Small Intestine

Creamer examined the structure of the mucosa of the small intestine in five patients with malignancy that arose outside the GI tract [36]. He concluded that 'weight loss and ill health' were associated

Neuropeptides (CRF)

Neuropeptides (CRF)

Neurotransmitters

GI Hormones (CCK)

Nutrients

Brain

Hypothalamus

Blood

Vagus Nerve

GI tract

Stomach (Gastric Emptying)

Small intestine (Absorption)

Fig. 1. The putative influence of non-gastrointestinal (GI) tumour on the regulation of brain and GI-tract activity, as these relate to gastric emptying and small bowel absorption. NTS, nucleus of the solitary tract with an abnormal small-intestinal mucosa. As shown in Fig. 2, the changes were consistent with atrophy, hypoplasia, and flattening of the mucosa. Dymock et al., in1967, similarly reported atrophy of the jejunal mucosa in six patients who had a non-GI malignancy [13]. The mechanism for the structural changes in the small intestine was not clear and no definitive hypothesis was proposed. However, based on these early clinical observations, it is apparent that the small intestine, especially the jejunal mucosa, was affected by the presence of a non-GI malignancy.

The factors identified to date that cause CACS also induce cellular damage in the small intestine and influence cellular function of the mucosa, leading to malabsorption, loss of nutrient intake, and, consequently, to further cachexia, which affects the prognosis and quality of life. Intestinal function can be examined by evaluating urinary D-xylose excretion, vitamin B12 and folic acid absorption, and stool fat excretion. D-Xylose excretion reflects the absorption of monosaccharides and is an ATP-dependent process [13, 37]. Stool fat excretion reflects fat absorption, and folic acid excretion represents the absorption of water-soluble vitamins. D-Xylose is absorbed in the jejunum, whereas fat is absorbed farther along the jejunum and must first be emulsified by bile to render it absorbable. Vitamin B12 is absorbed over a relatively limited area of the terminal ileum [13,37].

Figure 3 shows the data from 24 non-GI tract cancer patients who were studied by Klipstein and Smarth [38]. Other investigators [13,14,37] reported similar results, although the magnitude and range of the change varied widely in these uncontrolled observational studies, presumably influenced by the stage of each tumour and the duration of the patient's symptoms. Nevertheless, the data provide insight into the effects of non-GI tumours on gut mucosal function. These results can be sum-

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40

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Fig. 3. Absorption studies. Range of normal values is indicated by stippled areas. (From [38])

COB.

Fig. 3. Absorption studies. Range of normal values is indicated by stippled areas. (From [38])

Fig. 2. Photomicrographs of jejunal mucosa showing A normal appearance, B hypoplastic appearance, and C a flat mucosa. (From [36])

marised as follows: D-Xylose absorption was decreased, as was folic acid absorption although to a lesser degree [38]; fat excretion was increased [13] and vitamin B12 absorption ranged from normal to decreased [37, 38]. Based on these data, one concludes that the jejunum is the critical area of the gut most affected by the influence of non-GI neoplasias. Tests to assess limitations of absorption that are done via the oral route or gavage may be adversely influenced by delayed gastric motility. Impaired GE delays the entrance of nutrients into the small intestine, thereby potentially decreasing the relative rate of absorption of different compounds for a given time. The influence of gastric motility can be eliminated if absorption studies are done using closed-loop intestinal techniques.

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