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D-lactate is produced from carbohydrates that are not absorbed in the small intestine by bacteria residing in the colon. When large amounts are absorbed it can cause metabolic acidosis, altered mental status (from drowsiness to coma) and a variety of other neurologic symptoms, in particular dysarthria and ataxia. Although a temporal relationship has been described between elevations of plasma and urine D-lactate and the accompanying encephalopathy, the mechanism of neurologic manifestations has not been elucidated.
D-lactic acidosis is typically observed in patients with short-bowel syndrome and following jejunoileal bypass resulting in carbohydrate malabsorption. In addition, healthy children presenting with gastroenteritis may also develop the critical presentation of D-lactic acidosis.
Routine lactic acid determinations in blood will not reveal abnormalities because most lactic acid assays measure only L-lactate. Accordingly, D-lactate analysis must be specifically requested (eg, DLAC / D-Lactate, Plasma). However, as D-lactate is readily excreted in urine, this is the preferred specimen for D-lactate determinations.
Diagnosing D-lactate acidosis, especially in patients with jejunoileal bypass and short-bowel syndrome
Increased levels are diagnostic.
The test performed was D-Lactate. This is a product of bacterial overgrowth in the gastrointestinal tract. It should not be confused with L-lactate which accumulates in some metabolic acidosis.
1. Brandt RB, Siegel SA, Waters MG, Bloch MH: Spectrophotometric assay for D-(-)-lactate in plasma. Anal Biochem 1980;102(1):39-46
2. Petersen C: D-lactic acidosis. Nutr Clin Pract 2005 Dec;20(6):634-645