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Journal Scan

July 2015

D-lactic acidosis – a very rare form of metabolic acidosis explained

Summarized from Kowgli N, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. Gastroenterology Research and Practice 2015. Available on line at:

Health demands that the pH of blood is maintained within a narrow range (7.35-7.45). Monitoring this physiological imperative and detection of so-called acid-base disturbance, in which blood pH is either increased or decreased, is one of the principal clinical utilities of blood gas analysis. 

Metabolic acidosis – one of the four classes of acid-base disturbance identified by blood gas analysis – is most commonly the result of abnormal accumulation of lactic acid, either due to increased metabolic production, reduced elimination or a combination of the two. This most common form of metabolic acidosis should, strictly speaking, be called L-lactic acidosis rather than simply lactic acidosis, as is usually the case. 

The nomenclature, L-lactic acidosis recognizes that in nature lactic acid can exist in two stereoisomeric forms: L-lactic acid and D-lactic acid. In humans (and indeed all mammals) lactic acid exists almost exclusively as the L-isoform, and it is accumulation of this isoform that accounts for almost all cases of lactic acidosis. 

A recently published article focuses on the very rare instance in which lactic acidosis is caused not by accumulation of L-lactic acid, but rather accumulation of D-lactic acid. The authors provide the detail of D-lactic acidosis under five headings: pathophysiology, clinical features, diagnosis and treatment. 

Central to an understanding of the pathophysiology of D-lactic acidosis is the recognition that many bacterial species normally present in the colon produce D-lactic acid. An overgrowth of these colonic bacterial species, with resulting abnormally high production of D-lactic acid, occurs if abnormally high amounts of undigested dietary carbohydrate reach the colon. 

In health carbohydrates are digested and the products absorbed in the small intestine so that they do not normally reach the colon.  However, after surgical resection or shortening of the small intestine, dietary carbohydrate is presented directly to the colon where it serves as a substrate for fermentation of bacterial species, with resulting high production of D-lactic acid. 

As the authors detail, D-lactic acidosis thus occurs almost exclusively among those with short-bowel syndrome resulting from gastrointestinal surgery. The clinical features of D-lactic acidosis detailed by the authors are neurological in nature. 

They review current understanding about how D-lactic acidosis affects the brain and how this relates to clinical features. Discussion of diagnosis includes consideration of appropriate laboratory tests and how blood gases and electrolyte values can be of help. It is of course important that lactate measurement in these cases depends on measuring specifically D-lactate. Most available lactate assays measure only L-lactate.

In summary, a comprehensive review of D-lactic acidosis that includes in its cited references 33 single-case history reports accumulated over the 35 years since the condition was first recognized in 1979.



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Chris Higgins

has a master's degree in medical biochemistry and he has twenty years experience of work in clinical laboratories.

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