Health Sciences (Z01 ES025034); NIHR Imperial Biomedical Research Centre.