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A unique form of lactic acidosis can occur in patients with jejunoileal bypass or, less commonly, small bowel resection or other cause of the short bowel syndrome. (See "Management of the short bowel syndrome in adults".) In these settings, glucose and starch are metabolized in the colon into D-lactic acid, which is then absorbed into the systemic circulation [1-5]. The ensuing acidemia tends to persist, since D-lactate is not recognized by L-lactate dehydrogenase, the enzyme that catalyzes the conversion of the physiologically occurring L-lactate into pyruvate. Thus, D-lactate is slowly metabolized in humans.
Two factors tend to contribute to the overproduction of D-lactic acid in this disorder [3]:
A potential concern is whether patients undergoing continuous peritoneal dialysis are at risk for D-lactic acidosis, since the dialysate solution contains a racemic mixture of L- and D-lactate. Several small studies suggest that D-lactate does not accumulate in peritoneal dialysis [6,7]; it remains possible, however, that occasional patients might be at risk.
Patients with short bowel syndrome frequently demonstrate chronically elevated serum concentrations of D-lactate that are not sufficient to induce symptoms [8]. In some patients, however, carbohydrate loading leads to severe and symptomatic D-lactic acidosis. These patients typically present with episodic metabolic acidosis (usually occurring after high carbohydrate meals) and characteristic neurologic abnormalities including confusion, cerebellar ataxia, slurred speech, and loss of memory (table 1) [1-3,9]. In a review of 29 reported cases, for example, all patients exhibited some degree of altered mental status [9]. They may complain of or appear to be drunk in the absence of ethanol intake.
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