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As an adjunct to urine D-lactate (preferred), in the diagnosis of
D-lactate acidosis
D-lactate is produced from carbohydrates 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 clinical presentation of D-lactic acidosis.
Measured concentrations are diagnostic, but It is important to realize that
lactic acid determinations in blood will not reveal abnormalities because
routine lactic acid assays measure only L-lactate. Accordingly, D-lactate
analysis must be specifically requested.
0.0-0.25 mmol/L
Increased levels are consistent with D-lactic acidosis. However, because
D-lactate is readily excreted, urine determinations are preferred.
Urine is the preferred specimen to determine D-lactate.
1. Dahlquist NR, Perrault J, Callaway CW, Jones JD: D-Lactic
acidosis and encephalopathy after jejunoileostomy: response
to overfeeding and to fasting in humans. Mayo Clin Proc 1984;
59:141-145
2. Uribarri J, Oh MS, Carroll HJ: D-lactic acidosis. A review of
clinical presentation, biochemical features, and
pathophysiologic mechanisms. Medicine 1998;77:73-82
3. Hingorani AD, Chan NN: D-lactate encephalopathy. Lancet
2001;Nov 24;358(9295):1814