Volume 30, Issue 3 pp. 288-293
Original Article

Lactobacilli and Acidosis in Children With Short Small Bowel

Ger Bongaerts

Corresponding Author

Ger Bongaerts

Department of Medical Microbiology, Nijmegen, The Netherlands

Address correspondence and reprint requests to Dr. Ger Bongaerts, Department of Medical Microbiology, University Hospital of Nijmegen, St. Radboud, Box 9101, NL-6500 HB Nijmegen, The Netherlands.Search for more papers by this author
Jan Bakkeren

Jan Bakkeren

Department of Laboratory of Pediatrics and Neurology, University Hospital Nijmegen Sint Radboud, Nijmegen, The Netherlands

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René Severijnen

René Severijnen

Department of Pediatric Surgery, Nijmegen, The Netherlands

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Wolfgang Sperl

Wolfgang Sperl

Kinderspital, Landeskrankenanstalten Salzburg, Salzburg, Austria

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Hans Willems

Hans Willems

Department of Clinical Chemistry, Nijmegen, The Netherlands

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Ton Naber

Ton Naber

Departments of Gastroenterology and Hepatology, Nijmegen, The Netherlands

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Ron Wevers

Ron Wevers

Department of Laboratory of Pediatrics and Neurology, University Hospital Nijmegen Sint Radboud, Nijmegen, The Netherlands

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Alfred van Meurs

Alfred van Meurs

Juliana Children's Hospital, The Hague, The Netherlands

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Jules Tolboom

Jules Tolboom

Department of Pediatrics, Nijmegen, The Netherlands

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First published: 01 March 2000
Citations: 9

Presented in part at the 7th Southeast European Symposium of Pediatric Surgery on Short Bowel Syndrome, May 22–23, 1998, in Graz, Austria.

ABSTRACT

Background:

In patients with a short small bowel, D-lactic acidemia and D-lactic aciduria are caused by intestinal lactobacilli. The purpose of this study was to obtain a detailed picture of the metabolic acidosis in young children with short small bowel.

Methods:

Feces, blood, and urine of children with short small bowel and acidosis were studied microbiologically and/or biochemically.

Results:

Previous findings were confirmed that more than 60% of the fecal flora of patients with small short bowel, who are not receiving antibiotics, consists of lactic acid-producing lactobacilli. In blood, D-lactic acid was the most prominent metabolite: the highest serum D-lactate (15.5 mmol/l) was observed in a sample taken immediately after the onset of hyperventilation. The highest D-lactate excretion was in urine collected some hours after the onset of hyperventilation, and amounted to 59 mol/mol creatinine. Acidosis in the patients with short small bowel was related to strongly increased serum D-lactate and anion gap and to strongly decreased serum bicarbonate and pH.

Conclusion:

In children with small short bowel and acidosis, the common intestinal flora of mainly lactobacilli abundantly produces D-lactic acid from easily fermentable carbohydrates. Thus, these bacteria directly cause shifts of bicarbonate, pH, and base excess and indirectly cause shifts of the anion gap, as well as hyperventilation. These kinetic parameters are strongly associated.

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