AIM： To characterize hyperlactatemia in patients with non-acetaminophen acute liver failure （ALF） in an attempt to clarify the mechanisms implicated and the role as a prognosis factor. METHODS： In the setting of l...AIM： To characterize hyperlactatemia in patients with non-acetaminophen acute liver failure （ALF） in an attempt to clarify the mechanisms implicated and the role as a prognosis factor. METHODS： In the setting of liver transplantation, 63 consecutive patients with non-acetaminophen acute liver failure were studied in relation to tissue oxygenation, hemodynamic and metabolic parameters. Before and after transplantation, the number of infected patients and outcome were registered. RESULTS： Acute ALF showed higher levels of lactate than subacute ALF （5.4 ± 1 mmol/L versus 2.2 ± 0.6 mmol/L, P= 0.01）. Oxygenation parameters were within the normal range. Lactate levels showed good correlation with respiratory quotient （r=0.759, P〈 0.005）, mean glucose administration （r= 0.664, P= 0.01） and encephalopathy （r= 0.698, P= 0.02）, but not with splanchnic arteriovenous difference in PCO2, pH and the presence of infection （P=0.1）. Portal vein lactate was higher （P〈0.05） than arterial and mixed venous lactate, suggesting its production of hyperlactatemia in the intestine and spleen. The presence of infection was an independent predictor of survival. CONCLUSION： Hyperlactatemia is not a prognosis factor due to byproduct of the overall acceleration in glycolysis.展开更多
All oral nucleoside analogues against hepatitis B virus,with an exception of telbivudine,have been reported causing lactic acidosis(LA).Here we report the first case of chronic hepatitis B developing severe refractory...All oral nucleoside analogues against hepatitis B virus,with an exception of telbivudine,have been reported causing lactic acidosis(LA).Here we report the first case of chronic hepatitis B developing severe refractory LA during telbivudine monotherapy.A 36-year-old man of Chinese origin received telbivudine antiviral treatment for chronic hepatitis B.After 11 mo of therapy,he developed anorexia,nausea,and vomiting with mild muscle weakness.The patient was found with elevated serum creatine phosphokinase up to 3683 U/L(upper limit of normal 170 U/L)and marked LA.LA did not resolve immediately following discontinuation of telbivudine.His condition began to improve after hemodialysis treatment for 16 times and usage of glucocorticosteroid.The patient fully recovered after 16 wk of treatment.This is the first documented case with severe LA caused by telbivudine monotherapy.Besides serum creatine phosphokinase,blood lactate level should also be closely monitored in patients receiving telbivudine.展开更多
Type A lactic acidosis resulted from hypoxic mitochondrial dysfunction is an independent predictor of mortality for critically ill patients. However, current therapeutic agents are still in shortage and can even be ha...Type A lactic acidosis resulted from hypoxic mitochondrial dysfunction is an independent predictor of mortality for critically ill patients. However, current therapeutic agents are still in shortage and can even be harmful. This paper reviewed data regarding lactic acidosis treatment and recommended that pyruvate might be a potential alkalizer to correct type A lactic acidosis in future clinical practice. Pyruvate is a key energy metabolic substrate and a pyruvate dehydrogenase(PDH) activator with several unique beneficial biological properties, including anti-oxidant and antiinflammatory effects and the ability to activate the hypoxia-inducible factor-1(HIF-1α)-erythropoietin(EPO) signal pathway. Pyruvate preserves glucose metabolism and cellular energetics better than bicarbonate, lactate, acetate and malate in the efficient correction of hypoxic lactic acidosis and shows few side effects. Therefore, application of pyruvate may be promising and safe as a novel therapeutic strategy in hypoxic lactic acidosis correction accompanied with multi-organ protection in critical care patients.展开更多
BACKGROUND Intraoperative hyperlactatemia often affects circulatory stability,vital organ function,and postoperative recovery,poses a serious prognostic risk,and requires considerable attention from anesthesiologists....BACKGROUND Intraoperative hyperlactatemia often affects circulatory stability,vital organ function,and postoperative recovery,poses a serious prognostic risk,and requires considerable attention from anesthesiologists.Here,we describe a case of hyperlactatemia during the postoperative resection of liver metastases after chemotherapy for sigmoid colon cancer.This did not affect the patient's circulatory stability or quality of awakening,which is rarely reported in clinical practice.We present our management experience with the aim of providing a reference for future studies and clinical practice.CASE SUMMARY A 70-year-old female patient was diagnosed with postoperative liver metastasis following chemotherapy for sigmoid colon cancer.Laparoscopic right hemicolectomy and cholecystectomy under general anesthesia were required.Metabolic disorders,primarily hyperlactatemia,often