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DOI: 10.1055/s-0042-117647
D-lactic acidosis – case report and review of the literature
D-Laktat-Azidose – Fallbericht und LiteraturübersichtPublikationsverlauf
17. Mai 2016
13. September 2016
Publikationsdatum:
10. Oktober 2016 (online)
![](https://www.thieme-connect.de/media/zfg/201701/lookinside/thumbnails/zfg-0039_10-1055-s-0042-117647-1.jpg)
Abstract
D-lactic acidosis is a rare complication that occurs mainly in patients with malabsorption due to a surgically altered gastrointestinal tract anatomy, namely in short bowel syndrome or after bariatric surgery. It is characterized by rapid development of neurological symptoms and severe metabolic acidosis, often with a high serum anion gap. Malabsorbed carbohydrates can be fermented by colonic microbiota capable of producing D-lactic acid. Routine clinical assessment of serum lactate covers only L-lactic acid; when clinical suspicion for D-lactic acidosis is high, special assays for D-lactic acid are called for. A serum level of more than 3 mmol/L of D-lactate confirms the diagnosis. Management includes correction of metabolic acidosis by intravenous bicarbonate, restriction of carbohydrates or fasting, and antibiotics to eliminate intestinal bacteria that produce D-lactic acid. We report a case of D-lactic acidosis in a patient with short bowel syndrome and review the pathophysiology of D-lactic acidosis with its biochemical and clinical features. D-lactic acidosis should be considered when patients with short bowel syndrome or other malabsorption syndromes due to an altered gastrointestinal tract anatomy present with metabolic acidosis and neurological symptoms that cannot be attributed to other causes. With the growing popularity of bariatric surgery, this metabolic derangement may be seen more frequently in the future.
Zusammenfassung
Die D-Laktat-Azidose ist eine seltene gefährliche Komplikation bei Patienten mit Malabsorption bedingt durch einen chirurgisch veränderten Gastrointestinaltrakt, speziell bei Kurzdarmsyndrom oder nach bariatrischer Bypass-Operation. Sie ist charakterisiert durch typische, sich schnell entwickelnde neurologische Symptome und eine schwere metabolische Azidose, welche häufig durch eine hohe Anionenlücke gekennzeichnet ist. D-Laktat entsteht bei der Fermentation malabsorbierter Kohlenhydrate durch spezifische Darmbakterien. Im klinischen Routinelabor wird ausschließlich L-Laktat bestimmt; bei begründetem Verdacht muss die Analyse von D-Laktat entsprechend angefordert werden. Ein Serumspiegel an D-Laktat von größer 3 mmol/l bestätigt die Diagnose. Das klinische Management der D-Laktat-Azidose umfasst die Korrektur der metabolischen Azidose durch intravenöse Verabreichung von Bicarbonat, die Restriktion von Kohlenhydraten oder Nahrungskarenz, und die Verabreichung von Antibiotika zur Eliminierung intestinaler D-Laktat-produzierender Bakterien. Der dargestellte Fall beschreibt die klinische Präsentation, Diagnose und Therapie der D-Laktat-Azidose bei einer Patientin mit Kurzdarmsyndrom; die anschließende Literaturübersicht geht auf die Pathophysiologie der D-Laktat-Azidose sowie deren biochemische und allgemeine klinische Charakteristika ein. Präsentieren sich Patienten mit Kurzdarmsyndrom oder Malabsorption bedingt durch bariatrische Bypass-Operation mit metabolischer Azidose und neurologischen Symptomen, die nicht anderen Ursachen zugeschrieben werden können, sollte an eine D-Laktat-Azidose gedacht werden. Durch die steigende Zahl von bariatrischen Operationen könnte diese metabolische Entgleisung künftig häufiger angetroffen werden.
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