Intestinal adaptation after massive intestinal resection
- 1Department of Surgery, Southmead Hospital, North Bristol NHS Hospitals Trust, Westbury on Trym, Bristol, UK
- 2Molecular and Cellular Biology, Division of Veterinary Pathology Infection and Immunity, University of Bristol, Langford, UK
- Correspondence to: MrA R Weale Department of Surgery, Southmead Hospital, North Bristol NHS Hospitals Trust, Westbury on Trym, Bristol BS10 5NB, UK; andyweale.org.uk
- Received 7 May 2004
- Accepted 29 July 2004
Abstract
Patients with short bowel syndrome require long term parenteral nutrition support. However, after massive intestinal resection the intestine undergoes adaptation and nutritional autonomy may be obtained. Given that the complications of parenteral nutrition may be life threatening or result in treatment failure and the need for intestinal transplantation, a more attractive option is to wean patients off nutrition support by optimising the adaptive process. The article examines the evidence that after extensive small bowel resection adaptation occurs in humans and focuses on the factors that influence adaptation and the strategies that have been used to optimise this process. The review is based on an English language Medline search with secondary references obtained from key articles. There is evidence that adaptation occurs in humans. Adaptation is a complex process that results in response to nutrient and non-nutrient stimuli. Successful and reproducible strategies to improve adaptation remain elusive despite an abundance of experimental data. Nevertheless given the low patient survival and quality of life associated with other treatments for irreversible intestinal failure it is imperative that clinical research continues into the optimisation of the adaptation.
- HPN, home parenteral nutrition
- SCFA, short chain fatty acid
- LCFA, long chain fatty acid
- IGF-I, insulin-like growth factor I
- IGF-II, insulin-like growth factor II
- EGF, epidermal growth factor
- TGFα, transforming growth factor α
- HBEGF, heparin binding epidermal epidermal-like growth factor
- GLP2, glucagon-like peptide 2
- HGF, hepatocyte growth factor
Footnotes
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Funding: Mr A R Weale is supported by the Freemason’s Research Fellowship from the Royal College of Surgeons of England.
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Conflicts of interest: none declared.







