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Since the first descriptions of the contaminated small bowel syndrome, controversy has raged about both its pathogenesis and the mechanism of the malabsorption which often accompanies it.1-4 One, still popular, theory is that in small bowel bacterial overgrowth the concentration of conjugated bile acids in the gut lumen is reduced, by bacterial deconjugation, to levels less than those required for adequate micelle formation. The result is malabsorption of fat. However, there is as much controversy over the part played by bile acid deconjugation in the fat malabsorption of small bowel bacterial overgrowth as there is about whether malabsorption per se is an inevitable consequence of colonisation of the small bowel by colonic bacteria. Clearly, the presentation of this syndrome varies widely from patient to patient and a full investigation of the relation between events in the intestinal lumen and symptoms would therefore be very useful when considering treatment. However, there are many unresolved practical problems in this field, not least of which are the difficulties of quantitating fat malabsorption and assessing the bacterial flora of the small bowel.
The best test of fat malabsorption is generally considered to be a faecal fat measurement made on a standardised fat intake and stool collection over at least five days. Unfortunately, neither patients nor laboratory staff appreciate this ideal. Numerous alternatives have been proposed, the most successful of which is, perhaps, the14C-triolein breath test. However, although this test’s sensitivity and specificity are high, in practice the relation between fat digestion and fat malabsorption is far from linear.5Consequently, the 14C-triolein test is of doubtful value in situations other than moderate to severe pancreatic insufficiency.
The classic way to diagnose small bowel bacterial overgrowth is to culture aspirates of the luminal contents of the small bowel. Although generally accepted as the gold standard, as many as three aspirates (near, mid and distal small bowel) may be required for diagnostic certainty. This need, together with that for facilities capable of detecting fragile anaerobes, often prohibits such an approach. A frequently used alternative is the bile acid breath test.6The problems of interpreting the results of this test if it is applied with a protocol different from that described originally, are legendary. In the context of small bowel bacterial overgrowth it is insensitive and non-specific.
Fortunately, the bacteria of the large bowel are usually kept in their place, and by at least two mechanisms: gut propulsion and gastric acid secretion. The notion that diminished gastric acid secretion may be associated with intestinal bacterial overgrowth is not new. However, most studies have focused on the stomach and duodenum and apart from work by Shindo and colleagues,7 8 little attention has been given to possible changes in the jejunal flora. Shindo et al found that jejunal aspirates from patients and volunteers receiving cimetidine were overgrown with bacteria. The in vitro ability of these aspirates to deconjugate gycocholic acid mirrored positive in vivo bile acid breath tests, the results of which were significantly reduced towards normal by administration of tetracycline. Last year, in a prospective, randomised trial, Thorens et al found, perhaps not surprisingly, that treatment with omeprazole was more likely to produce gastric and duodenal overgrowth than was that with cimetidine.9 Thorens et al, who assessed bacterial overgrowth by aspiration and culture, did not aspirate the jejunal lumen but they did conclude that neither treatment induced malabsorption . . .as indicated by no changes in serum vitamin B12, beta carotene and albumin!
In this issue (see page 266) Shindo et al report that 12 of 21 patients (the oldest was 71) treated with omeprazole developed jejunal bacterial overgrowth. Most of the bacterial species present in jejunal fluid, aspirated from a site 30 cm past the ligament of Treitz, after just two weeks of omeprazole (20 mg/day), were capable of deconjugating the bile acids present in ox bile. Omeprazole treatment was also associated with significant increases in the exhaled14CO2 during the bile acid breath test, which were eliminated by co-administration of oral tetracycline for one week. The authors emphasise that they did not determine whether the stomach or the jejunum was the site of the breath test deconjugation (they were using a modified breath test which allowed no firm conclusions to be drawn as to the site of deconjugation). Nevertheless, omeprazole treatment was associated with fat malabsorption as judged by the14C-triolein breath test, and tetracycline apparently restored fat absorption to normal.
Although many questions are raised by this study (such as what are the relations among flora composition, flora migration, pH and propulsion, and what is the effect of the ileal brake mechanism on the bile acid breath test profile?), the authors have attempted to delineate, for perhaps the first time, the link between bacterial overgrowth, bile acid deconjugation and fat malabsorption in a group of patients receiving omeprazole. A clinical colleague tells me that although malabsorption is not listed as a side effect of omeprazole treatment, diarrhoea is. This raises the interesting question of what clinical importance to lend to Shindo et al’s observations.
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