Splanchnic and leg exchange of amino acids and ammonia in acute liver failure

BACKGROUND & AIMS: In patients with acute liver failure, hyperammonemia is associated with cerebral herniation. We examined the splanchnic and leg exchange of amino acids, urea, and ammonia in such patients. METHODS: Bedside liver vein catheterization was used in 22 patients after development of hepatic encephalopathy grades III-IV. Femoral venous blood was sampled in 7 of these patients. RESULTS: Arterial amino acid concentration (8.1 +/- 4.1 mmol/L) was increased 4-fold above normal. Glutamine (2.4 +/- 1.8 mmol/L) and alanine (0.57 +/- 0.35 mmol/L) were by far the predominant amino acids exchanged in the splanchnic and leg circulation. In the splanchnic circulation, there was a net uptake of glutamine (241 +/- 353 micromol/min) and ammonia and alanine were released in an almost 1:1 stoichiometry (r(2) = 0.47; P < 0.001). In the leg, ammonia and alanine were removed and glutamine released. The leg ammonia concentration difference was correlated to that of glutamine (r(2) = 0.80; P = 0.008) and alanine (r(2) = 0.67; P = 0.03). CONCLUSIONS: Splanchnic metabolism of glutamine in combination with decreased hepatic function was responsible for the splanchnic release of ammonia and alanine. These processes were reversed in skeletal muscle. Stimulation of skeletal muscle metabolism of ammonia could be a important target for future treatment of patients with acute liver failure.     

Cerebral metabolism of ammonia and amino acids in patients with fulminant hepatic failure.

BACKGROUND & AIMS: High circulating levels of ammonia have been suggested to be involved in the development of cerebral edema and herniation in fulminant hepatic failure (FHF). The aim of this study was to measure cerebral metabolism of ammonia and amino acids, with special emphasis on glutamine metabolism. METHODS: The study consisted of patients with FHF (n = 16) or cirrhosis (n = 5), and healthy subjects (n = 8). Cerebral blood flow was measured by the 133Xe washout technique. Blood samples for determination of ammonia and amino acids were drawn simultaneously from the radial artery and the internal jugular bulb. RESULTS: A net cerebral ammonia uptake was only found in patients with FHF (1.62 +/- 0.79 micromol x 100 g(-1) x min(-1)). The cerebral glutamine efflux was higher in patients with FHF than in the healthy subjects and cirrhotics, -6.11 +/- 5.19 vs. -1.93 +/- 1.17 and -1.50 +/- 0.29 micromol x 100 g(-1) x min(-1), respectively (P < 0.05). Patients with FHF who subsequently died of cerebral herniation (n = 6) had higher arterial ammonia concentrations, higher cerebral ammonia uptake, and higher cerebral glutamine efflux than survivors. Intervention with short-term mechanical hyperventilation in FHF reduced the net cerebral glutamine efflux, despite an unchanged net cerebral ammonia uptake. CONCLUSIONS: Patients with FHF have an increased cerebral glutamine efflux, and short-term hyperventilation reduces this efflux. A high cerebral ammonia uptake and cerebral glutamine efflux in patients with FHF were associated with an increased risk of subsequent fatal intracranial hypertension.     

Correlations between zinc, amino acids and ammonia in liver cirrhosis

In view of the universal metabolic importance of zinc in the organism, it was the purpose of the present work to determine the concentrations of zinc in serum, of amino acids and ammonia in plasma of patients with liver cirrhosis, and investigate that correlations might exist between these substances. The study involved 18 patients with decompensated liver cirrhosis without coma and eleven with coma. The subjects with normal livers were used as controls. While confirming known data (reduced zinc levels, imbalance of plasma amino acids, hyperammonaemia in chronic liver diseases) the findings also revealed correlations between the above substances. A negative correlations existed between zinc and ammonia. Decreases in zinc serum levels were accompanied by increases in plasma ammonia concentrations in hepatic coma (p less than 0.05). Plasma levels of amino acids did not correlate with serum zinc concentrations.     

