Current state of medical rehabilitation for adult short bowel syndrome patients with intestinal failure
PURPOSE OF REVIEW: Short bowel syndrome intestinal failure (SBS-IF) occupies a unique position at the interface between chronic organ failure management and intestinal transplantation (iTx). Historically, patients with SBF-IF progressed inevitably toward lifelong home parenteral support (HPS) dependence and, in a small and highly selected subset with impending HPS failure, ultimately to iTx. Recent advances in pro-adaptive pharmacological strategies, focusing on glucagon-like peptide (GLP)-2 and GLP-1-based approaches as adjuncts to conventional antimotility and antisecretory therapies, are reviewed, with implications for decision-making across the SBS-IF disease trajectory presented. RECENT FINDINGS: SBS-IF is now recognized as a dynamic and modifiable form of organ failure. Targeted pro-adaptive interventions reduce HPS dependence and improve patient-centered outcomes. Conventional antimotility and antisecretory therapies remain foundational, whereas GLP-2 analogues are the first pathophysiology-targeted, pro-adaptive therapies in SBS-IF, while GLP-1 receptor agonists have emerged as promising adjuncts in selected patients, particularly those with high-output phenotypes. SUMMARY: Multidisciplinary intestinal failure rehabilitation and gut-directed pharmacotherapy have altered the natural history of SBS-IF. Medical rehabilitation has shifted iTx from a default end-stage therapy to a targeted rescue option reserved for irreversible HPS failure, to be considered after optimized rehabilitation but before the transplant window is lost.
Authors
- Palle Bekker Jeppesen (ORCID: https://orcid.org/0000-0001-9680-6938)
Institutions
- University of Copenhagen (DK)
- Center for Digestive and Liver Diseases (US)
Publication Details
- Journal
- Current Opinion in Organ Transplantation
- Published
- 2026-06-16
- DOI
- https://doi.org/10.1097/mot.0000000000001296
- Primary Topic
- Clinical Nutrition and Gastroenterology
- Type
- article
- Field-Weighted Citation Impact
- 0.00