Irritable Bowel Syndrome Message Boards

Heather,
Thanks for your lengthy reply. I will read all the links you have added when my baby has her nap!.
I know I said I wouldn't pester you again, but I did ask about the theories on Gut Fermentation Syndrome, Small Intestine Bacteria Overgrowth and Leaky Gut Syndrome. I ask you this as my gastroenterologist seem to be keen to give me antibiotics (Metranodizole?) for what he thinks maybe an imabalance in my intestinal flora (dysbiosis). What do you think about the theories on this. I'll add a document which addresses this with my mail along with this link:
www.gsdl.com/assessments/bacterial_overgrowth/appguide/index4.html

The Changing Nature of Small Intestine Bacterial Overgrowth
Phillip P Toskes MD
Department of Medicine, Box 100277 JHMHC, University of Florida, Gainesville, FL, 32610, USA.
Current Gastroenterology Reports 1999 1:267-268 (published 1 August 1999)

First paragraph (this article has no abstract)

Small intestine bacterial overgrowth is also known as the blind loop, stagnant loop, or stasis syndrome, the syndrome associated with the excessive numbers of bacteria in the proximal small intestine. The pathophysiology of this condition involves competition between the bacteria and the human host for ingested nutrients. This leads to intraluminal bacterial catabolism of nutrients, often with production of and inury to the enterocyte. A complex array of clinical symptoms ensues, resulting in intestinal malabsorption, weight loss, and malnutrition. These symptoms and signs can be reversed with appropriate antimicrobial therapy.

A number of defense mechanisms in the human prevent excessive bacterial overgrowth in the small intestine. These include gastric acid secretion, normal intestinal motility, an intact ileocecal sphincter, immunoglobulin within intestinal secretions, and bacteriostatic properties of pancreatic and biliary secretions. By far the two most important defense mechanisms are normal intestinal motility and normal gastric acid secretion.

Many clinical conditions are associated with small intestine bacterial overgrowth. Traditionally, these conditions have been associated with small intestine anatomic abnormalities (gastrojejunostomy, duodenal-jejunal diverticulosis, surgical blind loops, obstruction), small intestine motor disturbances (scleroderma, idiopathic intestinal pseudo-obstruction, absent or disordered migrating motor complex, diabetic autonomic neuropathy), or an abnormal communication between the proximal and distal gastrointestinal tract (gastrocolic or jejunocolic fistula, resection of diseased ileocecal valve). These patients developed cobalamin (vitamin B12) deficiency with megaloblastic anemia, fat malabsorption, carbohydrate malabsorption, protein depletion, osteomalacia, vitamin K deficiency, and night blindness.

As a result of improvements in medical therapy, instances of these structural abnormalities in patients occur less frequently as predisposing settings for bacterial overgrowth. In our extensive experience with small intestine bacterial overgrowth, the most common predisposing conditions now appear to be dysmotility of the stomach and small intestine; hypochlorhydria and achlorhydria (either occurring naturally in the patient or as a result of extreme acid suppression with proton pump inhibitors); chronic pancreatitis; and inflammatory bowel disease. The symptoms and signs have also changed. No longer are cobalamin deficiency, steatorrhea, and osteomalacia frequent findings. Now patients are more commonly evaluated because of unexplained diarrhea, weight loss, bloating and flatulence, abdominal pain, and nausea.

In the past, diagnosis was difficult because the only accurate test was a small bowel aspiration, a cumbersome process for the patient and an expensive one if done properly. A number of more simple and indirect tests based on the metabolic actions of the enteric bacteria were proposed to assist in the diagnosis of blind-loop syndrome. Quantification of urinary excretion of indican, phenols, drug metabolites, and conjugated para-aminobenzoic acid did not adequately distinguish patients with bacterial overgrowth from patients with other kinds of malabsorption. Analysis of intestinal aspirates for deconjugated bile acids or volatile fatty acids was difficult and suffered from many of the limitations of intestinal cultures. Free serum bile acids are increased in some patients with blind-loop syndrome, but the positivity of this test depends on the presence of bacteria that deconjugate bile salts, ie, Bacteroides species. Another approach to diagnosing bacterial overgrowth was the timed analysis of breath excretion of volatile metabolites produced by intraluminal bacteria. Measures of both expired labeled CO2 after oral administration of carbon 14C-labeled substrates and breath hydrogen after administration of nonlabeled fermentable substrates were evaluated. Both the cholyglycine breath test and the hydrogen breath test were found to be lacking in sensitivity and specificity.