非生物人工肝支持系统治疗肝功能衰竭的血清氨基酸谱变化

目的 分析肝功能衰竭患者接受非生物人工肝支持系统(ALSS)治疗引起的血清氨基酸谱变化,阐述非生物ALSS治疗肝功能衰竭的有效性.方法 对2009年6月至2010年8月间146例肝功能衰竭患者行非生物ALSS治疗,观察治疗前后患者血清氨基酸谱的变化情况,并对不同预后、不同肝功能衰竭类型以及处于不同肝功能衰竭时期患者的血清氨基酸水平的变化进行研究.计量资料采用配对样本的t检验.结果 非生物ALSS治疗后,血清谷氨酸和赖氨酸下降明显[(395.62±200.24)μumol/L比(260.05±169.56)μmol/L,(436.73±326.18)μmol/L比(407.12±292.01)μmol/L;t＝8.611,t＝2.659;均P＜0.01],苏氨酸、支链氨基酸/芳香族氨基酸显著上升[(1302.90±1288.70)μmol/L比(1406.70±1272.34)μmol/L,1.23±0.53比1.36±0.57;t＝2.895,t＝1.061;均P＜0.01].在预后不同的患者间、不同肝功能衰竭类型以及处于不同时期的肝功能衰竭患者间,谷氨酸、酪氨酸、精氨酸以及蛋氨酸等治疗前后差异有统计学意义.结论 非生物ALSS治疗可以改善肝功能衰竭患者血清氨基酸紊乱状况.不同肝功能衰竭分类、分期以及不同预后患者的血清氨基酸谱在非生物ALSS治疗后有显著不同的变化.

Abstract：

Objective To analyze the patterns of amino acid changes in liver failure patients treated with non-bioartificial liver support system (ALSS), and to explore the efficacy of ALSS in liver failure treatment. Methods A total of 146 liver failure patients treated with ALSS from June 2009 to August 2010 were recruited in this study. Paired blood samples were collected from every patient and serum amino acids and ammonia were tested by automatic amino acid analyzer. The changes of amino acids in patients with different prognoses, different types/phases of liver failure were evaluated.Measurement data were compared by paired t test. Results After ALSS treatment, liver failure patients experienced a significant decrease in serum glutamic acid and lysine [(395.62±200.24)μmol/Lvs (260. 05±169.56) μmol/L and (436. 73±326. 18)μmol/L vs (407. 12±292.01) μmol/L,respectively; t= 8. 611 and 2. 659, respectively; both P＜0.01)], while experienced greatly increases in threonine and branched-chain amino acids/aromatic amino acid ratio [( 1302. 90 ±1288.70) μmol/L vs (1406.70 ±1272. 34) μmol/L and 1. 23 ± 0. 53 vs 1. 36 ± 0.57, respectively; t = 2. 895 and 1. 061,respectively; both P＜0. 01)]. The changes of glutamic acid, tyrosine, arginine and methionine before and after ALSS treatment in patients with different prognoses, different types/phases of liver failure were all significantly different. Conclusions ALSS treatment could improve the serum amino acid disorder in liver failure patients. The amino acids in patients with different types/phases or different prognoses of liver failure change significantly after ALSS treatment.     

非生物人工肝支持系统治疗肝功能衰竭的血清氨基酸谱变化

Objective To analyze the patterns of amino acid changes in liver failure patients treated with non-bioartificial liver support system (ALSS), and to explore the efficacy of ALSS in liver failure treatment. Methods A total of 146 liver failure patients treated with ALSS from June 2009 to August 2010 were recruited in this study. Paired blood samples were collected from every patient and serum amino acids and ammonia were tested by automatic amino acid analyzer. The changes of amino acids in patients with different prognoses, different types/phases of liver failure were evaluated.Measurement data were compared by paired t test. Results After ALSS treatment, liver failure patients experienced a significant decrease in serum glutamic acid and lysine [(395.62±200.24)μmol/Lvs (260. 05±169.56) μmol/L and (436. 73±326. 18)μmol/L vs (407. 12±292.01) μmol/L,respectively; t= 8. 611 and 2. 659, respectively; both P＜0.01)], while experienced greatly increases in threonine and branched-chain amino acids/aromatic amino acid ratio [( 1302. 90 ±1288.70) μmol/L vs (1406.70 ±1272. 34) μmol/L and 1. 23 ± 0. 53 vs 1. 36 ± 0.57, respectively; t = 2. 895 and 1. 061,respectively; both P＜0. 01)]. The changes of glutamic acid, tyrosine, arginine and methionine before and after ALSS treatment in patients with different prognoses, different types/phases of liver failure were all significantly different. Conclusions ALSS treatment could improve the serum amino acid disorder in liver failure patients. The amino acids in patients with different types/phases or different prognoses of liver failure change significantly after ALSS treatment.     

