Search

Background: Diets rich in lipid are used to provide energy density in treating children with severe malnutrition, but the extent to which their digestion and absorption can cope with the load effectively is uncertain., Aim: To determine the extent of impaired digestion or absorption, in three groups of eight malnourished children (aged 5-23 months) using isotopic probes of the predominant fatty acids in coconut and corn oil used to fortify the diet., Methods: Each child received oral doses of one of three (13)C labelled triglycerides (trilaurin, triolein, or trilinolein). The recovery of (13)C label in stool either as triglyceride (TAG) or fatty acid (FA), was used to assess digestion and absorption. In a separate test, the recovery of label in stool following an oral dose of [(13)C]-glycocholate was measured to assess bile salt malabsorption., Results: The median recovery of label in stool was 9% (range 1-29%) of administered dose. Following treatment there was a reduction in stool (13)C excretion for the labelled TAG (<1%). In half the subjects, label was recovered as TAG in stool (median 0.6%, range 0-44%). Most label in stool was recovered as FA (median 30%, range 0-100%). Following [(13)C]-glycocholate, label was recovered in excess in about one third of studies., Conclusion: Abnormalities in the gastrointestinal handling of lipid were observed in over 50% of children with severe malnutrition, reflecting problems in absorption, although impaired solubilisation or hydrolysis could also be contributory factors. The underlying lesion improves as treatment progresses, leading to concomitant improvement in function.

Aim: To examine the gastrointestinal handling and metabolic disposal of emulsified [1-13C]palmitic acid esterified into a triglyceride in nine healthy children and seven patients with cystic fibrosis on enzyme replacement treatment., Methods: After an overnight fast, each child was given 10 mg/kg body weight [1,1,1-13C]tripalmitin with a standardised test meal of low natural 13C abundance. The total enrichment of 13C was measured using isotope ratio mass spectrometry in stool collected for a period of up to five days and in breath samples collected over a 24 hour period., Results: The mean proportion of administered 13C label excreted in stool was 6% (range, 1-12.7%) in healthy children and 24.6% (range, 0-64%) in patients with cystic fibrosis. Healthy children excreted 31.3% of the administered label on their breath (range, 14.2-42.9%). Correcting the excretion of administered 13C label on the breath for differences in digestion and absorption in patients with cystic fibrosis increased the difference between individuals from 0-31.3% of administered dose (mean, 17.9%) to 0-49.1% of absorbed dose (mean, 23.2%) and was poorly related to the amount of 13C label in stool., Conclusion: Measurements of breath 13CO2 do not consistently reflect the gastrointestinal handling of emulsified 13C labelled tripalmitin because of differences in digestion and absorption in cystic fibrosis. Further studies need to examine whether "breath tests" alone can predict with confidence the gastrointestinal handling of other 13C labelled triglycerides and fatty acids.

Aim: To examine the gastrointestinal handling of [1-13C]palmitic acid given as the free acid by measuring the excretion of 13C label in stool in 16 healthy children and 11 patients with cystic fibrosis on their habitual enzyme replacement treatment., Methods: After an overnight fast, each child ingested 10 mg/kg body weight [1-13C]palmitic acid with a standardised test meal of low natural 13C abundance. A stool sample was collected before the test and all stools were collected thereafter for a period of up to five days. The total enrichment of 13C in stool and the species bearing the 13C label was measured using isotope ratio mass spectrometry., Results: The proportion of administered 13C label excreted in stool was 24.0% (range 10.7-64.9%) in healthy children and only 4.4% (range 1.2-11.6%) in cystic fibrosis patients. The enrichment of 13C in stool was primarily restricted to the species consumed by the subjects (that is as palmitic acid)., Conclusions: There does not appear to be a specific defect in the absorption of [1-13C]palmitic acid in patients with cystic fibrosis. The reasons why cystic fibrosis patients appear to absorb more of this saturated fatty acid than healthy children is not clear and requires further investigation.

Interleukin-8 (IL-8) and tumour necrosis factor-alpha (TNF-alpha) concentrations were measured in faecal samples from nine patients with cystic fibrosis and nine healthy age matched controls. The patients were assessed with Shwachman score, apparent energy absorption, pancreatic enzyme dosage, simple spirometry, and presence of pseudomonal colonisation. Median (range) wet stool IL-8 and TNF-alpha concentrations in patients were 32,113 pg/g (21,656-178,128) and 3187 pg/g (368-17,611) respectively, compared with < 43.5 pg (IL-8)/g (< 22-4079) and 99 pg (TNF-alpha)/g (< 0.26-231) in controls. IL-8 concentration was negatively correlated with Shwachman score (r = -0.79) and pancreatic enzyme dosage (r = -0.77), but not with energy absorption. Seven patients were mature enough to cooperate with spirometry. Their IL-8 concentrations correlated with percentage predicted forced expiratory volume in one second (r = -0.78). IL-8 concentration was greater in four patients with, than five without, established pseudomonal colonisation: median difference 134,583 pg/g. TNF-alpha concentration was not correlated with measures of disease severity. Faecal IL-8 concentration might reflect the severity of pulmonary inflammation in cystic fibrosis and could provide an easily obtainable marker of disease activity.

Stool energy losses and the sources of energy within the stool were determined in 20 healthy controls and 20 patients with cystic fibrosis while on their habitual pancreatic enzyme replacement treatment. Stool energy losses were equivalent to 3.5% of gross energy intake in healthy children (range 1.3-5.8%). Despite a comparable gross energy intake, stool energy losses were three times greater in patients with cystic fibrosis than controls averaging 10.6% of gross energy intake (range 4.9-19.7%). Stool lipid could account for only 29% and 41% of the energy within the stool in controls and patients with cystic fibrosis respectively and was poorly related to stool energy. Approximately 30% of the energy within the stool could be attributable to colonic bacteria in both the healthy children and patients with cystic fibrosis. These results suggest that stool energy losses in healthy children are relatively modest but that even when patients with cystic fibrosis are symptomatically well controlled on pancreatic enzyme replacement, raised stool energy losses may continue to contribute towards an energy deficit sufficient to limit growth in cystic fibrosis. As the energy content per gram wet weight remains relatively constant (8 kJ/g), stool energy losses may be estimated from simple measurements of stool wet weight.