Z Gastroenterol 2017; 55(01): 75-82
DOI: 10.1055/s-0042-117647
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

D-lactic acidosis – case report and review of the literature

D-Laktat-Azidose – Fallbericht und Literaturübersicht
Elisabeth Fabian
1   Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Austria
,
Ludwig Kramer
2   1st Department of Internal Medicine with Gastroenterology, Hietzing Hospital, Vienna, Austria
,
Franz Siebert
3   Department of Internal Medicine, Barmherzige Brueder Hospital, St. Veit on the Glan, Austria
,
Christoph Högenauer
4   Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Austria
,
Reinhard Bernd Raggam
5   Division of Angiology, Department of Internal Medicine, Medical University of Graz, Austria
,
Heimo Wenzl
4   Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Austria
,
Guenter J. Krejs
4   Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Austria
› Author Affiliations
Further Information

Publication History

17 May 2016

13 September 2016

Publication Date:
10 October 2016 (online)

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.

 
  • References

  • 1 Oh MS. Phelps KR. Traube M. et al. D-lactic acidosis in a man with short-bowel syndrome. New Engl J Med 1979; 301: 249-252
  • 2 Petersen C. D-lactic acidosis. Nutr Clin Pract 2005; 20: 634-645
  • 3 Adeva-Andany M. López-Ojén M. Funcasta-Calderón R. et al. Comprehensive review on lactate metabolism in human health. Mitochondrion 2014; 17: 76-100
  • 4 Philp A. Macdonald AL. Watt PW. Lactate--a signal coordinating cell and systemic function. J Exp Biol 2005; 208: 4561-4575
  • 5 Huckabee WE. Relationships of pyruvate and lactate during anaerobic metabolism. I. Effects of infusion of pyruvate or glucose and of hyperventilation. J Clin Invest 1958; 37: 244-254
  • 6 Vernon C. Letourneau JL. Lactic acidosis: recognition, kinetics, and associated prognosis. Crit Care Clin 2010; 26: 255-283
  • 7 Levy B. Lactate and shock state: the metabolic view. Curr Opin Crit Care 2006; 12: 315-321
  • 8 Bellomo R. Bench-to-bedside review: lactate and the kidney. Crit Care 2002; 6: 322-326
  • 9 Levraut J. Ciebiera JP. Chave S. et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J Respir Crit Care Med 1998; 157: 1021-1026
  • 10 Thornalley PJ. The glyoxalase system: new developments towards functional characterization of metabolic pathway fundamental to biological life. Biochem J 1990; 269: 1-11
  • 11 Talasniemi JP. Pennanen S. Savolainen H. et al. Analytical investigation: assay of D-lactate in diabetic plasma and urine. Clin Biochem 2008; 41: 1099-1103
  • 12 Flick MJ. Konieczny SF. Identification of putative mammalian D-lactate dehydrogenase enzymes. Biochem Biophys Res Commun 2002; 295: 910-916
  • 13 Yasuda T. Ozawa S. Shiba C. et al. D-lactate metabolism in patients with chronic renal failure undergoing CAPD. Nephron 1993; 63: 416-422
  • 14 Ewaschuk JB. Naylor JM. Zello GA. D-lactate in human and ruminant metabolism. J Nutr 2005; 135: 1619-1625
  • 15 Kowlgi NG. Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. Gastroenterol Res Pract 2015; 476215
  • 16 De Vrese M. Koppenhoefer B. Barth CA. D-lactic acid metabolism after an oral load of DL-lactate. Clin Nutr 1990; 9: 23-28
  • 17 Oh MS. Uribarri J. Alveranga D. et al. Metabolic utilization and renal handling of D-lactate in men. Metabolism 1985; 34: 621-625
  • 18 Kang KP. Lee S. Kang SK. D-lactic acidosis in humans: review of update. Electrolyte Blood Press 2006; 4: 53-56
  • 19 Hove H. Mortensen PB. Colonic lactate metabolism and D-lactic acidosis. Dig Dis Sci 1995; 40: 320-330
  • 20 Cherbut C. Aubé AC. Blottière HM. et al. Effects of short-chain fatty acids on gastrointestinal motility. Scand J Gastroenterol Suppl 1997; 222: 58-61
  • 21 Halperin ML. Kamel KS. D-lactic acidosis: turning sugar into acids in the gastrointestinal tract. Kideny Int 1996; 49: 1-8
  • 22 Enerson BE. Drewes LR. Molecular features, regulation, and function of monocarboxylate transporters: implications for drug delivery. J Pharm Sci 2003; 92: 1531-1544
  • 23 Zhang DL. Jiang ZW. Jiang J. et al. D-lactic acidosis secondary to short bowel syndrome. Postgrad Med J 2003; 79: 110-112
  • 24 Uchida H. Yamamoto H. Kisaki Y. et al. D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics. J Pediatr Surg 2004; 39: 634-636