非生物人工肝支持系统治疗肝功能衰竭的血清氨基酸谱变化

Objective To analyze the patterns of amino acid changes in liver failure patients treated with non-bioartificial liver support system (ALSS), and to explore the efficacy of ALSS in liver failure treatment. Methods A total of 146 liver failure patients treated with ALSS from June 2009 to August 2010 were recruited in this study. Paired blood samples were collected from every patient and serum amino acids and ammonia were tested by automatic amino acid analyzer. The changes of amino acids in patients with different prognoses, different types/phases of liver failure were evaluated.Measurement data were compared by paired t test. Results After ALSS treatment, liver failure patients experienced a significant decrease in serum glutamic acid and lysine [(395.62±200.24)μmol/Lvs (260. 05±169.56) μmol/L and (436. 73±326. 18)μmol/L vs (407. 12±292.01) μmol/L,respectively; t= 8. 611 and 2. 659, respectively; both P＜0.01)], while experienced greatly increases in threonine and branched-chain amino acids/aromatic amino acid ratio [( 1302. 90 ±1288.70) μmol/L vs (1406.70 ±1272. 34) μmol/L and 1. 23 ± 0. 53 vs 1. 36 ± 0.57, respectively; t = 2. 895 and 1. 061,respectively; both P＜0. 01)]. The changes of glutamic acid, tyrosine, arginine and methionine before and after ALSS treatment in patients with different prognoses, different types/phases of liver failure were all significantly different. Conclusions ALSS treatment could improve the serum amino acid disorder in liver failure patients. The amino acids in patients with different types/phases or different prognoses of liver failure change significantly after ALSS treatment.     

Cerebral herniation in patients with acute liver failure is correlated with arterial ammonia concentration

Cerebral edema leading to cerebral herniation (CH) is a common cause of death in acute liver failure (ALF). Animal studies have related ammonia with this complication. During liver failure, hepatic ammonia removal can be expected to determine the arterial ammonia level. In patients with ALF, we examined the hypotheses that high arterial ammonia is related to later death by CH, and that impaired removal in the hepatic circulation is related to high arterial ammonia. Twenty-two patients with ALF were studied retrospectively. In addition, prospective studies with liver vein catheterization were performed after development of hepatic encephalopathy (HE) in 22 patients with ALF and 9 with acute on chronic liver disease (AOCLD). Cerebral arterial-venous ammonia difference was studied in 13 patients with ALF. In all patients with ALF (n = 44), those who developed CH (n = 14) had higher arterial plasma ammonia than the non-CH (n = 30) patients (230 +/- 58 vs. 118 +/- 48 micromol/L; P <. 001). In contrast, galactose elimination capacity, bilirubin, creatinine, and prothrombin time were not different (NS). Cerebral arterial-venous differences increased with increasing arterial ammonia (P <.001). Arterial plasma ammonia was lower than hepatic venous in ALF (148 +/- 73 vs. 203 +/- 108 micromol/L; P <.001). In contrast, arterial plasma ammonia was higher than hepatic venous in patients with AOCLD (91 +/- 26 vs. 66 +/- 18 micromol/L; P <.05). Net ammonia release from the hepatic-splanchnic region was 6.5 +/- 6. 4 mmol/h in ALF, and arterial ammonia increased with increasing release. In contrast, there was a net hepatic-splanchnic removal of ammonia (2.8 +/- 3.3 mmol/h) in patients with AOCLD. We interpret these data that in ALF in humans, vast amounts of ammonia escape hepatic metabolism, leading to high arterial ammonia concentrations, which in turn is associated with increased cerebral ammonia uptake and CH.     

