Enterotoxigenic Intestinal Bacteria in Tropical Sprue

Klipstein, Frederick A.; Schenk, Eric A.

doi:10.1016/s0016-5085(75)80272-1

Cited by 56 publications

(40 citation statements)

References 37 publications

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“…Ethanol levels were found to be lower in the intestine than in the stomach. Ethanol has been demonstrated in concentrations from 11-144 mg/100 ml in jejunal aspirates from humans suffering from tropical sprue, when high levels of micro-organisms were also detected (Klipstein et al 1973). Levels of blood ethanol from 0.15-4.12 mg/100 ml (mean 1.8 mg/100 ml) have been detected in 7/20 patients after jejunoileal bypass for morbid obesity (Mezey et al 1975).…”

Section: A Chemical Methodsmentioning

confidence: 99%

Possible Sources of Ethanol Ante‐ and Post‐mortem: its Relationship to the Biochemistry and Microbiology of Decomposition

Corry

1978

Journal of Applied Bacteriology

170

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Section: A Chemical Methodsmentioning

confidence: 99%

Possible Sources of Ethanol Ante‐ and Post‐mortem: its Relationship to the Biochemistry and Microbiology of Decomposition

Corry

1978

Journal of Applied Bacteriology

170

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“…4 Enhanced production of endogenous ethanol as a result of bacterial overgrowth has been demonstrated in jejunal blind-loop contents of rats. 5 In m an signi® cant endogenous ethanol levels have been found in jejunal aspirates of patients with tropical sprue, 6 and in venous blood of patients after jejunoileal bypass for morbid obesity. 7 In gastric juice ethanol levels up to 27 mM have been measured in patients using cim etidine or antacids.…”

Section: Icrobial Alcoho L Dehydrogenases and Alcoho Lic Ferm Entationmentioning

confidence: 99%

Microbial metabolism of ethanol and acetaldehyde and clinical consequences

Salaspuro

1997

Addiction Biology

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Many bacteria possess marked alcohol dehydrogenase activity and in the presence of ethanol they produce reactive and toxic acetaldehyde. Acetaldehyde production mediated by microbial alcohol dehydrogenases has been demonstrated in the oropharynx and bronchopulmonary washings. Also the most important gastric pathogen, Helicobacter pylori, and many skin bacteria associating with pathological dermatological conditions, possess alcohol dehydrogenase activity and produce acetaldehyde from ethanol. The most richly colonized site of the human body, however, is the large intestine, and therefore bacterial acetaldehyde production is most important in this organ. Alcohol ingested orally is transported to the colon by blood circulation and, after the distribution phase, intracolonic ethanol levels are equal to those in the blood. In the large bowel ethanol is oxidized by a bacteriocolonic pathway. In this pathway intracolonic ethanol is at first oxidized by bacterial alcohol dehydrogenase to acetaldehyde. Then acetaldehyde is oxidized either by colonic mucosal or bacterial aldehyde dehydrogenase to acetate. Part of intracolonic acetaldehyde may also be absorbed via the portal vein and metabolized in the liver. Bacteriocolonic pathway offers a new explanation for the disappearance of a part of ethanol calories. Due to the low aldehyde dehydrogenase activity of colonic mucosa acetaldehyde accumulates in the colon. Accordingly, during ethanol oxidation highest acetaldehyde levels of the body are found in the colon and not in the liver. High intracolonic acetaldehyde may contribute to the pathogenesis of alcohol-induced diarrhoea. Acetaldehyde has been proven to be a carcinogen in experimental animals. It may therefore contribute to the increased risk of colon polyps and colon cancer found to be associated with heavy alcohol consumption in man. Intracolonic acetaldehyde may also be an important determinant of blood acetaldehyde level and a possible hepatotoxin. In addition to acetaldehyde, gut-derived endotoxin is another potential candidate in the pathogenesis of alcohol-related liver injury.

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“…In contrast to the results from southern India, crypt enterocyte damage has not been reported from other regions. At least in Puerto Rico there appears to be a relationship between the colonization of the small intestine by toxin-producing coliforms and the diarrhoea and malabsorption in tropical sprue [16,18]. These patients also respond dramatically to therapy with broad spectrum antibiotics [19,40].…”

Section: Pathophysiology Of Tropical Spruementioning

confidence: 99%

Tropical sprue

Mathan

1990

Springer Semin Immunopathol

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Enterotoxigenic Intestinal Bacteria in Tropical Sprue

Cited by 56 publications

References 37 publications

Possible Sources of Ethanol Ante‐ and Post‐mortem: its Relationship to the Biochemistry and Microbiology of Decomposition

Possible Sources of Ethanol Ante‐ and Post‐mortem: its Relationship to the Biochemistry and Microbiology of Decomposition

Microbial metabolism of ethanol and acetaldehyde and clinical consequences

Tropical sprue

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