  • 25 Satoh T. Narisawa K. Konno T. et al. D-lactic acidosis in two patients with short bowel syndrome: bacteriological analyses of the fecal flora. Eur J Pediatr 1982; 138: 324-326
  • 26 Caldarini MI. Pons S. D’Agostino D. et al. Abnormal fecal flora in a patient with short bowel syndrome. An in vitro study on effect of pH on D-lactic acid production. Dig Dis Sci 1996; 41: 1649-1652
  • 27 Mayeur C. Gratadoux JJ. Bridonneau C. et al. Faecal D/L lactate ratio is a metabolic signature of microbiota imbalance in patients with short bowel syndrome. PloS One 2013; 8: e54335
  • 28 Takahashi K. Terashima H. Kohno K. et al. A stand-alone synbiotic treatment for the prevention of D-lactic acidosis in short bowel syndrome. Int Surg 2013; 98: 110-113
  • 29 Hove H. Nordgaard-Andersen I. Mortensen PB. Faecal DL-lactate concentration in 100 gastrointestinal patients. Scan J Gastroenterol 1994; 29: 255-259
  • 30 Coronado BE. Opal SM. Yoburn DC. Antibiotic-induced D-lactic acidosis. Ann Intern Med 1995; 122: 839-842
  • 31 Flourie B. Messing B. Bismuth E. et al. D-lactic acidosis and encephalopathy in short-bowel syndrome occurring during antibiotic treatment. Gastroenterol Clin Biol 1990; 14: 596-598
  • 32 Gavazzi C. Stacchiotti S. Cavalletti R. et al. Confusion after antibiotics. Lancet 2001; 357: 1410
  • 33 Jorens PG. Demey HE. Schepens PJ. et al. Unusual D-lactic acid acidosis from propylene glycol metabolism in overdose. J Toxicol Clin Toxicol 2004; 42: 163-169
  • 34 Mann NS. Russman HB. Mann SK. et al. Lactulose and severe lactic acidosis. Ann Intern Med 1985; 103: 637
  • 35 Bustos D. Pons S. Pernas JC. et al. Fecal lactate and short bowel syndrome. Dig Dis Sci 1994; 39: 2315-2319
  • 36 Kaneko T. Bando Y. Kurihara H. et al. Fecal microflora in a patient with short-bowel syndrome and identification of dominant lactobacilli. J Clin Microbiol 1997; 35: 3181-3185
  • 37 Dahlquist NR. Perrault J. Callaway CW. et al. D-lactic acidosis and encephalopathy after jejunoileostomy: response to overfeeding and to fasting in humans. Mayo Clin Proc 1984; 59: 141-145
  • 38 Bongaerts G. Tolboom J. Naber T. et al. D-lactic acidemia and aciduria in pediatric and adult patients with short-bowel syndrome. Clin Chem 1995; 41: 107-110
  • 39 Tubbs PK. The metabolism of D-alpha-hydroxy acids in animal tissues. Ann N Y Acad Sci 1965; 119: 920-926
  • 40 Vella A. Farrugia G. D-lactic acidosis: pathophysiologic consequence of saprophytism. Mayo Clin Proc 1998; 73: 451-456
  • 41 Cross SA. Callaway CW. D-lactic acidosis and selected cerebellar ataxias. Mayo Clin Proc 1984; 59: 202-205
  • 42 Scully TB. Kraft SC. Carr WC. et al. D-lactate-associated encephalopathy after massive small-bowel resection. J Clin Gastroenterol 1989; 11: 448-451
  • 43 Karton M. Rettmer RL. Lipkin EW. Effect of parenteral nutrition and enteral feeding on D-lactic acidosis in a patient with short bowel. JPEN J Parenter Enteral Nutr 1987; 11: 586-589
  • 44 White L. D-lactic acidosis: more prevalent than we think?. Practical Gastroenterol 2015; 39: 26-45
  • 45 Godey F. Bouasria A. Ropert M. et al. Don’t forget to test for D-lactic acid in short bowel syndrome. Am J Gastroenterol 2000; 95: 3675-3677
  • 46 Munakata S. Arakawa C. Kohira R. et al. A case of D-lactic acid encephalopathy associated with use of probiotics. Brain Dev 2010; 32: 691-694
  • 47 Narula RK. El Shafei A. Ramaiah D. et al. D-lactic acidosis 23 years after jejuno-ileal bypass (case report). Am J Kidney Dis 2000; 36: E9
  • 48 Uribarri J. Oh MS. Carroll HJ. D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms. Medicine (Baltimore) 1998; 77: 73-82
  • 49 Spillane K. Nagendran K. Prior PF. et al. Serial electroencephalograms in a patient with D-lactic acidosis. Electroencephalogr Clin Neurophysiol 1994; 91: 403-405
  • 50 Nightingale JMD. Lennard-Jones JE. Gertner DJ. et al. Colonic preservation reduces the need for parenteral therapy, increases incidence of renal stones, but does not change the high prevalence of gall stones in patients with a short bowel. Gut 1992; 33: 1493-1497
  • 51 Bongaerts G. Bakkeren J. Severijnen R. et al. Lactobacilli and acidosis in children with short small bowel. J Pediatr Gastroenterol Nutr 2000; 30: 288-293
  • 52 Boomer L. Liu Y. Mahler N. et al. Scaffolding for challenging environments: materials selection for tissue engineered intestine. J Biomed Mater Res A 2014; 102: 3795-3802