The liver in heart failure

Severe congestive heart failure is associated with two distinct forms of liver dysfunction: jaundice that is related to passive congestion and acute hepatocellular necrosis that is caused by impaired perfusion. Cardiac cirrhosis (fibrosis) may result from prolonged recurrent congestive heart failure. Ischemic hepatitis (shock liver) usually manifests as asymptomatic elevation of the serum aminotransferase levels after an episode of hypotension, although the clinical presentation may mimic that of acute viral hepatitis. In most cases, ischemic hepatitis is of little clinical consequence and is self-limited. Acute liver failure may occur in patients with preexisting cirrhosis, severe chronic heart failure, or sustained hepatic ischemia.     

肝硬化上消化道出血并发缺血性肝炎的临床特征与预后

目的 研究乙型肝炎肝硬化上消化道出血患者中缺血性肝炎的发生率、临床特点及其对预后的影响.方法 回顾性分析了264例乙型肝炎肝硬化合并上消化道出血患者的资料,其中缺血性肝炎患者11例,分层随机抽样法选择同期无缺血性肝炎患者30例为对照,分析缺血性肝炎的临床特点.各种构成比及率的比较采用x2检验或直接概率法;出血前后各指标比较采用配对t检验,组间比较采用两独立样本t检验. 结果缺血性肝炎的发生率为4.17%,平均年龄为(43.1±5.7)岁,较对照组[(52.3±11.1)岁]年轻(P<0.05).ALT、AST快速升高超过正常值上限20倍,10 d内迅速恢复,伴有总胆红素、乳酸脱氢酶、碱性磷酸酶、γ-谷氨酰转肽酶的明显升高,胆碱酯酶下降,尿素氮、肌酐及白细胞数明显升高,与对照组比较差异有统计学意义(P<0.05).缺血性肝炎组病死率为54.5%(6/11),明显高于对照组的16.7%(5/30),P<0.05;感染、肝肾综合征,肝性脑病是其主要的死亡原因.缺血性肝炎组患者失血量200～3600 ml不等,休克患者占63.6%(7/11),出血量与缺血性肝炎无明显的相关性.结论 年龄小、失血性休克、肝脏储备功能差是乙型肝炎肝硬化患者发生缺血性肝炎的危险因素.肝硬化消化道出血并发缺血性肝炎患者,及时应用抗菌素防治感染,减少内毒素血症对于改善预后很重要.     

Hypoxic hepatitis: clinical and hemodynamic study in 142 consecutive cases

The centrilobular liver cell necrosis observed in hypoxic hepatitis is generally attributed to failure of hepatic blood perfusion. Accordingly, this injury of the liver is commonly recognized under the terms "shock liver" or "ischemic hepatitis." During a 10-year period, 142 episodes of hypoxic hepatitis were consecutively identified in the intensive care unit of a general hospital, and the clinical, biological, and hemodynamic parameters were prospectively collected on individual files. We conducted the current study to assess retrospectively the role of the hemodynamic mechanisms of tissue hypoxia: ischemia, passive venous congestion, and hypoxemia. Among the 142 episodes of hypoxic hepatitis, 138 were separated in 4 main groups based on clinical features: decompensated congestive heart failure (80 cases), acute cardiac failure (20 cases), exacerbated chronic respiratory failure (19 cases), and toxic/septic shock (19 cases). An elementary hemodynamic evaluation, including blood pressure, central venous pressure, and arterial blood gas analysis, was carried out in every episode and a more complete hemodynamic assessment through pulmonary artery catheterization was performed in 61 episodes.The hemodynamic mechanisms responsible for hypoxic hepatitis were different in the 4 groups. In congestive heart failure and acute heart failure, the hypoxia of the liver resulted from decreased hepatic blood flow (ischemia) due to left-sided heart failure and from venous congestion secondary to right-sided heart failure. In chronic respiratory failure, liver hypoxia was mainly due to profound hypoxemia. In toxic/septic shock, oxygen delivery to the liver was not decreased but oxygen needs were increased, while the liver was unable to use oxygen properly. In all conditions underlying hypoxic hepatitis, except toxic/septic shock, a shock state was observed in only about 50% of the cases. Therefore, the expressions "shock liver" or "ischemic hepatitis" are misleading and should be replaced by the more general term "hypoxic hepatitis."     

