肝硬化患者的胆囊结石发生率及其与肝功能分级的关系

目的研究肝硬化患者胆囊结石的发生率与肝功能分级的关系。方法回顾性分析195例肝硬化患者的临床资料,以同期230例健康体检者为对照组。结果肝硬化患者的胆囊结石发病率明显高于健康对照组（43．1％比6．1％,P〈0．01）,且胆囊结石发病率与肝功能损害程度呈正相关,Child—PughB级和C级患者的胆囊结石发病率显著高于A级患者（A级25．5％比B级52．4％比C级44．7％,P〈0．01）。不同病因的肝硬化患者的胆囊结石发病率差异无统计学意义。胆囊结石为肝硬化患者合并急性胆囊炎、急性胰腺炎的主要原因（54．8％）,经积极抗炎、利胆等对症治疗后大部分患者症状好转。结论肝硬化患者的胆囊结石发病率明显增加,并与肝脏疾病的进展呈正相关。     

腺苷脱氨酶活性与肝脏疾病的关系

目的：探讨腺苷脱氨酶在肝脏疾病中的诊断价值。方法：应用全自动生化分析仪检测肝病患者血清腺苷脱氨酶（ADA）及肝功能各项指标。结果：脂肪肝患者血清ADA无明显升高；慢性乙型肝炎、急性肝炎、肝硬化及肝硬化合并肝癌患者血清ADA活性明显增高，与正常组比较有统计学意义（P〈0．01）；肝硬化患者、肝硬化合并肝癌患者血清ADA活性较慢性乙型肝炎患者明显升高，两组比较有统计学意义P〈0．01）；急性肝炎患者经治疗血清ADA明显降低，与发病早期比较有统计学意义（P〈0．05）；肝病患者血清ADA与白球蛋白比值、前白蛋白呈负相关，与总胆红素呈正相关。结论：肝病患者血清ADA增高提示肝病慢性化、逐渐进展，反映肝脏损害程度加重，肝脏储备、合成功能逐渐降低。     

肝硬化患者中血清总胆汁酸测定的临床意义

背景：胆汁酸在肝内合成和分泌，因此可以作为反映肝细胞损害的指标之一。目的：探讨肝硬化患者血清总胆汁酸（TBA）测定的临床意义。方法：收集42例肝硬化患者的肝功能资料，比较TBA与其他常规肝功能指标的敏感性差异。结果：肝硬化组的TBA显著高于健康对照组（P＜0．01），其水平为健康对照组的6．9倍，异常率为74％，显著高于丙氨酸转氨酶（ALT）、γ－谷氨酰转移酶（γ－GT）和碱性磷酸酶（ALP）（P＜0．01）。肝硬化失代偿期患者的TBA水平显著高于代偿期患者（P＜0．01）。结论：TBA是反映肝硬化患者肝细胞损害的敏感指标之一。     

