SUMMARY The effects of cytotoxic therapy on the structure and function of the proximal jejunum were studied in six patients receiving intravenous cyclophosphamide (300 mg/M2), methotrexate (40 mg/M2), and 5-fluorouracil (600 mg/M2) as adjuvant therapy for breast cancer. Using a steady state, triple lumen tube perfusion system the absorption of water and electrolytes was measured before and 48 h after administration of the cytotoxic agents. Jejunal biopsies were obtained at each perfusion. Median (range) water absorption fell from 126 (40-142) to 84 (46-142) ml/h/30 cm, with parallel changes for electrolytes; none of the changes was significant. Brush border disaccharidases did not change at 48 h after chemotherapy, while mature enterocytes appeared normal by both light and electron microscopy. Crypt cells and immature enterocytes, however, showed focal vacuolation by light microscopy, corresponding to the occurrence of large residual bodies (secondary lysosomes) containing partially degraded fragments of damaged crypt cells. The confinement of ultrastructural changes to the immature cell population may explain the failure of this study to show a consistent change in the absorptive function of the jejunum 48 h after chemotherapy.Cytotoxic therapy can cause structural and functional changes in the human proximal intestine. '-3 This effect may be important in the development of gastrointestinal symptoms such as diarrhoea and may lead to malabsorption of orally administered drugs, including cytotoxic agents.4 5 Smith et a!6 could find no change in xylose absorption and faecal fat estimation in patients with biopsy proved depression of crypt cell mitosis, but most previous studies of cytotoxic damage have examined changes of gastrointestinal function and structure independently.The technique of small intestinal perfusion is a sensitive method for detecting changes in the transport of water and electrolytes across the jejunal mucosa and might therefore show relatively minor abnormalities of enterocyte function more readily than conventional intestinal absorption tests.7 We have used small intestinal perfusion to investigate IPresent address:

This randomised study aimed to compare the biochemical tolerance of three parenteral regimens administered during the first 48 hours of life. Twenty nine infants were randomised to either: (a) glucose 10%; (b) glucose 100/o/amino acids; (c) glucose 100/olamino acids/lipid.

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1. Zinc metabolism was studied in 11 patients with alcoholic cirrhosis and 13 healthy volunteers using the isotope tracer 65Zn. 2. Intestinal absorption, whole-body content and total daily elimination of zinc were all increased in alcoholic cirrhosis, but the biological half-life of zinc did not differ from controls. 3. Hepatic zinc concentration was reduced in alcoholic cirrhosis and correlated with changes in hepatic alcohol dehydrogenase activity. 4. Patients with alcoholic cirrhosis in this study were not demonstrated to be zinc-deficient.

1. Rats were fed with the elemental diet Vivonex for 1 or 3 months and their jejunal histology was compared with that of an equal number of rats fed on a normal diet. 2. After 1 month of Vivonex feeding a significant reduction in the ratio of crypt height: villus height (CH:VH) was found in the Vivonex-fed rats (n = 4) compared with the control rats (n = 4) (P less than 0.05). 3. After 3 months the CH:VH ratio was also reduced in the Vivonex-fed rats (n = 18) compared with control rats (n = 18) (P less than 0.002). Villus height was significantly increased (P less than 0.002) and crypt height decreased (P less than 0.05). 4. Jejunal protein content, alkaline phosphatase and disaccharidase activity were also determined in 12 control and 12 Vivonex-fed rats from the 3 months study. 5. Alkaline phosphatase activity was increased from a control value of 201 +/- 8 to 243 +/- 15 munits/cm in the Vivonex-fed rats (n = 12) (P less than 0.05) but no significant changes in lactase, sucrase or maltase activites were found. The observed decrease in the CH:VH ratio suggested an improved survival of the mature enterocyte population during elemental diet feeding.