Oldenbeuving G, McDonald J R, Goodwin M L, Sayilir R, Reijngoud D J, Gladden L B, Nijsten M W N
University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.
Anaesth Intensive Care. 2014 Jul;42(4):507-11. doi: 10.1177/0310057X1404200413.
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.
乳酸可替代葡萄糖作为代谢底物。我们报告了一名急性肝衰竭患者，尽管其血糖水平为0.7 mmol/L且乳酸水平极高，达25 mmol/L，但患者仍保持清醒。低血糖合并高乳酸血症这种组合可能看似矛盾，因为葡萄糖是乳酸的主要前体，且乳酸可通过科里循环再转化为葡萄糖。我们评估了与严重低血糖合并严重高乳酸血症潜在机制相关的文献。我们还评估了文献中关于高乳酸血症对严重低血糖具有保护作用的证据。发现了四种表现为低血糖合并高乳酸血症的综合征：1）对乙酰氨基酚所致急性肝衰竭，2）重症疟疾，3）淋巴瘤，4）葡萄糖 - 6 - 磷酸酶缺乏症。受损的科里循环是所有这些代谢状态的关键组成部分。显然，肝脏在耗尽其糖原储备后，失去了通过糖异生途径生成葡萄糖的能力，从而也失去了清除乳酸的能力。已有报道称，数名乳酸酸中毒且血糖水平低于1.7 mmol/L但未昏迷的患者。这些观察结果及其他数据一致表明，在实验和临床条件下，乳酸保护下的低血糖至少在短期内是一种可行的状态。严重低血糖合并高乳酸血症反映了乳酸代谢糖异生途径的衰竭。乳酸保护下的低血糖的存在意味着，出现这种代谢状态的患者不应自动被认为已遭受持续性不可逆脑损伤。此外，在伴有高乳酸血症的情况下，旨在实现低血糖的治疗可能是可行的。