功能磁共振成像在乙型肝炎相关慢性肝病检测中的应用

目的 探讨功能磁共振成像指标与慢性乙型肝炎、肝硬化程度动态变化的关系，并与血清肝纤维化标志物作对照分析。方法 对47例慢性肝病患者[慢性乙型肝炎6例，肝硬化41例（其中ChildA级14例，ChildB级12例；ChildC级15例）]及10名正常人（对照组）进行扩散加权成像（DWI），用不同的b值及b值差计算肝脏表观扩散系数（ADC）。灌注加权成像（PWI）测量肝脏强化参数：到达灌注峰值时间（TP）、血容量分布及肝脏强化曲线最大上升斜率（MSI）。相位对比法（PC）测门静脉血流速度、每分钟流量。所有入选者同时检测血清肝纤维化标志物：透明质酸（HA），Ⅲ型前胶原（PCⅢ）、层黏连蛋白（LN）和Ⅳ型胶原（CⅣ）。结果 （1）DWI：Child C级肝硬化组与对照组比，ADC3差异有统计学意义（P〈0．01），Child A、B级肝硬化组与对照组之间ADC3差异也有统计学意义（P值均〈0．05）。慢性乙型肝炎组和Child C级肝硬化组间ADC3差异有统计学意义（P〈0．01）。（2）PWI：Child A、B、C级肝硬化较对照组TP明显延长（P值均〈0．01）。肝脏MSI比较，对照组明显大于Child A、B、C级肝硬化组，差异有统计学意义，P值均〈0．01。（3）Child A、B、C级肝硬化组门静脉血流速度较慢性乙型肝炎组和对照组显著下降，差异有统计学意义，P值均〈0．01。（4）Child A、B、C级肝硬化组HA较慢性乙型肝炎组和对照组显著升高，差异有统计学意义，P值均〈0．01）；Child A、B．C级肝硬化组LN也明显高于慢性乙型肝炎组和对照组，P值均〈0．01；Child A，B、C级肝硬化组PCⅢ指标较对照组显著升高，P值均〈0．01。结论 功能磁共振成像指标能反映出慢性乙型肝炎、肝硬化的动态变化，对肝硬化的诊断及临床治疗有重要的参考价值。     

恩替卡韦联合中药内服外敷治疗乙型肝炎肝硬化随机多中心临床研究

目的评价中药内服外敷治疗乙型肝炎肝硬化的临床疗效及安全性。方法入组病例随机分组为对照组与治疗组,对照组单用恩替卡韦抗病毒治疗,治疗组加用中药内服外敷;观察肝功能、凝血功能、肝纤维化指标、超声、肝脏硬度值及中医证候积分。结果与对照组相比,中药内服外敷治疗24周患者ALT、AST、TBil、Alb、PT 明显改善（P＜0．01或 P＜0．05）;治疗48周AST、Alb、PT明显改善（P＜0．01）。与对照组相比,治疗组24周 HA、LN、PⅢP、Ⅳ-C及48周时HA、LN、Ⅳ-C均明显改善（P＜0．01）。肝脏硬度值（LSM ）基线水平比较,治疗组较高（P＜0．01）,治疗48周后,治疗组LSM下降显著（P＜0．05）。与对照组相比,内服外敷联合恩替卡韦治疗乙型肝炎肝硬化48周时,HBsAg滴度下降程度差异有统计学意义（P＜0．01）;治疗组48周脾脏厚度缩小程度差异有统计学意义（P＜0．05）。与对照组相比,治疗组24周中医证候积分未见明显改善（ P＞0．05）;治疗组48周显效率明显提高（ P＜0．01）,总有效率差异无统计学意义（93．3％比85％,P＞0．05）。结论中药内服外敷可有效改善乙型肝炎肝硬化患者肝功能,抑制肝纤维化及脾肿大进展程度,改善中医临床证候,对HBV有一定的抑制作用。     

慢性肝病患者血清总胆汁酸测定的临床意义

目的探讨各种慢性肝病患者血清总胆汁酸测定的临床意义。方法测定慢性肝病（脂肪肝、肝硬化及原发性肝癌）患者血清总胆汁酸浓度及其它肝功能指标[丙氨酸氨基转移酶（ALT）、门冬氨酸氨基转移酶（AST）、总胆红素（TBIL）],并与对照组进行比较。结果（1）慢性肝病患者血清TBA水平较对照组均升高,肝硬化及原发性肝癌患者血清TBA水平与对照组比较有显著性差异（P〈0.05）,且肝硬化患者升高更加显著（P〈0.01）;（2）肝硬化患者TBA随着child-pugh分级A、B、C级的升高逐渐递增,且C级与A、B级之间TBA水平比较有显著性差异（P〈0.01）;（3）脂肪肝、肝硬化及原发性肝癌患者的TBA阳性率分别为28.6%、88.3%和100%,肝硬化患者的TBA阳性率高于ALT、AST和TBIL;（4）肝硬化患者Child-Pugh C级TBA阳性率与A、B级比较差异有显著性（P〈0.05）,Child-Pugh分级B、C级TBA阳性率显著高于其他肝功能实验指标（P〈0.05）。结论血清TBA水平是反映肝实质损害的一项灵敏指标,对监测肝病的病情发展、严重程度、预后及治疗效果等方面具有重要的参考价值,而且在分析肝硬化患者肝损害方面比常规肝功能项目更为灵敏。     

