D-Lactic Acidosis: Pathologic Consequence of Saprophytism

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Presentation transcript:

D-Lactic Acidosis: Pathologic Consequence of Saprophytism Adrian Vella, M.D., Gianrico Farrugia, M.D. Mayo Clinic Proceedings Volume 73, Issue 5, Pages 451-456 (May 1998) DOI: 10.1016/S0025-6196(11)63729-4 Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 1 Overview of pathogenesis of D-lactic acidosis. High carbohydrate load in colon creates acidic conditions favorable to overgrowth of lactobacilli and other D-lactate forming organisms. When D-lactate is absorbed in excess, such as after a large carbohydrate-rich meal, metabolism is overwhelmed, an outcome that results in episodes of acidosis and encephalopathy. Mayo Clinic Proceedings 1998 73, 451-456DOI: (10.1016/S0025-6196(11)63729-4) Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 2 D-Lactate metabolism. Small amounts of D-lactate can be metabolized to pyruvate through D-2 hydroxyacid dehydrogenase (D-2-HDH). Acetyl CoA = acetyl coenzyme A; ATP = adenosine triphosphate; LDH = lactate dehydrogenase; PDH = pyruvate dehydrogenase; TCA = tricarboxylic acid. Mayo Clinic Proceedings 1998 73, 451-456DOI: (10.1016/S0025-6196(11)63729-4) Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 3 D-Lactate metabolism during D-lactic acidosis. When metabolism of D-lactate through D-2-hydroxyacid dehydrogenase is overwhelmed, D-lactate enters bloodstream. High carbohydrate loads, and possibly low insulin levels, inhibit pyruvate dehydrogenase (PDH) and further increase blood levels of D-lactate. DLLR = DL-lactate racemase. For explanations of other abbreviations, see Figure 2. Mayo Clinic Proceedings 1998 73, 451-456DOI: (10.1016/S0025-6196(11)63729-4) Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions