Energy metabolism in patients with acute and chronic liver disease

Energy expenditure and substrate oxidation rate for fat, glucose and protein were evaluated by indirect calorimetry in 20 normal individuals, 35 patients with acute hepatitis and 22 patients with biopsy-proven alcoholic cirrhosis in the postabsorptive state. Measurements were done in the resting state after an overnight fast (10 to 12 hr). Oxygen consumption (ml/min/1.73 m2) in normal subjects, in patients with acute hepatitis and in patients with cirrhosis was 206.5 +/- 4.0 (mean +/- S.E.M.), 216.4 +/- 4.7 and 228.8 +/- 7.1 (p less than 0.05 vs. controls), respectively. When related to body surface area (kcal/min/1.73 m2), resting energy expenditure did not differ between normal subjects (0.98 +/- 0.02), patients with acute hepatitis (1.03 +/- 0.02) and cirrhotic patients (1.06 +/- 0.03). However, when related to 24-hr urinary creatinine excretion as an estimate of lean body mass, energy expenditure was increased in cirrhosis (p less than 0.0001). In cirrhosis an inverse association between the severity of liver disease according to Pugh and oxygen consumption and resting energy expenditure was found. In cirrhotic patients the percentages of total calories derived from fat (86% +/- 5%), carbohydrate (2% +/- 4%) and protein (12% +/- 1%) were different from those of normal controls who metabolized 45% +/- 4%, 38% +/- 4%, 17% +/- 1%, respectively. In acute hepatitis no alterations in metabolism could be found apart from a decreased protein oxidation rate. In conclusion no appreciable changes in energy metabolism exist in acute hepatitis. The pattern of fuel use in cirrhosis resembles that in starvation.(ABSTRACT TRUNCATED AT 250 WORDS)     

肝硬化与骨代谢障碍

<正>慢性肝病引起的肝性骨病,在原发性胆汁性肝硬化、酒精性肝硬化和肝炎肝硬化最为常见。有研究指出,慢性肝病骨质疏松患者继发性骨折发生率达到20%~([1])。骨组织的细胞成分包括成骨细胞、骨细胞和破骨细胞,骨转换包括骨形成和骨吸收,其中成骨细胞的活化促进骨形成(bone formation),破骨细胞的活化促进骨吸收(bone resorption)。在慢性肝     

慢性肝病患者骨代谢变化的临床意义

为探讨慢性乙型肝炎（下称慢乙肝），乙肝肝硬化（下称肝硬化）与骨代谢的关系，分别对32例慢乙肝，32例肝硬化和31例对照组患者进行了骨钙素（BGP），甲状旁腺激素M（PTHM），血钙，血磷及尺桡骨骨密度（BMD）检测。结果显示，肝硬化组血清BGP水平较肝炎组和对照组明显降低（P＜0．05，＜0．01），血清PTHM水平较肝炎组及对照组升高（P＜0．05，＜0．05），两肝病组血钙水平较对照组明显下降（P均＜0．001），BMD较对照组降低（P＜0．001，＜0．01）；肝硬化组和肝炎组BGP均与BMD呈正相关。提示慢性病毒性肝病可出现调钙激素异常变化，且其骨质疏松随肝病加重而呈加重趋势。     

Angioma-like liver lesions in patients with chronic liver disease]

OBJECTIVE: The aim of this study was to evaluate in our healthcare area the clinical, ultrasonographic, and evolutionary features of patients with chronic liver disease and angioma-like liver lesions on ultrasonography. MATERIALS AND METHODS: We conducted a retrospective study amongst patients seen at the Ultrasonography Unit, Gastroenterology Department between January 2000 and June 2004. Included in the study were patients that presented with clinical and/or laboratory complaints consistent with chronic liver disease of any etiology, and those in which abdominal ultrasounds revealed the existence of at least one angioma-like liver lesion. All relevant epidemiological, clinical, ultrasonographic, and evolutionary data were carefully collected and recorded. RESULTS: In the course of our study, 58 patients were diagnosed with chronic liver disease and angioma-like liver lesions, of which 13 showed clinical, laboratory, ultrasonographic, and/or histological signs of liver cirrhosis. In 50% of patients these lesions were less than 10 mm in diameter, and in most cases were located in the right hepatic lobe. During an average follow-up period of 35 months (6-168 months) we verified that, in two patients, these lesions, initially interpreted as angiomas were in fact malignancies (one hepatocellular carcinoma and one metastatic adenocarcinoma of the gallbladder). In both cases, the patients were cirrhotic. Thus, our study revealed that 15% of lesions found in cirrhotic patients initially interpreted as angiomas were actually malignant.CONCLUSIONS: Our study revealed that, in patients with chronic liver disease, particularly in cirrhotic patients, a considerable percentage of ultrasonographic lesions originally interpreted as angiomas are in fact malignant tumors.     

Nutritional support in patients with chronic liver disease

Malnutrition is highly prevalent among patients with chronic liver disease and is nearly universal among patients awaiting liver transplantation. Malnutrition in patients with cirrhosis leads to increased morbidity and mortality rates. Furthermore, patients who are severely malnourished before transplant surgery have a higher rate of complications and a decreased overall survival rate after liver transplantation. In light of the high incidence of malnutrition among patients with chronic liver disease and the complications that result from malnutrition in these patients, it is essential to assess the nutritional status of all patients with liver disease, and to initiate treatment as indicated. This review addresses the etiologies of malnutrition, methods used to assess nutritional status, and appropriate treatment strategies.     

Fulminant hepatitis in patients with chronic liver disease

The changing epidemiology of hepatitis A virus (HAV) in the UK has led to a decline in natural immunity against the virus. It is estimated that in the UK, HAV is responsible for 10%-20% of cases of liver failure, and an overall mortality rate of 0.1%. It is clear that certain factors predispose patients to more severe HAV disease and increased mortality, although the reasons for this have yet to be elucidated. The age at which infection occurs clearly influences the outcome, with the risk of severe hepatitis increasing sharply after the age of 40 years. Intravenous drug users, homosexual men, individuals with an excessive alcohol intake or patients with chronic liver disease are also at increased risk of severe disease. An analysis of data from King's College Hospital was performed to determine the factors that influence the outcome or clinical course of HAV infection in at-risk patients. Data compiled from 1991 to 1998 revealed 187 cases with confirmed HAV, 45 of whom developed severe hepatitis. Outcomes were varied, eight (17.7%) patients developed acute liver failure and two (4.4%) died.     

Peptic ulceration in patients with chronic liver disease

A prospective study was undertaken to determine the frequency of peptic ulceration in different forms of chronic liver disease and the effect of corticosteroid treatment. One hundred sixty-three patients with chronic liver disease underwent upper gastrointestinal endoscopy, 106 for investigation of dyspeptic symptoms and the remaining 57 for assessment of the presence of varices. Twenty-four peptic ulcers were found (14.7%), 12 duodenal, 8 gastric, and 4 prepyloric. Ulcers were found in 5 of 15 patients with hepatitis B surface-antigen-positive chronic active liver disease (33%), 10 of 46 patients with alcoholic liver disease (22%), 5 of 35 with primary biliary cirrhosis (14%), 2 of 19 with miscellaneous chronic liver diseases (10%), and 2 of 25 with cryptogenic cirrhosis (8%). Ulcers were not demonstrated in any of the 23 patients with hepatitis B surface-antigen-negative chronic active hepatitis. Thirty-one patients were receiving prednisolone therapy, 5 had peptic ulcer compared with 19 of the remaining 132 patients. This difference was not significant. Fifty-nine patients presented with gastrointestinal bleeding on 88 separate occasions. Peptic ulcer was the cause in 6% of these. In chronic liver disease peptic ulcers occurred with differing frequencies in different forms of the disease. This was unaffected by corticosteroid therapy. Peptic ulcers were rarely the cause of gastrointestinal bleeding.     

Lipid absorption, bile acids, and cholesterol metabolism in patients with chronic liver disease

Faecal bile acids and neutral sterols of cholesterol origin were decreased in patients with chronic liver disease, while urinary bile acids were constantly, but never greatly, increased. Thus, production of cholesterol and its conversion to bile acids was decreased in these patients. Faecal fat was only slightly increased, even in cases with a very low bile salt output, but it was negatively correlated with faecal bile acids. The reduced capacity of these patients to synthesize bile acids was shown by the fact that cholestyramine treatment, although it decreased urinary bile acids, increased faecal bile acids only slightly. The resin constantly increased faecal neutral sterols, while the increase of faecal fat was insignificant. Thus, the absorption of fats, as compared with that of sterols, was less strongly reduced by interruption of the enterohepatic circulation of bile salts. In one cirrhotic patient markedly increased faecal bile acids apparently caused cholerrhoeic diarrhoea, which was easily controlled with cholestyramine. The latter consistently increased elimination of cholesterol in cirrhotic patients, but serum cholesterol was not consistently decreased, and in these patients, in contrast to the control subjects, it was difficult to detect changes in cholesterol synthesis with the acetate-mevalonate test and serum methyl sterols.     

Expired hydrocarbons in patients with chronic liver disease

Fifty patients with various types of liver disease and twenty-one healthy subjects were examined for lipoperoxidation in vivo by gaschromatographic assay of volatile hydrocarbons (ethane, ethylene, propane, n-butane, n-pentane) in breath gases. In 15 patients with alcoholic cirrhosis the amount of expired pentane was greater than in all the other groups examined. No significant increase of exhaled ethane, in contrast, was detected in the same patients. These results seem to indicate that pentane is a more sensitive index than ethane for ethanol-induced lipoperoxidation. This simple and non-invasive method opens up promising new opportunities for clarifying in humans, the role of lipoperoxidation in ethanol-induced liver damage, as well as in other chronic liver disease.     

Pregnancy in patients with chronic liver disease.

The pregnant patient with established chronic liver disease presents a unique situation in medicine. Although neither the pregnancy nor the liver disease is likely to specifically worsen the other, the combination can result in fatal complications for mother and infant. Fertility is decreased in patients with advanced liver disease and may provide a degree of protection for many patients who would be at increased risk should they become pregnant; however, pregnancy may occur even with advanced liver disease, and it is necessary to anticipate and plan for possible complications of the specific hepatic disease encountered. Counseling prior to pregnancy is the best policy, with consideration to transplantation prior to childbearing or to sterilization if it is more appropriate. Most problems associated with advanced liver disease are managed as in the nonpregnant patient; however, variceal bleeding may be a particularly difficult problem, and management here may necessitate portacaval shunt surgery.     

Platelet autoantibodies in patients with chronic liver disease

The thrombocytopenia in chronic liver disease (CLD) has been attributed mainly to hypersplenism, although other factors such as reduced mean life span with increased platelet turnover have also been demonstrated. Immunological abnormalities have been described in the pathogenesis and progression of CLD. In this sense, many studies have reported elevated levels of platelet associated IgG (PAIgG) in patients with CLD, and it has been suggested that PAIgG could represent true antiplatelet antibody. In this study we used a glycoprotein (GP)-specific immunoassay (MACE) to determine whether PAIgG or circulating antiplatelet antibodies, reacted against the GPIIb/IIIa or GPIb/IX complexes, in patients with CLD. Thirty-six patients with CLD of diverse etiology were studied (20 female, mean age 53 years, range 38–75 years). 23 out of 36 patients (64%) had anti-GP antibodies in MACE. Particularly, 12 had anti-GPIb, 4 anti-GPIIb/IIIa, and 7 had both types of autoantibodies. The existence of these anti-GP antibodies was not related with the blood platelet count or etiology of CLD. These data show that in patients with CLD of diverse origin, there is a high prevalence of autoantibodies reacting specifically with platelet membrane GP, which constitutes the first evidence of the specific nature of platelet-bound IgG in CLD. These findings suggest that in patients with CLD, an immune mechanism may participate in inducing or aggravating the thrombocytopenia.     

Alterations of glucose metabolism in chronic liver disease

The prevalence of glucose intolerance has been studied by oral glucose tolerance test in 670 patients affected by chronic liver disease. The glycometabolic status was evaluated by criteria given by WHO in 1980. Sixty-nine subjects appeared to be affected by chronic persistent hepatitis and 140 by chronic active hepatitis. In these patients the prevalence of diabetic responses (DR) did not differ much from that of the general population in our geographic area. In contrast, a markedly higher frequency of DR appeared in a cirrhotic group of 401 patients compared to non-cirrhotic subjects. The cirrhotics, divided according to different disease stages, showed a higher DR frequency in decompensated patients than in well compensated patients, the prevalence reaching 63% in the former subgroup. The coincident presence of hepatocarcinoma - documented in 60 other cirrhotic patients - does not modify the prevalence of diabetes. Other risk factors for diabetes such as age, sex, and family history have been considered. Our results suggest that: (1) all these factors seem not to play a major role in the pathogenesis of alterations of glucose metabolism in patients suffering from chronic liver disease, and therefore (2) liver cirrhosis by itself might be a risk factor in the disturbance of glucose tolerance.     

Increase of mexiletine plasma levels due to delayed hepatic metabolism in patients with chronic liver disease

The clinical relevance of changes in pharmacokinetics of oralmexiletine (600 mg daily dose) was studied in 82 patients withventricular arrhythmias and impaired liver, renal or heart function(control group n = 51, patients with liver cirrhosis n = 9,with renal insufficiency n = 14, or heart failure n = 8). Increasedplasma levels of mexiletine were found in patients with chronicliver disease (2.21 ± 0.94 µg/ml, versus, 0.63± 0.22µg/ml of controls, P < 0.01). Plasma levels in patients with renal insufficiency or heartfailure were not significantly different from the controls.The resulting elevated plasma levels in patients with livercirrhosis emphasize the importance of hepatic metabolism inthe elimination of mexiletine. Drug monitoring must be considerednecessary in patients with impaired liver function.     

举足轻重,持续关注肝病营养问题

正肝病营养,尤其是终末期和危重症患者的营养问题,在国际国内受到了越来越多的重视。在营养筛查、评定、营养支持治疗和随访管理等领域均涌现了一些有价值的新理念和新方法。1国际国内共识/指南陆续更新/出台,循证医学证据不断升级近年来,一些国际肝病和营养相关学会陆续发