14112例脂肪肝相关因素分析

目的：探讨脂肪性肝病（脂肪肝）的相关影响因素。方法分析14112健康查体者的临床资料,分析脂肪肝的相关影响因素。结果14112名受检者中,检出脂肪肝2874例,脂肪肝患病率为20．29％。其中男性患病率明显高于女性（ P＜0．01）;随着年龄增长脂肪肝患病率显著增加,在21～60岁体检人员中,男性检出率高于女性,在＞60岁者中女性的检出率高于男性;脂肪肝检出率随着体重指数增加显著上升。脂肪肝患者转氨酶异常发生率显著高于非脂肪肝者（P＜0．01）。结论性别、年龄、体质量指数、转氨酶与脂肪肝发病率有关。重点干预30～60岁肥胖男性及脂肪肝并转氨酶异常者有助于预防脂肪肝。     

血清甲状腺素检测对肝硬化患者的临床意义

目的：探讨肝硬化患者血清甲状腺激素水平的变化及其临床意义。方法：回顾分析经相关检查确诊的肝硬化患者125例。根据肝功能Child—Pugh分级分为A级、B级、C级3组,36例健康体检者为对照组,分别分析其游离三碘甲状腺原氨酸（F13）、游离甲状腺素（FT4）水平,并结合肝功能分级进行比较。结果：肝硬化患者血清FT3、FT4水平显著低于健康对照组（P〈0．01）,肝功能Child-Pugh B级组患者血清FT3、FT4水平显著低于A级组患者（P〈0．05）,肝功能Child-PushC级组患者血清FF3、FT4水平显著低于B级组患者（P〈0．01）。结论：肝硬化患者进行血清甲状腺素水平的检测有助于判断其病情严重程度及预后。     

血清总胆汁酸和4项肝纤维化指标与肝硬化Child-Pugh分级的关系

背景：血清总胆汁酸（TBA）以及肝纤维化指标Ⅲ型前胶原（PCU1）、Ⅳ型胶原（C-Ⅳ）、层黏蛋白（LN）和透明质酸（HA）水平可判断肝硬化程度，但国内外研究关于肝纤维化指标与Child-Pugh分级关系的结果并不完全一致。目的：研究肝硬化患者血清TBA含量以及PCⅢ、C-Ⅳ、LN、HA水平与肝硬化Child-Pugh分级的关系。方法：按Child．Pugh分级标准将42例肝硬化患者分为A、B、C三级，酶法测定血清TBA含量，放射免疫测定法检测空腹血清PCⅢ、C．IV、LN、HA水平。结果：血清TBA含量随Child．Pugh分级增高而升高，不同分级间有显著差异（P〈0．01）。肝功能C级患者血清PCU1水平显著高于A级患者（P〈0．05），各级肝功能患者间血清C-Ⅳ水平均无显著差异，肝功能C级患者血清LN水平显著高于A级和B级患者（P〈0．01，P〈0．05），肝功能B级和C级患者血清HA水平均显著高于A级患者（P〈0．01）。结论：血清TBA含量能灵敏地反映肝硬化患者肝功能损害程度，对指导肝硬化患者肝功能分级具有很好的参考价值；联合检测肝硬化患者血清PCU1、LN、HA对指导肝功能的分级也有一定意义。     

老年脂肪肝的生化检测与相关疾病的分析

目的：比较各项生化检查在脂肪肝诊断中的作用与了解分析脂肪肝与相关疾病的情况。方法：将受检人员进行体重，血压，心电，超声波，血生化检测。结果：脂肪肝组血清胆碱酯酶（CHE）活性升高最为显著（P＜0．01），有87％以上的脂肪肝患者血清CHE活性明显升高，老年脂肝组与某些相关疾病极其显著（P＜0．01），结论：老年脂肪肝与某些疾病密切相关，血清CHE活性明显增高是脂肪肝最突的生化特征。     

