Consult the medical resource doctors trust

UpToDate is one of the most respected medical information resources in the world, used by over 360,000 doctors and thousands of patients to find answers to medical questions.

  • Content written by a faculty of over 4,000 physicians from leading medical institutions
  • Unbiased: free of advertising or pharmaceutical funding
  • Evidence-based treatment recommendations
  • Continuously updated to incorporate new medical findings

Related articles included with a subscription

D-Lactic acidosis

As a subscriber you will have access to the full contents of this article

INTRODUCTION

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]:

  • There is overgrowth of gram-positive anaerobes, such as Lactobacilli, which are most able to produce D-lactate.
  • There is usually relatively little glucose and starch delivered to the colon because of extensive small intestinal absorption. However, delivery of these substrates is markedly enhanced when the small bowel is bypassed, removed, or diseased.

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.

CLINICAL MANIFESTATIONS

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.

To continue reading this article you need to subscribe.

Read the rest of this article and others like it

The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use (click here) ©2010 UpToDate, Inc.
white circle LOG IN
white circle DEMO