Ischemic hepatitis in patients with heart failure

Ischemic hepatitis is characterized by a marked and reversible elevation in either the serum alanine or aspartate aminotransferase level in a appropriate clinical setting that could lead to a reduction in hepatic blood flow, mainly in patients with heart failure. To establish the diagnosis other causes of hepatitis, such as virus and drugs, must be previously excluded. Centrilobular necrosis is the main histologic feature. In the present study we describe the three cases of ischemic hepatitis seen in our medical service during a period of one year. Its prevalence was 2.7% among all patients with heart failure admitted in our centre during the same period.     

丹红软肝胶囊对肝纤维化患者血小板生长因子的影响

目的:研究丹红软肝胶囊对肝纤维化患者血小板生长因子(PDGF)的影响.方法:以108例慢性乙型肝炎肝纤维化患者为观察对象,随机分为两组,治疗组56例采用丹红软肝胶囊治疗,对照组52例服用复方鳖甲软肝片,均治疗6个月,观察治疗前后患者血清肝功能、肝纤维化指标及PDGF含量的变化.结果:治疗6个月时,治疗组患者肝纤维化血清指标透明质酸(HA)、层粘连蛋白(LN)、Ⅳ型胶原(Ⅳ-C)和Ⅲ型前胶原( PCⅢ)水平较治疗前均显著降低(P＜0.05);肝功能丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)与治疗前比较均显著改善(P＜0.05);PDGF含量较治疗前明显降低(P＜0.05).上述指标与对照组比较差异无显著性意义(P＞0.05).结论:丹红软肝胶囊可能通过抑制PDGF的分泌来抑制肝纤维化的发生发展.     

Hypoxic hepatitis. Prospective, clinical and hemodynamic study of 45 cases

The authors report 45 episodes of centrilobular liver cell necrosis, called ischemic hepatitis, in 43 cardiac patients. In 75 percent of the episodes, centrilobular liver cell necrosis was preceded by a period of progressive deterioration of myocardiac function. In 100 percent of the episodes, liver cell necrosis occurred after an acute clinical event inducing a transient fall of cardiac output. Shock was observed in only 47 percent of the episodes. The biological hallmarks of this centrilobular liver cell necrosis were a massive increase in serum aminotransferase levels and in 85 percent of the episodes, a decrease in the prothrombine time below 50 percent of control level. The mortality rate, 15 days after admission, was 42 percent. Prognosis was mainly related to cardiac function. The hemodynamic comparison between the 45 episodes of centrilobular liver cell necrosis and 22 cases of cardiogenic shock without liver cell necrosis showed that, besides hepatic ischemia, passive venous congestion of the liver and arterial hypoxemia were also involved in the onset of liver cell necrosis in these cardiac patients. Among these 45 episodes of liver cell necrosis of cardiac origin, a unique case of hepatic necrosis secondary to major hypoxemia and passive venous congestion, despite an high cardiac output was observed and is reported in detail. Accordingly, the appellation "hypoxic hepatitis" seems to be more appropriate than "ischemic hepatitis".     

恩替卡韦治疗乙型肝炎肝硬化伴肝源性糖尿病的临床疗效研究

目的探究恩替卡韦治疗乙型肝炎肝硬化伴肝源性糖尿病的临床疗效。方法选取该院于2017年1月—2019年2月收治的160例乙型肝炎肝硬化伴肝源性糖尿病患者作为该次的研究对象,采用随机数表法将其平均分为两组,对照组患者采取常规护肝及降糖药物治疗,观察组患者在常规药物治疗的基础上联合恩替卡韦进行治疗,治疗后对比两组患者的肝功能各项指标以及血糖水平改善情况。结果采用不同药物进行治疗后,观察组患者的谷丙转氨酶(ALT)、天门冬氨酸氨基转移酶(AST)、血清白蛋白(ALB)、总胆红素(TBIL)等各项肝功能指标均优于对照组,差异有统计学意义(P<0.05);观察组患者的空腹血糖、餐后2 h血糖以及糖化血红蛋白的水平均明显低于对照组,差异有统计学意义(P<0.05)。结论在对乙型肝炎肝硬化伴肝源性糖尿病患者进行治疗时,在常规药物治疗的基础上联合恩替卡韦进行治疗,能够有效改善患者的各项肝功能指标,具有更高的降糖效果,值得广大医院进行推广和研究。     

