Small Intestinal Bacterial Overgrowth
Small Intestinal Bacterial Overgrowth
Patients with SIBO may be clinically asymptomatic or have symptoms that fit the diagnostic criteria of irritable bowel syndrome (IBS). There are few studies, which have focused on identifying the predominant clinical symptoms in patients with SIBO. Those that have, suggest that the most common symptom caused by SIBO is diarrhoea, followed by abdominal pain and then bloating (Table 2).
Although many other symptoms have been described in SIBO, the significance of these symptoms is difficult to ascertain, given that the majority of studies have not used validated symptom questionnaires. Moreover, some studies describe patients with one symptom, where others describe patients with up to 20 abnormal symptoms. Other features of SIBO have also been identified, namely signs of nutrient malabsorption: weight loss, fat-soluble vitamin deficiencies and deficiencies of vitamin B12, iron, serum bile acids and red blood cell folate.
Weight loss resulting from SIBO has been described. Fat, protein and carbohydrate malabsorption may lead to reduced availability of nutrients to the host and subsequent weight loss. Steatorrhoea (fat malabsorption) may result from SIBO and is principally due to bacterial deconjugation of bile acids and subsequent deficiency of intraluminal conjugated bile acids. It has been postulated that in SIBO, the microbiota are responsible for deaminating dietary protein in the lumen of the GI tract. As a consequence, there is a diversion of dietary nitrogen into urea formation, with the result that it becomes unavailable for protein anabolism by the human host.
Carbohydrate malabsorption can result from SIBO due to reduced disaccharidase function and increased intraluminal carbohydrate degradation by bacteria. This macronutrient malabsorption coupled with chronic GI symptoms, which often include bloating, cramps and diarrhoea, may result in reduced dietary intake secondary to disease-related anorexia and subsequent weight loss.
With vitamin D deficiency, osteomalacia or hypocalcaemia can occur and osteoporosis is a recognised complication of SIBO. Bone mineral density in the femoral neck and lumbar spine has been reported to be lower in patients with SIBO than in a reference population.
There have been reports of vitamin E deficiency syndromes (neuropathy, T-cell abnormalities) in SIBO and a single case-report of night blindness caused by vitamin A deficiency secondary to SIBO. Levels of vitamin K, however, are usually normal or raised in the context of SIBO as a result of bacterial synthesis of menaquinone.
Megaloblastic, macrocytic anaemia can occur in SIBO and is due to vitamin B12 (cobalamin) deficiency. Polyneuropathy due to vitamin B12 deficiency has also been described and is attributed to greatly reduced absorption of both free and intrinsic-factor-bound vitamin B12. Facultative Gram-negative aerobes and anaerobes are shown to be capable of competitively utilising vitamin B12.
Iron deficiency anaemia can occur in SIBO. Although the exact mechanism is not known, it is likely due to injury to the mucosa caused by bacterial toxins, short-chain fatty acids and/or unconjugated bile acids. Such injury may inhibit iron absorption.
The immune system plays a role as evidenced by the high prevalence of SIBO in patients who have immunodeficiency. Duodenal and jejunal immunoglobulin A immunocytes have been shown to be significantly increased in the mucosa of patients with SIBO.
Clinical Features of SIBO
Patients with SIBO may be clinically asymptomatic or have symptoms that fit the diagnostic criteria of irritable bowel syndrome (IBS). There are few studies, which have focused on identifying the predominant clinical symptoms in patients with SIBO. Those that have, suggest that the most common symptom caused by SIBO is diarrhoea, followed by abdominal pain and then bloating (Table 2).
Although many other symptoms have been described in SIBO, the significance of these symptoms is difficult to ascertain, given that the majority of studies have not used validated symptom questionnaires. Moreover, some studies describe patients with one symptom, where others describe patients with up to 20 abnormal symptoms. Other features of SIBO have also been identified, namely signs of nutrient malabsorption: weight loss, fat-soluble vitamin deficiencies and deficiencies of vitamin B12, iron, serum bile acids and red blood cell folate.
Weight Loss
Weight loss resulting from SIBO has been described. Fat, protein and carbohydrate malabsorption may lead to reduced availability of nutrients to the host and subsequent weight loss. Steatorrhoea (fat malabsorption) may result from SIBO and is principally due to bacterial deconjugation of bile acids and subsequent deficiency of intraluminal conjugated bile acids. It has been postulated that in SIBO, the microbiota are responsible for deaminating dietary protein in the lumen of the GI tract. As a consequence, there is a diversion of dietary nitrogen into urea formation, with the result that it becomes unavailable for protein anabolism by the human host.
Carbohydrate malabsorption can result from SIBO due to reduced disaccharidase function and increased intraluminal carbohydrate degradation by bacteria. This macronutrient malabsorption coupled with chronic GI symptoms, which often include bloating, cramps and diarrhoea, may result in reduced dietary intake secondary to disease-related anorexia and subsequent weight loss.
Fat-soluble Vitamin Deficiencies
With vitamin D deficiency, osteomalacia or hypocalcaemia can occur and osteoporosis is a recognised complication of SIBO. Bone mineral density in the femoral neck and lumbar spine has been reported to be lower in patients with SIBO than in a reference population.
There have been reports of vitamin E deficiency syndromes (neuropathy, T-cell abnormalities) in SIBO and a single case-report of night blindness caused by vitamin A deficiency secondary to SIBO. Levels of vitamin K, however, are usually normal or raised in the context of SIBO as a result of bacterial synthesis of menaquinone.
Vitamin B12 and Iron Deficiency
Megaloblastic, macrocytic anaemia can occur in SIBO and is due to vitamin B12 (cobalamin) deficiency. Polyneuropathy due to vitamin B12 deficiency has also been described and is attributed to greatly reduced absorption of both free and intrinsic-factor-bound vitamin B12. Facultative Gram-negative aerobes and anaerobes are shown to be capable of competitively utilising vitamin B12.
Iron deficiency anaemia can occur in SIBO. Although the exact mechanism is not known, it is likely due to injury to the mucosa caused by bacterial toxins, short-chain fatty acids and/or unconjugated bile acids. Such injury may inhibit iron absorption.
Altered Immunological Parameters
The immune system plays a role as evidenced by the high prevalence of SIBO in patients who have immunodeficiency. Duodenal and jejunal immunoglobulin A immunocytes have been shown to be significantly increased in the mucosa of patients with SIBO.
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