1977例急性、亚急性、慢加急性肝衰竭患者的病因与转归分析

目的 探讨急性肝衰竭(ALF)、亚急性肝衰竭(SALF)、慢加急性肝衰竭(ACLF)的病因. 方法回顾性总结1977例肝衰竭患者的临床资料,对病因、年龄、性别、转归等方面进行比较分析.结果 ALF的前三位病因是:HEV感染(33.96%)、HBV感染(13.21%)与药物性肝病(9.43%);SALF为药物性肝病(31.53%)、HEV感染(16.22%)、HBV感染(9.91%);ACLF为HBV感染(90.29%)、洒精性肝病(2.65%)、HBV与HEV重叠感染(2.26%).常见嗜肝病毒感染者占90.09%(1781例),其中单HBV感染占92.93%(1655例).在HBV感染者中(1655例),26～55岁患者占77.10%(1276例).2005-2007年酒精性肝衰竭患者39例,占酒精性病因患者的81.25%(48例);2006-2007年药物性肝衰竭共23例,占药物性病因的56.10%(41例).除药物性肝损伤外,其他病因均男性多于女性.三类肝衰竭总治愈,好转率为35.56%,HEV感染性肝衰竭的治愈,好转率高于药物性肝衰竭(x2=4.42,P<0.05),其他组间差异无统计学意义.结论 不同类型肝衰竭主要病因不同;HBV感染居肝衰竭病因之首,酒精性、药物性肝衰竭呈上升趋势;HEV感染性肝衰竭治愈、好转率相对较高.     

D-penicillamine and plasmapheresis in acute liver failure secondary to Wilson's disease.

We report a case of a 19-year-old woman with acute liver failure, Coomb? negative hemolytic anemia, and renal failure as initial manifestations of Wilsoń disease with recovery following medical treatment. The clinical picture and low serum transaminase and alkaline phosphatase levels gave us a clue to suspect Wilsoń disease and to initiate plasmapheresis and D-penicillamine soon after admission. The serum and urinary copper levels were elevated with low serum ceruloplasmin. We proceeded to ambulatory follow-up with medical treatment with D-penicillamine. A few months later, during the course of a laparoscopic cholecystectomy because of symptomatic gallstone disease, a liver biopsy sample was obtained that showed histological liver fibrosis and strongly elevated levels of liver tissue copper.     

Plasma amino acids imbalance in patients with liver disease

The venous plasma amino acid patterns have been determined in 12 normal individuals and in 71 shunted and nonshunted cirrhotics in various grades of hepatic encephalopathy. The free amino acids have been determined by an amino autoanalyzer; the total and free tryptophan have been measured by a spoctrophotofluorimetric method. In 14 instances arterial plasma amino acid patterns have been measured simultaneously. High levels of aromatic and sulfurated amino acids and low levels of branched-chain amino acids have been constantly found in all cirrhotics. Methionine, phenylalanine, valine, leucine, tyrosine, and free tryptophan showed a statistical difference between controls and all other groups. These altered patterns did not correlate either with the grade or the evolution of the coma or with the presence of the surgical anastomosis. No statistical differences were lated with the grade and evolution of the hepatic encephalopathy was free tryptophan. The molar ratios between the amino acids sharing the same transport system across the blood-brain-barrier have been considered. A very good correlation with the grade of the mental disorder was found with the ratios free tryptophan/phenylalanine-tyrosine-methionine-valine-leucine-isoleucine and free tryptophan/branched-chain amino acids.This work was supported by Grant 30.3.1971, no. 118, 500.6/Contract 72, from Ministero della Sanita. Dir. Gen. Sery. Med. Soc., Div. VI.     

The effects of ammonia tolerance tests on the cerebrospinal fluid concentrations of amino acids and indoleamines in patients with liver cirrhosis.

To study the effect of ammonia administration on amino acids and indoleamines in cerebrospinal fluid (CSF) and on amino acids, insulin, and glucagon in plasma in humans with liver cirrhosis, we performed seven ammonia tolerance tests on six patients with stable liver cirrhosis. The grade of encephalopathy was determined by psychometric tests. Only one of the patients had pronounced encephalopathy. The other patients had no or only slight encephalopathy. The plasma concentrations of valine, leucine, isoleucine, phenylalanine, tyrosine, and methionine decreased after the ammonia load, whereas no changes were found in the plasma concentrations of glucagon and insulin. In CSF the concentrations of glutamine, aromatic amino acids, and indoleamines increased only in the patient who had pronounced encephalopathy, whereas no changes were found in the other patients. The effect of an ammonia load on the concentrations of neutral amino acids in CSF in patients with pronounced encephalopathy remains to be demonstrated.     

Synthesis of urea after stimulation with amino acids: relation to liver function.