Our laboratory put forth a 1-gram 14C-labeled xylose breath test that appears to be sensitive and specific. In a number of laboratories, when patients were selected and proven to have overgrowth by intestinal culture and an early time period (ie, 30 minutes after the administration of the substrate) was employed, this test had a very acceptable sensitivity and specificity (80-90%). Clinicians, however, did not utilize these breath tests very often and were not comfortable with performing small bowel aspirations of secretions and culturing of the secretions. Patients were actually given a trial of a broad-spectrum antibiotic like tetracycline for 2 weeks, after which the results were evaluated. Unfortunately, in many cases the overgrowth flora, particularly those of the Bacteroides species, have now become resistant to tetracycline. Our laboratory has been performing the 14C- and now the 13C-xylose breath test for a number of years and offering these tests clinically to physicians for evaluation of their patients. We recently reviewed 100 consecutive patients who had a xylose breath test ordered by a large number of practicing clinicians. The evaluation of that review was very interesting. Only 15% of the patients had a history of gastrointestinal surgery. The most common coexisting conditions were the ones discussed above, ie, motility disturbances, lack of acid secretion, and chronic pancreatitis. These three conditions accounted for nearly 90% of the patients with a positive xylose breath test. In the opinion of these referring clinicians, symptoms of bloating, distention, and flatulence remarkably improved following antimicrobial therapy in those patients with a positive xylose breath test. Clinicians should be aware that patients presenting with a dysmotility syndrome, achlorhydria, or chronic pancreatitis might have concomitant bacterial overgrowth as the source of their main complaints. Some of the symptoms of the overgrowth are also part of the basic disease complex that one would see, for example, in a patient with gastroparesis.

Treatment has also undergone a dramatic change. It used to be the case that when a patient with structural lesions presented with bacterial overgrowth and vitamin B12 deficiency or steatorrhea, 2 weeks on an appropriate antimicrobial program would cause the symptoms to cease and improve the absorption of fat and vitamin B12. Such a patient would stay well, often for many months, after only a 2-week course of therapy.

Now some principles of treatment are emerging, based on our experience, that change the whole approach to these patients. First of all, it is important to realize that both aerobic and anaerobic bacteria are significant in the genesis of these symptoms. Therefore any antimicrobial agent that only suppresses anaerobic bacteria, as had been often done in the past, will not suffice in a number of patients with these new symptoms. One must choose a therapeutic agent that acts against both of these large groups of bacteria. We commonly use amoxicillin/clavulanic acid, 825 mg orally twice a day for 10 days. In patients allergic to penicillin, we have used agents such as cephalosporin and metronidazole. It is not uncommon for a patient to receive 10 to 14 days of one of these effective programs and for the patient to do well with regard to cessation of symptoms but then quickly experience a relapse. For this reason, patients are now frequently given cyclical therapy for 1 week out of every month. If the cyclical program is not successful, then a 30-day treatment with appropriate antimicrobial agents is employed. Most patients respond to the 30-day treatment quite well and can then go back on cyclical therapy. Some patients do not respond to any antimicrobial agent. In these patients it is noteworthy that octreotide (25-50 mg) at bedtime will effectively induce a normalization of motility in the small intestine and clear the patient of bacterial overgrowth.

Nutritional support is an important aspect of a therapeutic program. To reduce diarrhea and steatorrhea, a lactose-free diet and substitution of a large part of dietary fat with medium-chain triglycerides may be necessary. Formulations are now available that contain literally all of their fat as medium-chain triglycerides. Patients with cobalamin malabsorption should receive monthly injections of this vitamin. Deficiencies of other nutrients, such as calcium, should be addressed.

Clinicians should have a low threshold for suspecting bacterial overgrowth as the cause of malabsorption because the entity is rather common

Synonyms and related keywords: acquired monosaccharide intolerance of infancy, blind-loop syndrome, contaminated small bowel syndrome, small intestinal stasis syndrome, stagnant loop syndrome

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