Clinlab Navigator

D Lactic acidosis

A unique form of lactic acidosis can occur in patients with jejunoileal bypass or, less commonly, small bowel resection or other causes of the short bowel syndrome. Two major factors contribute to the overproduction of D-lactic acid in these situations: overgrowth of gram-positive anaerobes, such as Lactobacilli, and increased delivery of glucose and starch to the colon after the small bowel is bypassed, removed or diseased. Antimicrobial therapy can occasionally precipitate D-lactic acidosis in susceptible individuals by promoting overgrowth of Lactobacilli.

D-lactic acid is absorbed into the systemic circulation and the ensuing acidemia tends to persist because D-lactate is not metabolized by lactate dehydrogenase, the enzyme that normally catalyzes the conversion of physiologically occurring L-lactate into pyruvate.

Patients with short bowel syndrome frequently demonstrate chronically elevated serum concentrations of D-lactate that are not sufficient to induce symptoms. In some patients, however, carbohydrate loading leads to severe and symptomatic D-lactic acidosis. Affected 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. It is not known if these symptoms are actually due to D-lactate itself or to some other toxin produced in the colon and absorbed in parallel with D-lactate.

The diagnosis of D-lactic acidosis should be strongly considered in the patient presenting with an increased serum anion gap, normal serum concentration of L-lactate, negative plasma ketoacid level, negative urine ketones and the characteristic history, signs and symptoms.

The plasma anion gap may not be increased in proportion to the decrease in serum bicarbonate because D-lactate is not well reabsorbed by the renal tubules and is more readily excreted in the urine, thereby lowering the anion gap.

Confirmation of the diagnosis requires measurement of D-lactate that uses a special enzymatic assay employing D-lactate dehydrogenase. The standard assay for lactate uses L-lactate dehydrogenase and does not detect D-lactate. A random urine sample is the preferred specimen because D-lactate is readily excreted in urine. Reference range is 0.0-0.25 mmol/L. Increased levels are diagnostic of D-lactic acidosis.

AddThis Social Bookmark Button