Cirrhosis in children with celiac disease

BACKGROUND: Liver involvement represents an extra-intestinal feature of celiac disease (CD) and shows a clinical spectrum varying from nonspecific reactive hepatitis to cirrhosis. Here we report the association of cirrhosis with CD in 5 children. PATIENTS AND METHODS: The mean age of the patients was 9.4 +/- 2.8 years. Viral, metabolic, and autoimmune etiology of liver disease was ruled out. Intestinal and liver biopsies were performed to confirm the histologic diagnosis in all subjects. RESULTS: Three of the patients had chronic diarrhea and hepatosplenomegaly in whom diagnoses of CD and cirrhosis were established at presentation simultaneously. In the other 2 patients, CD was diagnosed following an initial diagnosis of cirrhosis. At diagnosis, alanine aminotransferase (range, 64-271 IU/L) and aspartate aminotransferase (range, 90-225 IU/L) values were elevated. After 1 to 5 years of a gluten-free diet (GFD), normalization of serum aminotransferase levels and clinical improvement were observed in 3 patients with strict GFD. The other 2 patients without improvement of the liver disease had poor dietary compliance. CONCLUSION: CD may be associated with severe hepatic damage in children and strict GFD may have beneficial effect on the course of liver disease. Serologic screening of CD should be included in differential diagnosis of chronic liver disease of unknown origin.     

Blood level of mitochondrial aspartate aminotransferase as an indicator of the extent of ischemic necrosis of the rat liver

To assess the severity of ischemic liver injury, we examined release of mitochondrial aspartate aminotransferase (EC 2.6.1.1) and its cytoplasmic isozyme from the ischemic rat liver into the circulation. Their patterns of leakage were quite different: the level of cytoplasmic aspartate aminotransferase reached a peak soon after the circulation to the ischemic liver was restored, while that of mitochondrial aspartate aminotransferase increased slowly, reaching a maximum after more than 10 hr. On anoxic incubation of mitochondria isolated from the normal liver, oxidative phosphorylation capacity was lost within 2 hr, at which time no leakage of matrix enzymes was observed: more than 10 hr after-loss-of-oxidative phosphorylation were needed for the matrix enzymes to leak out of the mitochondrial membrane. Since the viability of cells is considered to depend on the capacity of oxidative phosphorylation, it is highly likely that the delayed appearance of mitochondrial aspartate aminotransferase in blood indicates the postmortem changes of injured cells. In fact, the cumulative activity of mitochondrial aspartate aminotransferase but not cytoplasmic aspartate aminotransferase in circulation after ischemic liver injury correlated fairly well with the decrease of total adenine nucleotides which were monitored to measure viable cells. The difference between mitochondrial aspartate aminotransferase and cytoplasmic aspartate aminotransferase as quantitative indices of hepatic necrosis may be due to the relative stability of the former and significant inactivation of the latter during hepatic ischemia. Therefore, the determination of mitochondrial aspartate aminotransferase in blood may be useful in the assessment of liver necrosis after ischemic injury.     

Hypoxic hepatitis: the point of view of the clinician

Hypoxic hepatitis better known under the terms of ischemic hepatitis or shock liver is the clinical manifestation of an acute liver cell necrosis consecutive to liver hypoxia. The clinical syndrome is defined as a massive but rapidly resolutive increase in serum aminotransferase activities (AT) occurring in a clinical setting of hemodynamic failure. Actually, when confronted to a case of massive increase in serum AT in the setting of cardiac or respiratory failure, the diagnosis of HH may be assumed without liver biopsy if another cause of hepatocyte necrosis such as viral hepatitis or drug induced hepatitis may be excluded. To our opinion, in these patients often aged and in poor general condition, it is particularly important to exclude herpes simplex virus infection and paracetamol intoxication. In case of doubt, a mere ultrasonography of the liver will be helpful. Indeed the majority of these patients will have a dilation of hepatic veins due to passive congestion of the liver. There is no specific liver therapy and the prognosis is poor depending on the severity of the underlying condition. In this point of view, we report what could be of interest for the hospital clinician.     

Acute liver injury that followed food-dependent exercise-induced anaphylaxis.