Hepatic urea synthesis is the organism's main channel for the disposal of nitrogen and it may be an 'essential' liver function. In six control subjects and five patients with cirrhosis of the liver urea synthesis was studied during continuous infusion for six to 24 hours of about 3 mmol alpha-amino nitrogen/h X kg body weight. The urea synthesis rate was calculated in intervals of two hours as urinary excretion with correction for accumulation in the total body water and for hydrolysis of urea in the gut. The peripheral venous plasma alpha-amino nitrogen concentration increased from 3 to about 14 mmol/l and the urea nitrogen synthesis rate from 25 to about 215 mmol/h. In all cases the urea synthesis rate rose linearly with the alpha-amino concentration throughout the examined range. The slope of this linear relationship is an expression of the hepatic conversion of alpha-amino nitrogen to urea nitrogen ('functional hepatic nitrogen clearance'). The functional hepatic nitrogen clearance was 22.4 l/h in control subjects and 13.7 1/h (P < 0.025) in the patients with cirrhosis. It was correlated with quantitative measures of the liver function (the galactose elimination capacity, r = 0.84, and the clearance of antipyrine, 4 = 0.80). These observations, while confirming the abundant capacity of the urea synthesis system, imply that a given urea synthesis rate requires a higher alpha-amino level in patients with reduced liver function.     

Association of reduced extracellular brain ammonia, lactate, and intracranial pressure in pigs with acute liver failure

We previously demonstrated in pigs with acute liver failure (ALF) that albumin dialysis using the molecular adsorbents recirculating system (MARS) attenuated a rise in intracranial pressure (ICP). This was independent of changes in arterial ammonia, cerebral blood flow and inflammation, allowing alternative hypotheses to be tested. The aims of the present study were to determine whether changes in cerebral extracellular ammonia, lactate, glutamine, glutamate, and energy metabolites were associated with the beneficial effects of MARS on ICP. Three randomized groups [sham, ALF (induced by portacaval anastomosis and hepatic artery ligation), and ALF+MARS] were studied over a 6-hour period with a 4-hour MARS treatment given beginning 2 hours after devascularization. Using cerebral microdialysis, the ALF-induced increase in extracellular brain ammonia, lactate, and glutamate was significantly attenuated in the ALF+MARS group as well as the increases in extracellular lactate/pyruvate and lactate/glucose ratios. The percent change in extracellular brain ammonia correlated with the percent change in ICP (r(2) = 0.511). Increases in brain lactate dehydrogenase activity and mitochondrial complex activity for complex IV were found in ALF compared with those in the sham, which was unaffected by MARS treatment. Brain oxygen consumption did not differ among the study groups. Conclusion: The observation that brain oxygen consumption and mitochondrial complex enzyme activity changed in parallel in both ALF- and MARS-treated animals indicates that the attenuation of increased extracellular brain ammonia (and extracellular brain glutamate) in the MARS-treated animals reduces energy demand and increases supply, resulting in attenuation of increased extracellular brain lactate. The mechanism of how MARS reduces extracellular brain ammonia requires further investigation.     

Opportunistic infection in patients with acute liver failure

Background

Treatment with systemic corticosteroids is often used for acute liver failure (ALF), but this has increased the number of profoundly immunocompromised patients and cases of opportunistic infection.

Methods

Between January 2007 and December 2012, all patients (n = 51) referred to the Chiba University Hospital for treatment of ALF were studied. Patients with prothrombin activity of 40 % or less of the standardized values were defined as having ALF. Patient age, sex, cause of ALF, alanine aminotransferase and total bilirubin levels, prothrombin activity and total amount of corticosteroid were analyzed to determine the factors associated with the occurrence of opportunistic infection.

Results

Opportunistic infections occurred in 21.6 % (n = 11) of ALF patients. Thirty-five patients underwent systemic corticosteroid therapy, and 31.4 % of those patients showed opportunistic infections. Cytomegalovirus (n = 9, 81.8 %) and Pneumocystis jiroveci (n = 6, 54.5 %) were the microorganisms frequently suspected as the causes of opportunistic infection. In 7 (63.6 %) of the 11 cases of opportunistic infection, 2 or more species of microorganism were detected. Seven patients (63.6 %) with opportunistic infection were cured by treatment. Cox regression analysis for the patients who underwent systemic corticosteroid therapy steroid treatment revealed that age over 52 years (compared to younger patients: odds ratio = 9.62, 95 % confidence interval = 1.22–76.9) was only the predictive factor for the occurrence of opportunistic infection.

