d-lactate encephalopathy

Joseph R. Thurn, Gordon L. Pierpont, Carl W. Ludvigsen, John H. Eckfeldt

Research output: Contribution to journalArticlepeer-review

77 Scopus citations

Abstract

Although d-lactate is not a product of human intermediary metabolism, absorption of d-lactate produced by abnormal intestinal bacteria can cause systemic acidosis in patients who have undergone gastrointestinal surgery, particularly jejunoileal bypass. In order to learn more about the prevalence of d-lactate encephalopathy, its occurrence in other disorders, and how well D-lactate concentration correlates with clinical symptoms, serum D-lactate levels were determined in several specific populations. d-lactate was undetectable (less than 0.5 mmol/liter) in 72 healthy volunteers and 57 obese persons. In 33 patients who had jejunoileal bypass, 16 reported symptoms consistent with d-lactate encephalopathy since surgery. Nine of these 16 had d-lactate levels greater than 0.5 mmol/liter (range 0.7 to 11.5 mmol/liter). Levels of, d-lactate fluctuated over time, and in two patients, markedly elevated levels correlated with an encephalopathy accompanied by hyperchloremic metabolic acidosis and elevated anion gap. In 470 randomly chosen hospitalized patients, d-lactate level greater than 0.5 mmol/ liter was found in 13 (2.8 percent), and 60 percent of these had a history of gastrointestinal surgery or disease. It is concluded that elevated serum D-lactate levels are relatively common in patients with jejunoileal bypass, and although more rare, occur in other gastrointestinal disorders as well. The symptoms of D-lactate encephalopathy are quite sensitive, but not necessarily specific for this disorder.

Original languageEnglish (US)
Pages (from-to)717-721
Number of pages5
JournalThe American Journal of Medicine
Volume79
Issue number6
DOIs
StatePublished - Dec 1985

Bibliographical note

Funding Information:
From the Departments of Medicine, and Laboratory Medicine and Pathology, Minneapolis Veterans Administration Medical Center and University of Minnesota Hospitals, Minneapolis, Minnesota. This work was supported in part by a grant from the Minnesota Medical Foundation and by the Veterans Administration. Requests for reprints should be addressed to Dr. Cordon L. Pier-pont, Department of Cardiology 616/l 1 lC, Veterans Administration Medical Center, 54th Street and 48th Avenue South, Minneapolis, Minnesota 55417. Manuscript accepted February 5, 1985.

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