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      D-Lactic Acidosis: An Underrecognized Complication of Short Bowel Syndrome

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      Gastroenterology Research and Practice
      Hindawi Publishing Corporation

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          Abstract

          D-lactic acidosis or D-lactate encephalopathy is a rare condition that occurs primarily in individuals who have a history of short bowel syndrome. The unabsorbed carbohydrates act as a substrate for colonic bacteria to form D-lactic acid among other organic acids. The acidic pH generated as a result of D-lactate production further propagates production of D-lactic acid, hence giving rise to a vicious cycle. D-lactic acid accumulation in the blood can cause neurologic symptoms such as delirium, ataxia, and slurred speech. Diagnosis is made by a combination of clinical and laboratory data including special assays for D-lactate. Treatment includes correcting the acidosis and decreasing substrate for D-lactate such as carbohydrates in meals. In addition, antibiotics can be used to clear colonic flora. Although newer techniques for diagnosis and treatment are being developed, clinical diagnosis still holds paramount importance, as there can be many confounders in the diagnosis as will be discussed subsequently.

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          D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms.

          This report describes a case of d-lactic acidosis observed by the authors and then reviews all case reports of d-lactic acidosis in the literature in order to define its clinical and biochemical features and pathogenetic mechanisms. The report also reviews the literature on metabolism of d-lactic acid in humans. The clinical presentation of d-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings. Development of the syndrome requires the following conditions 1) carbohydrate malabsorption with increased delivery of nutrients to the colon, 2) colonic bacterial flora of a type that produces d-lactic acid, 3) ingestion of large amounts of carbohydrate, 4) diminished colonic motility, allowing time for nutrients in the colon to undergo bacterial fermentation, and 5) impaired d-lactate metabolism. In contrast to the initial assumption that d-lactic acid is not metabolized by humans, analysis of published data shows a substantial rate of metabolism of d-lactate by normal humans. Estimates based on these data suggest that impaired metabolism of d-lactate is almost a prerequisite for the development of the syndrome.
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            Faecal D/L Lactate Ratio Is a Metabolic Signature of Microbiota Imbalance in Patients with Short Bowel Syndrome

            Our objective was to understand the functional link between the composition of faecal microbiota and the clinical characteristics of adults with short bowel syndrome (SBS). Sixteen patients suffering from type II SBS were included in the study. They displayed a total oral intake of 2661±1005 Kcal/day with superior sugar absorption (83±12%) than protein (42±13%) or fat (39±26%). These patients displayed a marked dysbiosis in faecal microbiota, with a predominance of Lactobacillus/Leuconostoc group, while Clostridium and Bacteroides were under-represented. Each patient exhibited a diverse lactic acid bacteria composition (L. delbrueckii subsp. bulgaricus, L. crispatus, L. gasseri, L. johnsonii, L. reuteri, L. mucosae), displaying specific D and L-lactate production profiles in vitro. Of 16 patients, 9/16 (56%) accumulated lactates in their faecal samples, from 2 to 110 mM of D-lactate and from 2 to 80 mM of L-lactate. The presence of lactates in faeces (56% patients) was used to define the Lactate-accumulator group (LA), while absence of faecal lactates (44% patients) defines the Non lactate-accumulator group (NLA). The LA group had a lower plasma HCO3− concentration (17.1±2.8 mM) than the NLA group (22.8±4.6 mM), indicating that LA and NLA groups are clinically relevant sub–types. Two patients, belonging to the LA group and who particularly accumulated faecal D-lactate, were at risk of D-encephalopathic reactions. Furthermore, all patients of the NLA group and those accumulating preferentially L isoform in the LA group had never developed D-acidosis. The D/L faecal lactate ratio seems to be the most relevant index for a higher D- encephalopathy risk, rather than D- and L-lactate faecal concentrations per se. Testing criteria that take into account HCO3− value, total faecal lactate and the faecal D/L lactate ratio may become useful tools for identifying SBS patients at risk for D-encephalopathy.
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              Short-bowel syndrome in children and adults.

              Short-bowel syndrome is the malabsorptive state that follows extensive resection of the small intestine. Potential long-term survival without parenteral nutrition heavily depends on stimulation of the process of intestinal adaptation, through which the remaining small intestine gradually increases its absorptive capacity. This process is heavily nutrient dependent, and aggressive use of enteral nutrition is required to stimulate its completion. A combination of osmotic sensitivities, nutrient malabsorption, bowel dilatation and dysmotility, and changes in bacterial flora influence the symptoms and the management of this disorder. Chronic complications include parenteral nutrition-induced liver disease, nutrient deficiency states, and, frequently, small bowel bacterial overgrowth. Intestinal transplantation has been successfully developed in some centers in the United States, and preliminary experience suggest a long-term survival of 50%-75%, better in patients receiving an isolated intestinal transplant than a combined liver/bowel transplant. The ultimate role of intestinal transplantation is still undergoing evaluation.
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                Author and article information

                Journal
                Gastroenterol Res Pract
                Gastroenterol Res Pract
                GRP
                Gastroenterology Research and Practice
                Hindawi Publishing Corporation
                1687-6121
                1687-630X
                2015
                22 April 2015
                : 2015
                : 476215
                Affiliations
                Department of Medicine, Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT 06102, USA
                Author notes

                Academic Editor: Anastasios Koulaouzidis

                Article
                10.1155/2015/476215
                4421027
                25977687
                58b8135c-cf39-4d74-81c7-66f17716e8ad
                Copyright © 2015 N. G. Kowlgi and L. Chhabra.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 November 2014
                : 28 March 2015
                : 8 April 2015
                Categories
                Review Article

                Gastroenterology & Hepatology
                Gastroenterology & Hepatology

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