Conclusion

Opportunistic infections are not rare in ALF patients, and the appropriate diagnosis and treatment of these infections are critical during ALF treatment.     

Hyperlactatemia in patients with non-acetaminophen-related acute liver failure

AIM:To characterize hyperlactatemia in patients withnon-acetaminophen acute liver failure(ALF)in anattempt to clarify the mechanisms implicated and therole as a prognosis factor.METHODS:In the setting of liver transplantation,63consecutive patients with non-acetaminophen acute liverfailure were studied in relation to tissue oxygenation,hemodynamic and metabolic parameters.Before andafter transplantation,the number of infected patientsand outcome were registered.RESULTS:Acute ALF showed higher levels of lactatethan subacute ALF(5.4±1 mmol/L versus 2.2±0.6mmol/L,P=0.01).Oxygenation parameters were withinthe normal range.Lactate levels showed good correlationwith respiratory quotient(r=0.759,P<0.005),meanglucose administration(r=0.664,P=0.01)andencephalopathy(r=0.698,P=0.02),but not withsplanchnic arteriovenous difference in PCO2,pH and thepresence of infection(P=0.1).Portal vein lactate washigher(P<0.05)than arterial and mixed venous lactate,suggesting its production of hyperlactatemia in theintestine and spleen.The presence of infection was anindependent predictor of survival.CONCLUSION:Hyperlactatemia is not a prognosisfactor due to byproduct of the overall acceleration inglycolysis.     

Short-term effects of an intravenous infusion of a nutrient solution containing amino acids, glucose and insulin on leucine turnover and amino acid metabolism in patients with liver failure

Tolerance to an intravenous nutrient infusion containing amino acids, glucose and insulin was assessed in 12 adult patients with clinical and biochemical evidence of liver failure. In six individuals, fasting plasma amino acid patterns and turnover rates were measured by a constant intravenous infusion of [1-14C]leucine tracer. In the remaining patients the same measurements were made after a 10 h intravenous infusion of a 'standard' commercial mixture of amino acids (3.4 g/h), dextrose (20 g/h) and insulin (1.6 units/h). On the second day, conditions were crossed over and measurements were repeated. With the exception of glycine, the infusion of the amino acid-containing solution failed to significantly increase plasma amino acid content. Plasma leucine flux measurements indicated that the explanation involved a reduction in input of amino acids derived from the breakdown of body proteins rather than an increased uptake of amino acids into protein; i.e., the rate of liberation of leucine from protein decreased by an average of 2.4 mmol/h (P less than 0.05) whilst intake only added 1.6 mmol/h. No consistent changes in encephalopathy were observed. In conclusion, the infusion of the amino acid solution together with glucose and insulin resulted in improved nutritional intake and had no deleterious short-term effects on encephalopathy. However, judging from the plasma amino acid concentrations, the composition of the commercial mixture could be improved by reducing the glycine content.     

慢加急性乙型肝炎肝衰竭患者贫血特点分析

目的探索慢加急性肝衰竭患者贫血的发生、转归及对短期生存的影响。方法纳入2011年12月至2013年1月我院住院的乙型肝炎病毒感染导致的慢加急性肝衰竭患者,中心实验室常规检测血常规、血肌酐、谷丙转氨酶、谷草转氨酶、白蛋白、总胆红素、凝血功能指标等。与慢性乙型肝炎及HBV相关的肝硬化患者比较,观察慢加急性肝衰竭患者贫血的发生、转归。结果在纳入的171例肝病患者中,40例慢性乙型肝炎患者贫血发生率为2.5%,49例肝硬化患者为34.7%,82例慢加急性肝衰竭患者住院时贫血发生率为45.1%(其中26.8%为轻度贫血,17.1%为中度贫血,1.2%为重度贫血);慢加急性肝衰竭患者贫血程度在住院1周内加重(122.4 g/L对112.7 g/L,P0.001);长期生存患者(n=42)恢复期贫血情况显著改善(147.5 g/L对入院时的112.7 g/L,P=0.001);住院首日血红蛋白水平(截断点125.5 g/L)是90天生存率的预测因素(曲线下面积=0.735,P0.001)。结论慢加急性肝衰竭患者贫血发生率高,对短期生存不利,而生存者贫血情况可缓慢恢复;入院时血红蛋白水平能预测短期预后。