Impact of splenectomy in patients with liver cirrhosis: Results from 18 patients in a single center experience

Aim: With the recent advances in medical or surgical treatments in chronic hepatic disorders, the indications for splenectomy in hepatic disorders have greatly expanded. We performed splenectomy for cirrhotic patients and investigated the effects of splenectomy on hepatic functional reserve and nutrition metabolism. Methods: Eighteen patients (Child–Pugh B/C: 12/6; Child–Pugh A: excluded) who underwent splenectomy at our institute between 2005 and 2008 were enrolled. Twelve patients (67%) had hepatocellular carcinoma (HCC), eight of whom met the Milan criteria. Results: Overall survival rate was 83.3% at 1 year and 62.7% at 2 years. The survival rate of six patients with liver cirrhosis classified a Child–Pugh C was 80.0% at 1 year and 60.0% at 2 years. Three patients underwent hepatic resection and nine patients received ablation therapy against hepatocelluar carcinoma. Portal pressure decreased after splenectomy in most patients (mean decrease, 4.7 mmHg). Four weeks after the operation, the markers of hepatic functional reserve, indocyanine green retention rate at 15 min (ICGR15) and Technetium‐99m‐galactosyl human serum albumin value (^99mTc‐GSA), improved from 38.5% to 35.1% and from 0.773 to 0.788 (LHL15), respectively. The non‐protein respiratory quotient (npRQ) did not change in short period after the operation. Other outcomes, including liver function test in cirrhotic patients with long‐term (1 year) follow‐up after splenectomy (n = 7), did not improve significantly. Post‐operative complications included portal thrombus (n = 2), ascites (n = 2) were observed in six patients (33%). Conclusion: Splenectomy improved hepatic functional reserve and nutritional metabolism in some cases. However, the long‐term outcomes should still be evaluated.     

Factors influencing the prevalence of gallstones in liver cirrhosis

BACKGROUND AND AIMS: To investigate the prevalence of gallstone disease in Chinese patients with liver cirrhosis and to identify risk factors for cholelithiasis. METHODS: Blood samples were tested and ultrasonographic examination of the upper abdomen was conducted to observe the prevalence of gallstones in 90 compensated cirrhotic patients (Child-Pugh A), 180 decompensated cirrhotic patients (Child-Pugh B, C) and 300 controls. Risk factors for gallstone formation (age, sex, pregnancy, family history) and the characteristics of liver cirrhosis (Child class, inside diameter of portal vein), and gallbladder (wall thickness) were assessed. RESULTS: Gallstones were found more often in cirrhotic patients (23.7%) than in controls (7.33%, P < 0.001). The prevalence of gallstones in decompensated cirrhotic patients was higher than that of the compensated cirrhotic patients (P < 0.001). Advanced age, female sex, family history of gallstones, gallbladder wall thickness 4 mm or greater and inside diameter of portal vein 13 mm or greater were significantly associated with gallstone disease in patients with liver cirrhosis. Multivariate analysis revealed that age (P < 0.001), sex (P = 0.0005) and thickness (4 mm or greater) of the gallbladder wall (P = 0.0064) were independently associated with gallstone disease in such patients. CONCLUSIONS: This study confirms the high prevalence of cholelithiasis in liver cirrhosis. Age and sex are risk factors for gallstones and gallbladder wall thickness could be an additional risk factor for the development of gallstone in patients with liver cirrhosis.     

