Small Intestinal Bacterial Overgrowth - SIBO

Small intestinal bacterial overgrowth (SIBO), defined as excessive bacteria in the small intestine, remains a poorly understood disease. It is now apparent that this disorder is more prevalent than previously thought. 

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Symptoms of SIBO are nonspecific and include bloating, abdominal distension, abdominal pain or discomfort, diarrhea, fatigue, and weakness, malabsorption, nutritional deficiencies, and metabolic bone disorders. The frequency and severity of symptoms likely reflect both the degree of bacterial overgrowth along with the extent of mucosal inflammation. However, symptoms may also reflect the underlying cause of SIBO, a small bowel dysmotility.

A number of diagnostic tests are currently available, although the optimal treatment regimen remains elusive. Recently there has been renewed interest in SIBO and its putative association with irritable bowel syndrome.

The absolute number of organisms, the type of microbial flora present plays an important role in the manifestation of signs and symptoms of overgrowth.For example, a predominance of bacteria that metabolize bile salts to unconjugated or insoluble compounds may lead to fat malabsorption or bile acid diarrhea. In contrast, microorganisms that preferentially metabolize carbohydrates to short-chain fatty acids and gas may produce bloating without diarrhea because the metabolic products can be absorbed. Gram-negative coliforms, such as Klebsiella species, may produce toxins that damage the mucosa, interfering with absorptive function and causing secretion, thereby mimicking tropical sprue.

SIBO in young and middle-aged adults appear to be low, whereas prevalence rates appear to be consistently higher in the older patients.

SIBO develops when the normal homeostatic mechanisms that control enteric bacterial populations are disrupted. The two processes that most commonly predispose to bacterial overgrowth are diminished gastric acid secretion and small intestine dysmotility. Disturbances in gut immune function and anatomical abnormalities of the GI tract also increase the likelihood of developing SIBO. Once present, bacterial overgrowth may induce an inflammatory response in the intestinal mucosa.

Gastric acid suppresses the growth of ingested bacteria, thereby limiting bacterial counts in the upper small intestine. Diminished acid production (hypochlorhydria) is a risk factor for SIBO, and can develop after colonization with Helicobacter pylori or as a consequence of aging.
Inhibition of acid secretion via histamine type 2 receptor blockers (H2RAs) or proton-pump inhibitors (PPIs) may predispose to SIBO.

Normal GI motility involves a complex, tightly coordinated series of events designed to move material through the GI tract. During periods of fasting, a migrating motor complex (MMC) develops approximately every 90-120 minutes to sweep residual debris through the GI tract. Several studies have demonstrated that abnormalities in the MMC may predispose to the development of SIBO.

Small bowel motility disorders also predispose to the development of SIBO, because bacteria may not be effectively swept from the proximal bowel into the colon. Disruption of the MMC is associated with bacterial overgrowth.

Other conditions that affect small bowel motility, which predispose patients to develop SIBO,

Structural abnormalities in the GI tract provide an ideal environment for bacterial colonization and overgrowth. GI tract surgeries that create a blind loop

Small bowel diverticula. Large duodenal and jejunal diverticula can harbor bacteria and lead to symptoms of SIBO. Strictures of the small intestine, which can develop after surgery, after radiation, in association with Crohn's disease, or secondary to medication use, also predispose to the development of SIBO.
Finally, resection of the ileocecal valve increases the risk of developing SIBO, because retrograde movement of bacteria from the colon into the small intestine can now readily occur.

Patients who are immunodeficient, whether due to an abnormal antibody response or T-cell response, are prone to bacterial overgrowth.

SIBO can develop in a variety of patient populations.

Irritable Bowel Syndrome
There is a significant amount of interest on the possible role of SIBO in the generation of IBS. Many IBS symptoms are nonspecific (bloating, distention, cramping, abdominal discomfort) and can mimic symptoms of SIBO. Long-standing and poorly controlled diabetes can injure the enteric nervous system leading to disordered GI motility.

SIBO develops in the elderly because of age-associated decline in GI tract motility.
Long-standing celiac disease can disturb gut motility, leading to small intestine dysmotility.
GI symptoms are common in patients with renal failure and include nausea, early satiety, bloating, and abdominal pain.

Surgically induced obstructive jaundice can lead to bacterial overgrowth and increased bacterial translocation from the GI tract.Clinical studies have shown that patients with advanced liver disease are more likely to have abnormalities in gut motility.

Acute necrotizing pancreatitis disturbs the jejunal MMC leading to SIBO.
Chronic alcohol use may predispose patients to SIBO.
Antibiotics can alter the normal balance of gut flora leading to changes in the population of bacteria within the GI tract.

Fat malabsorption occurs as a result of bacterial deconjugation of bile salts. In addition, free bile acids are toxic to the intestinal mucosa, resulting in mucosal inflammation and malabsorption.Deconjugated bile salts are reabsorbed in the jejunum rather than the ileum, leading to impaired micelle formation, fat malabsorption, and deficiencies in fat-soluble vitamins (A, D, E, and K). Fortunately, symptoms rarely develop; however, in severe cases night blindness (vitamin A), osteomalacia and tetany due to hypocalcemia (vitamin D), prolonged prothrombin times (vitamin K), or neuropathy, retinopathy, and impairments in T-cell function can occur.

Carbohydrate malabsorption develops as a result of premature breakdown of sugars by bacteria in conjunction with decreased disaccharidase activity secondary to disruption of the intestinal brush border. Protein malabsorption can occur because of digestion by bacteria, whereas protein-losing enteropathies can develop as a result of mucosal damage.

A common complication of bacterial overgrowth is cobalamin (vitamin B12) deficiency. Patients with normal intestinal enteric flora rely on gastric intrinsic factor to bind to vitamin B12 to permit absorption in the ileum.

The diagnosis of SIBO is controversial. Two tests are commonly employed: bacterial culture and breath tests.

All breath tests rely on the recovery and quantification of an exhaled gas produced by the bacterial metabolism of the ingested substrate. The development of inexpensive, commercially available gas chromatographs to measure exhaled hydrogen and/or methane has led to the widespread use of breath testing for the diagnosis of bacterial overgrowth.

Strict adherence to diet may lead to symptom improvement in patients with celiac disease and bacterial overgrowth.

Nutritional support, particularly in those patients with weight loss or vitamin and mineral deficiencies, is an important component of SIBO treatment. Supplementation and maintenance of vitamin B12 and fat-soluble vitamins, with correction of calcium and magnesium deficiencies, are key components of treatment. Lactase and fructase deficiency may develop due to inflammation of the small bowel brush border.

Attempts at treating SIBO with probiotics have shown mixed results.

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