We describe an unusual case of acute liver injury that followed food-dependent exercise-induced anaphylaxis (FDEIAn). A 45-year-old man who experienced anaphylactic shock induced by postprandial exercise and took alcohol that night was admitted the following day to our hospital because of general fatigue. Laboratory examinations revealed elevated hepatic enzymes (aspartate aminotransferase (AST) 6,110 IU, alanine aminotransferase (ALT) 4,178 IU). He had two similar episodes in the past. We speculated that acute liver injury in this case might be induced by interaction of anaphylactic shock and alcohol.     

Relationship between pyridoxal 5'-phosphate deficiency and aminotransferase levels in alcoholic hepatitis

The relationship between pyridoxal phosphate deficiency and activities of serum and liver aminotransferases was studied in 12 patients with alcoholic hepatitis. Plasma pyridoxal phosphate and the activities of liver aminotransferases were initially decreased in the patients, as compared with mean values in controls with normal hepatic histology. Addition of pyridoxal phosphate to liver homogenates increased liver alanine aminotransferase, but not aspartate aminotransferase, in all patients with initially low plasma pyridoxal phosphate. After 1 mo of abstinence from alcohol, with intake of an adequate diet and pyridoxine supplementation, plasma pyridoxal phosphate increased in all patients with initially low values (p less than 0.02). Serum aspartate aminotransferase decreased, whereas serum alanine aminotransferase increased, resulting in a decrease in their ratio in serum (p less than 0.001). Liver alanine aminotransferase increased (p less than 0.005), whereas liver aspartate aminotransferase remained unchanged. These data suggest that pyridoxal 5'-phosphate depletion is partially responsible for the low serum alanine to aspartate aminotransferase ratio that is typical of patients with alcoholic hepatitis.     

Effects of obstructive sleep apnea syndrome on serum aminotransferase levels in obese patients

PURPOSE: Obesity has been associated with obstructive sleep apnea and hepatic steatosis. We investigated the effects of obstructive sleep apnea and treatment with nasal continuous positive airway pressure (CPAP) on serum aminotransferase levels in obese patients. METHODS: We studied 40 obese men with obstructive sleep apnea syndrome. None had hepatitis B antigen or C antibody, autoimmune disease, or an excessive intake of alcohol. Serum levels of aspartate aminotransferase, alanine aminotransferase, triglyceride, glucose, insulin, and leptin were determined in the afternoon and in the morning immediately after sleep, before and after nasal CPAP treatment. RESULTS: Aminotransferase levels were abnormal in 35% (n = 14) of patients. Before treatment, mean (+/- SD) aspartate aminotransferase levels were higher in the morning than in the previous afternoon (presleep, 34 +/- 20 IU/L; postsleep, 39 +/- 28 IU/L; P = 0.006). The overnight mean increases in aminotransferase levels were less marked after the first night of nasal CPAP treatment (aspartate aminotransferase: from 6 +/- 11 IU/L to 2 +/- 6 IU/L, P = 0.0003; alanine aminotransferase: from 5 +/- 9 IU/L to 2 +/- 6 IU/L, P = 0.006). Leptin levels (n = 23) decreased significantly after treatment (P = 0.0002), whereas insulin resistance (calculated by the homeostasis model assessment method) and triglyceride levels were unchanged. Improvements in aspartate and alanine aminotransferase levels were maintained after 1 and 6 months of nasal CPAP treatment. CONCLUSION: Nasal CPAP therapy may have beneficial effects on serum aminotransferase abnormalities in obese patients who have obstructive sleep apnea.     

Continuous infusion of prostaglandin E1 via the superior mesenteric artery can prevent hepatic injury in hepatic artery interruption through passive portal oxygenation

AIMS/BACKGROUND: Hepatic artery interruption (HAI) causes severe ischemic liver damage, especially following hepatopancreatobiliary surgery. In order to inhibit a decrease in oxygen delivery after HAI, continuous infusion of PGE1 via the superior mesenteric artery (SMA) was administered in pigs and changes in hepatic blood flow and oxygen delivery were investigated. Furthermore, its effectiveness in the prevention of liver injury was evaluated by histology and serum enzyme levels. METHODS: Animals were subjected to HAI without PGE1 infusion (control group n=6) and to continuous infusion of PGE1 (0.02 microg/kg/min) into the SMA (PGE1 group n=6). RESULTS AND CONCLUSION: PGE1 infusion via the SMA not only increased the portal blood flow but also elevated the oxygen content of the portal blood. The reduction in oxygen delivery to the liver was 50% in the control group, and only 13% in the PGE1 group. Serum aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels 24 h after HAI in the control group were 3415+/-1283 IU/L and 9839+/-2959 respectively while in the PGE1 group they were 939+/-426 IU/L and 5510+/-1545 IU/L respectively. Histological examination showed massive necrosis in the control group at 72 h but only focal liver cell necrosis in the PGE1 group. Based on this finding and the fact that this treatment can be performed easily and safely, continuous infusion of PGE1 via the SMA may be a useful intervention to prevent severe liver damage after hepatic artery interruption.     

