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Culkin, Alison (2010) The nutritional management and immune status in patients with chronic intestinal failure. Doctoral thesis, London Metropolitan University.
Chronic intestinal failure is a rare but life threatening condition which may require long-term parenteral nutrition (LTPN) for survival. Patients with chronic intestinal failure are thought to experience a low grade inflammatory response which may contribute to the infectious and inflammatory complications that some of them develop which include catheter-related bloodstream infections (CRBSI) and parenteral nutrition associated liver disease (PNALD). This thesis describes studies undertaken to address these issues including the effect of patient education, altering the composition of parenteral nutrition and exploring novel immunological markers in these patients.
Patients with chronic intestinal failure need to adhere to a regimen involving specific dietetic and medical interventions in order to prevent malnutrition, dehydration and electrolyte disturbances. An evaluation of education using individualised written material was undertaken in 48 patients.
Improvements in knowledge of the intestinal failure regimen resulted in a reduction in parenteral requirements for energy (p=0.02), nitrogen (p=0.003), lipid (p=0.08), volume (p=0.02) and frequency (p=0.003) together with an improvement in quality of life.
Glutamine is an amino acid which has been shown to reduce infectious complications in other patient populations. A double-blind randomised controlled crossover trial of parenteral glutamine supplementation was completed in 22 LTPN patients. No significant reduction in the incidence of CRBSI was demonstrated. Taurine is an amino acid which is involved in bile acid conjugation and is thought to play a role in the development of PNALD. A double-blind randomised controlled crossover trial of parenteral taurine supplementation was completed in 11 LTPN patients. Taurine did not affect PNALD or infective complications. The lack of efficacy may have resulted from a type II error due to the low numbers of patients included in both these studies.
Patients with chronic intestinal failure have often had a significant portion of their intestine removed and are left with a short bowel (SB) resulting in a reduction in intestinal immune cells and gut-associated lymphoid tissue (GALT) which could leave them susceptible to infection possibly mediated through dendritic cell (DC) function. Sixteen patients with SB and 11 healthy volunteers underwent an investigation of their DC status. Patients had reduced total numbers of DC compared to healthy volunteers (p=0.04) including in the myeloid subset (p=0.005) which is predominately responsible for antigen presentation. DC are also responsible for imprinting homing markers on T lymphocytes in order to direct them back to the site of antigen encounter. The expression of the gut homing marker 137 integrin on DC was significantly reduced in patients with SB (p=0.01). Further work comparing eight SB patients with healthy volunteers demonstrated a selective loss of 137 on naive T lymphocytes (p=0.01). No such loss was identified on memory T lymphocytes.
In conclusion, patient management can be optimised and LTPN reduced through education but supplementation with glutamine and taurine does not reduce LTPN-complications in the doses given. Differences in DC and gut lymphocyte populations may explain susceptibility to infective and/or inflammatory complications.
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