Five‐year survival predictive factors in patients with excessive alcohol intake and cirrhosis. Effect of alcoholic hepatitis,smoking and abstinence

Abstract: Aim: To evaluate 5‐year survival predictive factors in hospitalised patients with excessive alcohol intake and cirrhosis, including in a multivariate analysis the severity of the liver disease, gastrointestinal bleeding, concomitant viral B or C infection, smoking status, presence of alcoholic hepatitis at inclusion and abstinence from alcohol during follow‐up. Methods: In a non‐concurrent cohort study, 122 patients with excessive alcohol intake and cirrhosis were followed up at least five years or till death. Two patients were lost to follow‐up. Results: The 5‐year survival rates were 43% in the 122 patients and 66%, 50% and 25% in Child–Pugh class A, B and C patients, respectively. In multivariate analysis, age (P = 0.01), Child–Pugh score (P = 0.0001), gastrointestinal bleeding (P = 0.01), presence of HBs Ag and/or anti‐HCV (P = 0.03), smoking (P = 0.01), absence of histologically proven alcoholic hepatitis (P = 0.05) and persistent alcohol intake (P = 0.002) were associated with significantly increased risk ratios of death. Conclusions: In hospitalised patients with excessive alcohol intake and cirrhosis: (1) age, liver failure, gastrointestinal bleeding, concomitant viral B or C infection and persistent alcohol intake are independent poor prognostic markers, (2) smoking may contribute to the aggravation of cirrhosis, and (3) alcoholic hepatitis, being a potentially reversible cause of liver failure, has a favourable prognostic significance.     

Enhanced expressions of apelin on proliferative hepatic arterial capillaries in human cirrhotic liver

Aim: Apelin (APLN), the endogenous ligand of angiotensin-like receptor 1 (APJ), is a peptide necessary for embryonic and tumor angiogenesis. Little is known about the localization and changes of APLN expression including the sinusoids in human cirrhotic liver, which might contribute to portal hypertension. This study was designed to elucidate the localization and change of APLN expression in human liver during the progression of cirrhosis. Methods: Twelve normal liver specimens, eight specimens of Child–Pugh grade A cirrhosis, and 10 specimens of Child–Pugh grade C cirrhosis were studied. APLN protein and gene expression was examined by immunohistochemistry, western blotting, immunoelectronic microscopy, and laser captured microdissection (LCM) followed by polymerase chain reaction (PCR) in sinusoid. Results: In control liver tissue, APLN was localized mainly on arterial endothelial cells and hepatic arterioles in the portal tract. In cirrhotic liver tissue, aberrant APLN expression was observed in periportal capillary endothelial cells corresponding to capillarized sinusoids, and in proliferated arterial capillaries in the fibrotic septa. Significant overexpression of APLN at protein level in cirrhotic liver was demonstrated by western blotting (P < 0.01 Child–Pugh A and C versus control, P < 0.01 Child–Pugh A versus C). APLN mRNA expression in the sinusoid was confirmed by LCM-PCR. Conclusion: In humans, APLN protein and gene were overexpressed in cirrhotic liver compared with normal liver, and the magnitude increased as cirrhosis progressed. Especially in end-stage cirrhosis, APLN was strongly expressed in proliferated arterial capillaries directly connected with the sinusoids, suggesting a role of APLN in the proliferation of arterial capillaries in cirrhosis.     

Increased bile acid concentration in liver tissue with cholesterol gallstone disease

Patients with cholesterol gallstone disease have a reduced pool of bile acids. Overly sensitive feedback inhibition of bile acid synthesis has been postulated to explain this size reduction. To test this hypothesis, hepatic bile acid concentration and the activity of cholesterol 7-hydroxylase, the rate-limiting enzyme for bile acid biosynthesis, were determined in ten patients with cholesterol gallstones and ten patients without gallstones. The bile acids present in liver tissue are the sum of those returning to liver and those newly synthesized in liver. If an overly sensitive feedback inhibition truly existed in our gallstone patients, a decreased concentration of hepatic bile acids would have been expected. However, patients with cholesterol gallstones had significantly higher total (143.3 ±25.5 vs 64.5±10.8 nmol/g liver,P<0.01), chenodeoxycholic=" (64.1±9.9=" vs=">P<0.01), deoxycholic=" (22.8±10.9=" vs=">P<0.05), and=" ursodeoxycholic=" acid=" (6.2±1.4=" vs=">P<0.01) concentrations=" than=" patients=" without=" gallstones.=" the=" activity=" of=" cholesterol=">-hydroxylase did not differ significantly between the two groups. Impaired hepatic transport or secretion of bile acids is strongly suspected in cholesterol gallstone patients. The findings of the present study showed no evidence of overly sensitive feedback inhibition of bile acid synthesis in cholesterol gallstone patients. Bile acid pool size may be affected by the inappropriate increase of hepatic bile acids rather than by overly sensitive feedback inhibition.     