Protective effects of tumor necrosis factor α antibody and ulinastatin on liver ischemic reperfusion in rats

AIM: To study the protective effects of tumor necrosis factor α (TNFα) antibody and ulinastatin on liver ischemic reperfusion in rats.METHODS: One hundred and twenty male SD rats were randomly divided into four groups: normal control group, ischemic group, TNFα antibody group and TNFα antibody + ulinastatin group. The animals were killed at 0, 3, 6, 9, 12 h after ischemia for 60 min and followed by reperfusion. Serum alanine aminotransferase (ALT), malondialdehyde (MDA) and liver histopathology were observed.RESULTS: After ischemic reperfusion, the serum ALT and MDA were remarkably increased, and the hepatic congestion was obvious. Treatment of TNFα antibody and ulinastatin could significantly decrease serum ALT and MDA levels, and relieve hepatic congestion.CONCLUSION: Ulinastatin and TNFα antibody can suppress the inflammatory reaction induced by hepatic ischemic reperfusion, and have protective effects on rat hepatic ischemic reperfusion injury.     

Protective effects of tumor necrosis factor antibody and ulinastatin on liver ischemic reperfusion in rats

AIM: To study the protective effects of tumor necrosis factor α(TNFα) antibody and ulinastatin on liver ischemic reperfusion in rats.METHODS: One hundred and twenty male SD rats were randomly divided into four groups: normal control group,ischemic group, TNFα antibody group and TNFα antibody + ulinastatin group. The animals were killed at 0, 3, 6, 9,12 h after ischemia for 60 min and followed by reperfusion.Serum alanine aminotransferase (ALT), malondialdehyde (MDA) and liver histopathology were observed.RESULTS: After ischemic reperfusion, the serum ALT and MDA were remarkably increased, and the hepatic congestion was obvious. Treatment of TNFα antibody and ulinastatin could significantly decrease serum ALT and MDA levels,and relieve hepatic congestion.CONCLUSION: Ulinastatin and TNFα antibody can suppress the inflammatory reaction induced by hepatic ischemic reperfusion, and have protective effects on rat hepatic ischemic reperfusion injury.     

Recovery from severe hepatitis caused by mushroom poisoning without liver transplantation.

BACKGROUND & AIMS: Toxic mushroom poisoning leads to a variety of clinical outcomes ranging from self-limited gastrointestinal symptoms to fulminant hepatic failure requiring orthotopic liver transplantation. We reviewed the outcomes of patients with severe acute hepatitis secondary to mushroom poisoning, treated with contemporary modalities. METHODS: We retrospectively reviewed patients admitted to our institution over a 5-year period with elevated transaminase levels (>1000 IU/L) attributed to recent mushroom ingestion. The patients' clinical course, laboratory data, and treatment regimen were recorded and analyzed. RESULTS: Eight patients who presented with severe hepatitis after mushroom ingestion qualified for analysis. The mean peak serum levels were: aspartate transaminase 5488 IU/L, alanine transaminase 7618 IU/L, and total bilirubin 10.5 mg/dL. The mean peak prothrombin time was 31 seconds. One patient developed acute renal failure requiring hemodialysis. Three patients developed encephalopathy ranging from grade I to III. All 8 patients survived without significant morbidity or need for liver transplantation. Subgroup analysis revealed that older patients spent more days in the intensive care unit and subsequently had longer hospital stays. The older group also had a trend toward more severe laboratory abnormalities. CONCLUSIONS: Patients with severe hepatitis from mushroom poisoning are thought to have a poor prognosis and frequently need liver transplantation for survival. We suggest that with early and aggressive multidisciplinary care, such patients have improved outcomes and may avoid liver transplantation.     