occur intraoperatively.After treatment,other indices quickly returned to normal,lactate levels decreased slowly,and hyperlactatemia persisted during the awakening period.However,this did not affect the patient's circulatory stability or awakening quality.This condition has rarely been clinically reported.Therefore,we report our management experience in order to guide clinical practice in this regard.Hyperlactatemia did not affect circulatory stability or the quality of awakening.We considered that active intraoperative rehydration avoided serious harm to the organism caused by hyperlactatemia due to insufficient tissue perfusion,while hyperlactatemia caused by decreased lactate clearance due to impaired liver function associated with surgical resection had a mild effect on the function of important organs.CONCLUSION Active intraoperative rehydration avoided serious harm to the organism caused by hyperlactatemia.Strengthening body temperature protection could improve lactate circulation.展开更多
BACKGROUND Mitochondrial myopathy is a rare genetic disease with maternal inheritance that may involve multiple organ systems.Due to the lack of typical characteristics,its clinical diagnosis is difficult,and it is of...BACKGROUND Mitochondrial myopathy is a rare genetic disease with maternal inheritance that may involve multiple organ systems.Due to the lack of typical characteristics,its clinical diagnosis is difficult,and it is often misdiagnosed or even missed.CASE SUMMARY The patient was a young college student.When he presented at the hospital,he had severe lactic acidosis,respiratory failure,and shock with multiple organ dysfunction syndrome(MODS).He was treated by mechanical ventilation,venoarterial extracorporeal membrane oxygenation,and other organ support.However,his condition continued to worsen.After a thorough and detailed medical and family history was taken,a mitochondrial crisis was suspected.A muscle biopsy was taken.Further genetic testing confirmed a mitochondrial gene mutation(TRNL13243A>G).The final diagnosis of mitochondrial myopathy was made.Although there is no known specific treatment,intravenous methylprednisone and intravenous immunoglobulin were started.The patient’s shock eventually improved.The further course was complicated by severe infection in multiple sites,severe muscle weakness,and recurrent MODS.After 2 mo of multidisciplinary management and intensive rehabilitation,the patient could walk with assistance 4 mo after admission and walk independently 6 mo after admission.CONCLUSION More attention should be paid to mitochondrial myopathy to avoid missed diagnosis and misdiagnosis.展开更多
文摘AIM： To characterize hyperlactatemia in patients with non-acetaminophen acute liver failure （ALF） in an attempt to clarify the mechanisms implicated and the role as a prognosis factor. METHODS： In the setting of liver transplantation, 63 consecutive patients with non-acetaminophen acute liver failure were studied in relation to tissue oxygenation, hemodynamic and metabolic parameters. Before and after transplantation, the number of infected patients and outcome were registered. RESULTS： Acute ALF showed higher levels of lactate than subacute ALF （5.4 ± 1 mmol/L versus 2.2 ± 0.6 mmol/L, P= 0.01）. Oxygenation parameters were within the normal range. Lactate levels showed good correlation with respiratory quotient （r=0.759, P〈 0.005）, mean glucose administration （r= 0.664, P= 0.01） and encephalopathy （r= 0.698, P= 0.02）, but not with splanchnic arteriovenous difference in PCO2, pH and the presence of infection （P=0.1）. Portal vein lactate was higher （P〈0.05） than arterial and mixed venous lactate, suggesting its production of hyperlactatemia in the intestine and spleen. The presence of infection was an independent predictor of survival. CONCLUSION： Hyperlactatemia is not a prognosis factor due to byproduct of the overall acceleration in glycolysis.
基金Supported by National Natural Science Foundation of ChinaNo.81071354 and 81271833+4 种基金National "973’ ’ProjectNo.2012CB519001National Science and Technology Major Project of ChinaNo.2012ZX10002007-001-002No.2013ZX10002001
文摘All oral nucleoside analogues against hepatitis B virus,with an exception of telbivudine,have been reported causing lactic acidosis(LA).Here we report the first case of chronic hepatitis B developing severe refractory LA during telbivudine monotherapy.A 36-year-old man of Chinese origin received telbivudine antiviral treatment for chronic hepatitis B.After 11 mo of therapy,he developed anorexia,nausea,and vomiting with mild muscle weakness.The patient was found with elevated serum creatine phosphokinase up to 3683 U/L(upper limit of normal 170 U/L)and marked LA.LA did not resolve immediately following discontinuation of telbivudine.His condition began to improve after hemodialysis treatment for 16 times and usage of glucocorticosteroid.The patient fully recovered after 16 wk of treatment.This is the first documented case with severe LA caused by telbivudine monotherapy.Besides serum creatine phosphokinase,blood lactate level should also be closely monitored in patients receiving telbivudine.