肝硬化患者胆囊运动功能与Child-Pugh分级的相关性研究

探讨肝硬化患者胆囊运动功能与Child-Pugh分级之间的关系。研究对象分为正常对照组14例和肝硬化组62例,并行Child—Pugh分级。全部受试者均行mTc—EHIDA肝胆动态显像得到:①潜伏期(LP);②排胆期(EP);计算③排胆分数(GBEF);④排胆率(ER)。比较正常对照组与肝硬化组GBEF、LP、ER,可见肝硬化患者GBEF和ER明显低于正常对照组(P<0．01),LP高于正常对照组(P<0．05)。Child-Pugh A级、B级、C级三组的胆石发生率和胆囊运动异常发生率分别为:7．7％和15．4％,19．0％和19．0％,35．7%和46．4％。Child-Pugh分级越高,胆囊运动异常发生率越高(P<0．05),胆结石发生率也越高(但P>0．05),同时胆囊壁厚度越厚(P<0．05)。肝硬化患者的胆囊运动功能减弱,且与肝功能损害程度有一定的关系。     

Assessment of adult patients with chronic liver failure for liver transplantation in 2015: who and when?

In 2015, there are a few absolute contraindications to liver transplantation. In adult patients, survival post‐liver transplant is excellent, with 1‐year survival rate >90% and 5‐year survival rates >80% and predicted median allograft survival beyond 20 years. Patients with a Child‐Turcotte Pugh score ≥9 or a model for end‐stage liver disease (MELD) score >15 should be referred for liver transplantation, with patients who have a MELD score >17 showing a 1‐year survival benefit with liver transplantation. A careful selection of hepatocellular cancer patients results in excellent outcomes, while consideration of extra‐hepatic disease (reversible vs irreversible) and social support structures are crucial to patient assessment. Alcoholic liver disease remains a challenge, and the potential to cure hepatitis C virus infection together with the emerging issue of non‐alcoholic fatty liver disease‐associated chronic liver failure will change the landscape of the who in the years ahead. The when will continue to be determined largely by the severity of liver disease based on the MELD score for the foreseeable future.     

Clinical factors predictive of insufficient liver enhancement on the hepatocyte-phase of Gd-EOB-DTPA-enhanced magnetic resonance imaging in patients with liver cirrhosis

Background

Estimating liver parenchymal enhancement prior to gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance (MR) imaging is crucial to accurate detection and characterization of focal hepatic lesions. We aimed to clarify the factors predictive of liver enhancement in a relatively large sample of patients.

Methods

Gd-EOB-DTPA-enhanced MR images of 328 patients with liver cirrhosis (Child–Pugh class A in 223 patients, class B in 71 patients, and class C in 34 patients) were analyzed retrospectively. The liver parenchymal signal intensity (SI) was measured in pre-contrast T1-weighted images and hepatocyte phase images. The relative enhancement (RE) was calculated: (hepatocyte phase SI–pre-contrast SI)/pre-contrast SI. We analyzed the correlation between hepatic function parameters and RE.

Results

RE of patients with Child–Pugh A cirrhosis was significantly higher than that of patients with Child–Pugh B or C cirrhosis (both P < 0.001). Among various clinical factors, platelet count, prothrombin activity, albumin, sodium, total bilirubin, aspartate aminotransferase, Model for End-stage Liver Disease (MELD) score, MELD-Na score, Child–Pugh score, and the presence of ascites were significantly correlated with RE. A multiple stepwise regression analysis revealed that MELD-Na, albumin, and the presence of ascites were the only factors that predicted liver parenchymal enhancement on hepatocyte-phase images.