Levels of plasma malondialdehyde and erythrocyte antioxidant enzyme activities in patients with chronic hepatitis B

BACKGROUND/AIMS: Hepatitis B virus infection, extensively seen throughout the world, can become highly chronic. Pathogenesis of chronic hepatitis is not yet known fully. It is shown that oxidative stress may play a role in pathogenesis and may regulate collagen synthesis and thus may contribute to the process of liver damage. This study is aimed at investigating the existence of oxidative stress in chronic hepatitis B cases and its relation with alanine aminotransferase and aspartate aminotransferase which are the serum indicators of liver damage; along with interaction of erythrocyte antioxidation enzyme activities in the same cases. METHODOLOGY: Eighty patients with chronic hepatitis B under follow-up, and 40 healthy volunteers were included in this study. In the control and patients groups, together with serological markers for viral etiology, alanine aminotransferase and aspartate aminotransferase levels; plasma malondialdehyde level; erythrocyte superoxide dismutase, glutathione peroxidase and catalase activities were analyzed. RESULTS: Malondialdehyde levels of chronic hepatitis B cases were statistically high compared to control group (p < 0.05). There was correlation between serum malondialdehyde levels and serum alanine aminotransferase, aspartate aminotransferase levels in the patient group (r = 0.324, p < 0.01, r = 0.273, p < 0.05). Average superoxide dismutase and catalase activities were found to be significantly low compared to control group (p < 0.001); average glutathione peroxidase activity were significantly high when considered statistically (p < 0.001). No correlation between serum alanine aminotransferase and aspartate aminotransferase levels and glutathione peroxidase, catalase and superoxide dismutase activities was found in the patients group (p > 0.05). CONCLUSIONS: In the study we showed that there is correlation between serum malondialdehyde level and alanine aminotransferase and aspartate aminotransferase levels of chronic hepatitis B patients. According to the results of our study, it might be thought that serum malondialdehyde level might be a marker of hepatocellular damage in chronic hepatitis B cases. We suggest that antioxidant treatment for chronic hepatitis B patients should be examined in future studies.     

Dietary iron restriction improves aminotransferase levels in chronic hepatitis C patients

BACKGROUND/AIMS: It is generally accepted that iron overload plays an important role in the pathogenesis of liver cell injury in chronic hepatitis C. The present study was undertaken to evaluate whether low-iron diet improves liver function tests in patients with chronic hepatitis C. METHODOLOGY: Seventeen patients with chronic hepatitis C (13 men and 4 women, 54 +/- 14 years old) that did not respond to, or were unsuitable for interferon therapy, were enrolled in this study. All patients had been pretreated with ursodeoxycholic acid for more than 12 months before the beginning of the study. Dietary iron intake was restricted to less than 7 mg/day, and the patients were followed up for 18 months. RESULTS: Mean daily iron intakes, calculated from food records, were 5.9 and 6.4 mg after 6 and 12 months, respectively. The mean serum ferritin decreased significantly from 362 ng/mL at entry to 179 ng/mL after 18 months. The serum unsaturated iron binding capacity level increased significantly from 163 micrograms/dL at entry to 203 micrograms/dL after 18 months. The serum aspartate aminotransferase decreased significantly from 62 IU/L at entry to 47 IU/L after 18 months, and serum alanine aminotransferase from 68 IU/L at entry to 53 IU/L after 18 months. Serum iron, hepatitis C virus-RNA titer and platelet count remained unchanged throughout the study. CONCLUSIONS: These results suggest that iron-restricted diet may be an important therapeutic modality for improving liver injury in patients with chronic hepatitis C.     

Ischemic hepatitis

Seven patients with cardiovascular disease had clinical episodes and marked transaminase elevations that suggested viral hepatitis, but all had morphologic evidence (from liver biopsy or autopsy specimens) that documented centrilobular necrosis (ischemic hepatitis) with no evidence of viral or drug injury. Several also had moderate or marked passive congestion of the liver so the liver biopsies of 15 additional patients were retrospectively reviewed. In this latter group congestion alone was associated with normal or minimal elevation in transaminases while all patients with notable (>5 times normal) transaminase elevations had centrilobular necrosis. Congestion alone, no matter how severe or prolonged, seems to do little if any damage to the liver. Centrilobular necrosis, or ischemic hepatitis, correlates with significant hypertransaminasemia, appears to result from failure of hepatic perfusion (with or without preceding hypotension), and presents with clinical and laboratory manifestations that suggest viral hepatitis.This study was supported, in part, by a grant from the James R. Dougherty, Jr. Foundation, Beeville, Texas.