{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T03:06:24Z","timestamp":1788577584769,"version":"build-2803163510"},"reference-count":24,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2014,7,1]],"date-time":"2014-07-01T00:00:00Z","timestamp":1404172800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Anaesth Intensive Care"],"published-print":{"date-parts":[[2014,7]]},"abstract":"<jats:p>Lactate can substitute for glucose as a metabolic substrate. We report a patient with acute liver failure who was awake despite a glucose level of 0.7 mmol\/l with very high lactate level of 25 mmol\/l. The hypoglycaemia+hyperlactataemia combination may be considered paradoxical since glucose is the main precursor of lactate and lactate is reconverted into glucose by the Cori cycle. Literature relevant to the underlying mechanism of combined deep hypoglycaemia and severe hyperlactataemia was assessed. We also assessed the literature for evidence of protection against deep hypoglycaemia by hyperlactataemia. Four syndromes demonstrating hypoglycaemia+hyperlactataemia were found: 1) paracetamol-induced acute liver failure, 2) severe malaria, 3) lymphoma and 4) glucose-6-phosphatase deficiency. An impaired Cori cycle is a key component in all of these metabolic states. Apparently the liver, after exhausting its glycogen stores, loses the gluconeogenic pathway to generate glucose and thereby its ability to remove lactate as well. Several patients with lactic acidosis and glucose levels below 1.7 mmol\/l who were not in a coma have been reported. These observations and other data coherently indicate that lactate-protected hypoglycaemia is, at least transiently, a viable state under experimental and clinical conditions. Severe hypoglycaemia+hyperlactataemia reflects failure of the gluconeogenic pathway of lactate metabolism. The existence of lactate-protected hypoglycaemia implies that patients who present with this metabolic state should not automatically be considered to have sustained irreversible brain damage. Moreover, therapies that aim to achieve hypoglycaemia might be feasible with concomitant hyperlactataemia.<\/jats:p>","DOI":"10.1177\/0310057x1404200413","type":"journal-article","created":{"date-parts":[[2019,1,14]],"date-time":"2019-01-14T17:45:02Z","timestamp":1547487902000},"page":"507-511","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":23,"title":["A Patient with Acute Liver Failure and Extreme Hypoglycaemia with Lactic Acidosis who was not in Coma: Causes and Consequences of Lactate-Protected Hypoglycaemia"],"prefix":"10.1177","volume":"42","author":[{"given":"G.","family":"Oldenbeuving","sequence":"first","affiliation":[{"name":"Universitiy of Groningen, University Medical Center Groningen, Groningen, the Netherlands"},{"name":"Intensive Care and Anesthesiology, University Medical Center Groningen, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. R.","family":"Mcdonald","sequence":"additional","affiliation":[{"name":"Universitiy of Groningen, University Medical Center Groningen, Groningen, the Netherlands"},{"name":"School of Kinesiology, Auburn University, Auburn, Alabama, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. L.","family":"Goodwin","sequence":"additional","affiliation":[{"name":"Universitiy of Groningen, University Medical Center Groningen, Groningen, the Netherlands"},{"name":"Weill Cornell Medical College, New York, New York, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Sayilir","sequence":"additional","affiliation":[{"name":"Universitiy of Groningen, University Medical Center Groningen, Groningen, the Netherlands"},{"name":"Department of Critical Care, Martini Hospital, Groningen, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. J.","family":"Reijngoud","sequence":"additional","affiliation":[{"name":"Universitiy of Groningen, University Medical Center Groningen, Groningen, the Netherlands"},{"name":"Digestive and Metabolic Diseases, University of Groningen, University Medical Center Groningen, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. B.","family":"Gladden","sequence":"additional","affiliation":[{"name":"Universitiy of Groningen, University Medical Center Groningen, Groningen, the Netherlands"},{"name":"Department of Kinesiology, Auburn University, Auburn, Alabama, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. W. 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