基金supported by the National Natural Science Foundation of China(No.81700181,No.81600148)
文摘Type A lactic acidosis resulted from hypoxic mitochondrial dysfunction is an independent predictor of mortality for critically ill patients. However, current therapeutic agents are still in shortage and can even be harmful. This paper reviewed data regarding lactic acidosis treatment and recommended that pyruvate might be a potential alkalizer to correct type A lactic acidosis in future clinical practice. Pyruvate is a key energy metabolic substrate and a pyruvate dehydrogenase(PDH) activator with several unique beneficial biological properties, including anti-oxidant and antiinflammatory effects and the ability to activate the hypoxia-inducible factor-1(HIF-1α)-erythropoietin(EPO) signal pathway. Pyruvate preserves glucose metabolism and cellular energetics better than bicarbonate, lactate, acetate and malate in the efficient correction of hypoxic lactic acidosis and shows few side effects. Therefore, application of pyruvate may be promising and safe as a novel therapeutic strategy in hypoxic lactic acidosis correction accompanied with multi-organ protection in critical care patients.
文摘BACKGROUND Intraoperative hyperlactatemia often affects circulatory stability,vital organ function,and postoperative recovery,poses a serious prognostic risk,and requires considerable attention from anesthesiologists.Here,we describe a case of hyperlactatemia during the postoperative resection of liver metastases after chemotherapy for sigmoid colon cancer.This did not affect the patient's circulatory stability or quality of awakening,which is rarely reported in clinical practice.We present our management experience with the aim of providing a reference for future studies and clinical practice.CASE SUMMARY A 70-year-old female patient was diagnosed with postoperative liver metastasis following chemotherapy for sigmoid colon cancer.Laparoscopic right hemicolectomy and cholecystectomy under general anesthesia were required.Metabolic disorders,primarily hyperlactatemia,often occur intraoperatively.After treatment,other indices quickly returned to normal,lactate levels decreased slowly,and hyperlactatemia persisted during the awakening period.However,this did not affect the patient's circulatory stability or awakening quality.This condition has rarely been clinically reported.Therefore,we report our management experience in order to guide clinical practice in this regard.Hyperlactatemia did not affect circulatory stability or the quality of awakening.We considered that active intraoperative rehydration avoided serious harm to the organism caused by hyperlactatemia due to insufficient tissue perfusion,while hyperlactatemia caused by decreased lactate clearance due to impaired liver function associated with surgical resection had a mild effect on the function of important organs.CONCLUSION Active intraoperative rehydration avoided serious harm to the organism caused by hyperlactatemia.Strengthening body temperature protection could improve lactate circulation.
基金The Science and Technology Department of Gansu Province,No.20JR5RA355 and No.22JR10KA009Talent Innovation and Entrepreneurship Project of Science and Technology Bureau of Chengguan District,Lanzhou,No.2020RCCX0030+1 种基金Lanzhou Science and Technology Development Guiding Plan Project,No.2019-ZD-37Fund of The First Hospital of Lanzhou University,No.Ldyyyn2020-79.
文摘BACKGROUND Mitochondrial myopathy is a rare genetic disease with maternal inheritance that may involve multiple organ systems.Due to the lack of typical characteristics,its clinical diagnosis is difficult,and it is often misdiagnosed or even missed.CASE SUMMARY The patient was a young college student.When he presented at the hospital,he had severe lactic acidosis,respiratory failure,and shock with multiple organ dysfunction syndrome(MODS).He was treated by mechanical ventilation,venoarterial extracorporeal membrane oxygenation,and other organ support.However,his condition continued to worsen.After a thorough and detailed medical and family history was taken,a mitochondrial crisis was suspected.A muscle biopsy was taken.Further genetic testing confirmed a mitochondrial gene mutation(TRNL13243A>G).The final diagnosis of mitochondrial myopathy was made.Although there is no known specific treatment,intravenous methylprednisone and intravenous immunoglobulin were started.The patient’s shock eventually improved.The further course was complicated by severe infection in multiple sites,severe muscle weakness,and recurrent MODS.After 2 mo of multidisciplinary management and intensive rehabilitation,the patient could walk with assistance 4 mo after admission and walk independently 6 mo after admission.CONCLUSION More attention should be paid to mitochondrial myopathy to avoid missed diagnosis and misdiagnosis.
