Following RYGB, pancreatic volume and steatosis adaptively decreased to "normal" levels with accompanying improvement in glucose homeostasis. Moreover, obesity-driven beta-cell expansion seems to be reversible; however, future studies must define a method to more accurately estimate functional beta-cell mass to increase our understanding of glucose homeostasis after RYGB.
Purpose About 20–25% of patients experience weight regain (WR) or insufficient weight loss (IWL) after bariatric metabolic surgery (BS). Therefore, we aimed to retrospectively assess the effectiveness of adjunct treatment with the GLP-1 receptor agonist semaglutide in non-diabetic patients with WR or IWL after BS. Materials and Methods Post-bariatric patients without type 2 diabetes (T2D) with WR or IWL (n = 44) were included in the analysis. The primary endpoint was weight loss 3 and 6 months after initiation of adjunct treatment. Secondary endpoints included change in BMI, HbA1c, lipid profile, hs-CRP, and liver enzymes. Results Patients started semaglutide 64.7 ± 47.6 months (mean ± SD) after BS. At initiation of semaglutide, WR after post-bariatric weight nadir was 12.3 ± 14.4% (mean ± SD). Total weight loss during semaglutide treatment was − 6.0 ± 4.3% (mean ± SD, p < 0.001) after 3 months (3.2 months, IQR 3.0–3.5, n = 38) and − 10.3 ± 5.5% (mean ± SD, p < 0.001) after 6 months (5.8 months, IQR 5.8–6.4, n = 20). At 3 months, categorical weight loss was > 5% in 61% of patients, > 10% in 16% of patients, and > 15% in 2% of patients. Triglycerides (OR = 0.99; p < 0.05), ALT (OR = 0.87; p = 0.05), and AST (OR = 0.89; p < 0.05) at baseline were negatively associated with weight loss of at least 5% at 3 months’ follow-up (p < 0.05). Conclusion Treatment options to manage post-bariatric excess weight (regain) are scarce. Our results imply a clear benefit of adjunct treatment with semaglutide in post-bariatric patients. However, these results need to be confirmed in a prospective randomized controlled trial to close the gap between lifestyle intervention and revision surgery in patients with IWL or WR after BS. Graphical abstract
Background Bariatric-metabolic surgery (BS) decreases the grade of steatosis, hepatic inflammation, and fibrosis in patients with severe obesity and non-alcoholic fatty liver disease (NAFLD). Mechanisms include substantial weight loss, but also simultaneous effects on glucose homeostasis. Therefore, we aimed to investigate the association between NAFLD and remission of type 2 diabetes (T2D) up to 8 years following different types of BS. Methods In a retrospective cohort study including 107 patients with obesity and T2D at baseline, the association between biopsy-proven NAFLD defined as steatosis in > 5% of hepatocytes at the time of surgery and T2D remission up to 8 years following different surgical procedures was investigated. Univariate regression analysis was used to examine the association between NAFLD and remission of T2D. Results Long-term remission of T2D was present in 56% of patients (n = 60). The presence of low-grade liver steatosis (grade 1) was associated with remission of T2D. Patients with a liver steatosis score ≥ 2 showed higher HbA1c levels at baseline. There were no significant differences in preoperative presence of lobular inflammation, hepatocyte ballooning, or fibrosis between patients who achieved T2D remission compared with those with no remission. Type of surgery did not affect remission of T2D. Conclusion Our results suggest that the presence of low-grade liver steatosis is associated with remission of T2D following sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB). Therefore, BS should be considered at an early NAFLD stage in patients with T2D. Graphical Abstract
Zusammenfassung Anamnese Eine 80-jährige Patientin stellte sich mit einer ausgeprägten Lymphadenopathie und Gewichtsverlust vor. Vorbekannt war eine seit 6 Jahren bestehende rheumatoide Arthritis. Es bestand eine basistherapeutische Behandlung mit Methotrexat (MTX) 10 mg 1-mal/Woche. Untersuchungen und Diagnose Anhand einer Lymphknotenbiopsie konnte eine klonale Vermehrung sowohl von EBV-positiven B- als auch T-Zellen nachgewiesen werden. Eine neu aufgetretene Anämie (Hb 10 g/dl), eine monoklonale Gammopathie vom Isotyp IgM sowie der Nachweis von 40 % EBV-positiven Plasmazellen im Knochenmark waren vereinbar mit der Diagnose eines IgM-Myeloms. Wir interpretierten dies als biklonale Epstein-Barr-Virus-induzierte MTX-assoziierte lymphoproliferative Erkrankung (MTX-LPD). Therapie und Verlauf Unmittelbar nach Absetzen von Methotrexat konnte eine relevante klinische Besserung beobachtet werden. In der Verlaufskontrolle nach 4 Monaten war die Gammaglobulin-Konzentration im Serum deutlich reduziert (von 51,1 auf 34,7 %) und eine erneute Immunelektrophorese des Serums war ohne Nachweis einer monoklonalen Gammopathie. Folgerung Anhand dieses Falls lässt sich die Assoziation einer RA mit lymphoproliferativen Erkrankungen bestätigen – hier als Assoziation einer RA mit einer biklonalen MTX-LPD bzw. einem Multiplen Myelom. Eine Therapie mit MTX sowie die Reaktivierung einer EBV-Infektion stellen dabei wichtige Einflussfaktoren dar.
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