Conclusion

The degree of liver parenchymal enhancement after Gd-EOB-DTPA administration was correlated with liver function parameters. Gd-EOB-DTPA-enhanced MR images require careful interpretation, particularly in patients with cirrhosis and clinical factors such as high MELD-Na score, hypoalbuminemia, or ascites.     

Clinicopathological analysis of non‐alcoholic steatohepatitis

OBJECTIVE : Based on liver biopsy samples collected during the past 10 years, the present study aimed to investigate the incidence of fatty liver, the relationship between fatty liver and other underlying liver diseases, and the clinical and pathological characteristics, and the risk factors of fatty liver. METHODS : From a total of 658 liver biopsy specimens collected from 1988 to 1997, there were 71 cases of fatty liver and 68 cases of non‐alcoholic fatty liver. Matched by sex and age, 155 specimens of non‐fatty liver were used as controls. All patients from which the biopsies were taken were tested for liver function, blood lipid profile, blood glucose and hepatitis virus markers. The liver biopsy samples were all investigated by the same pathologist. RESULTS : The prevalence of fatty liver among all the liver biopsies was 10.8%. The alanine aminotransferase, aspartate aminotransferase, total bilirubin and con‐jugated bilirubin levels in the fatty liver group were significantly lower than those in the non‐fatty liver group, whereas the triglyceride levels were higher. Pathologically, steatosis in patients with fatty liver was mainly located around the hepatic lobules, and macrovesicular steatosis was common. Of the 68 cases of non‐alcoholic fatty liver, hepatic cell necrosis was found in 35 cases (51.5%), inflammatory cell infiltration in 46 cases (67.6%) and fibrosis to various degrees in 19 cases (27.9%). CONCLUSION : Non‐alcoholic fatty liver is closely related to hyperlipidemia. In asymptomatic subjects with abnormal liver function, a liver biopsy is the only way to establish the type and severity of liver lesions.     

Relationships between blood levels of fat soluble vitamins and disease etiology and severity in adults awaiting liver transplantation

Background and Aims: Although malnutrition is common in liver disease, there are limited data on fat soluble vitamins in various diseases. The aims of this study were to: (i) determine fat soluble vitamin levels in patients assessed for liver transplantation; (ii) compare levels between different disease etiologies (hepatocellular and cholestatic) and between subgroups of hepatocellular disease; and (iii) assess the multivariate contribution to vitamin levels of etiology and various indicators of disease severity. Methods: This was a cross‐sectional study of 107 inpatients awaiting liver transplantation, mean age 47 years. Biochemical parameters included plasma retinol, 25‐hydroxycholecalciferol, and vitamin E. Biochemical (albumin, bilirubin and zinc) and clinical indicators (Child‐Pugh and Model of End Stage Liver Disease [MELD] scores) of disease severity were determined. Results: Deficiencies of retinol (< 1.0 µmol/L), 25‐hydroxycholecalciferol (< 50 nmol/L) and vitamin E (< 11 µmol/L) were present in 75%, 66% and 3%, respectively, of patients. Concentrations of retinol and vitamin E were lower in hepatocellular than cholestatic disease but 25‐hydroxycholecalciferol concentrations were similar. Child–Pugh score was higher in hepatocellular than cholestatic disease. Concentrations of retinol were lower in alcoholic liver disease (ALD) than hepatitis and Child–Pugh score was higher in ALD. For the whole group, levels of retinol, 25‐hydroxycholecalciferol and vitamin E were negatively related to Child–Pugh score, MELD score and bilirubin, and positively related to albumin. When Child–Pugh scores were controlled for, retinol was lower in the hepatocellular group. Conclusions: There was a high prevalence of fat soluble vitamin deficiencies with vitamin levels being related to disease severity. Retinol was lower in the hepatocellular group.