Optimization of Liver Iron Load Assessment by Pixel-Based T2* MRI in Thalassemic Patients

Purpose: To improve liver iron load assessment by investigating the precision of different approaches of T2* Measurement. Background: Iron overload is a major problem in the treatment of thalassemic patients. Liver iron concentration (LIC) is an important index toward the management of body iron load. The accuracy of iron load estimation may suffer from the methodology of T2* measurement and there is no complete agreement upon the best approach of T2* calculation. Methods: 32 β-thallasemic patients (18 male) with the mean age of 20.0 ± 6.5 years were involved in this study. A multi-echo fast gradient-echo technique on a 1.5 T MRI system was used to measure liver iron overload and the T2* map of liver was reconstructed on a pixel-by-pixel basis. The T2* map and MRI images were utilized to deter- mine accurate location of ROI (region of interest). The mean of T2* were computed from the ROIs. The reproducibility of calculated T2* values in two methods were obtained. Moreover, the mean of the pixel’s T2* was calculated in the entire liver parenchyma of one slice. The T2* value of the entire slice was compared with the ROI approach. Results: In the ROI based method, the CoV for the intra-observer reproducibility was 8.5% and for the inter-observer was 9.78%. In the pixel based method, the CoVs for intra-observer and inter-observer reproducibility were 2.79% and 3.91%. There was an acceptable correlation (r = 0.96) between the T2* values calculated by the ROI and the entire slice. Conclusions: The pixel-based approach is more precise to determine the appropriate placement of the ROI. The assessment of T2* in the entire slice reduces the user-based errors significantly.

Liver iron content determination by magnetic resonance imaging

Accurate evaluation of iron overload is necessary to establish the diagnosis of hemochromatosis and guide chelation treatment in transfusion-dependent anemia. The liver is the primary site for iron storage in patients with hemochromatosis or transfusion-dependent anemia, therefore, liver iron concentration (LIC) accurately re? ects total body iron stores. In the past 20 years, magnetic resonance imaging (MRI) has emerged as a promising method for measuring LIC in a variety of diseases. We review the potential role of MRI in LIC determination in the most important disorders that are characterized by iron overload, that is, thalassemia major, other hemoglobinopathies, acquired anemia, and hemochromatosis. Most studies have been performed in thalassemia major and MRI is currently a widely accepted method for guiding chelation treatment in these patients. However, the lack of correlation between liver and cardiac iron stores suggests that both organs should be evaluated with MRI, since cardiac disease is the leading cause of death in this population. It is also unclear which MRI method is the most accurate since there are no large studies that have directly compared the different available techniques. The role of MRI in the era of genetic diagnosis of hemochromatosis is also debated, whereas data on the accuracy of the method in other hematological and liver diseases are rather limited. However, MRI is a fast, non-invasive and relatively accurate diagnostic tool for assessing LIC, and its use is expected to increase as the role of iron in the pathogenesis of liver disease becomes clearer.

A randomized trial of iron depletion in patients with nonalcoholic fatty liver disease and hyperferritinemia

AIM: To compare iron depletion to lifestyle changes alone in patients with severe nonalcoholic fatty liver disease (NAFLD) and hyperferritinemia, a frequent feature associated with more severe liver damage, despite at least 6 mo of lifestyle changes.

Iron and liver fibrosis: Mechanistic and clinical aspects

Liver fibrosis is characterised by excessive deposition of extracellular matrix that interrupts normal liver functionality. It is a pathological stage in several untreated chronic liver diseases such as the iron overload syndrome hereditary haemochromatosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and diabetes. Interestingly, regardless of the aetiology, iron-loading is frequently observed in chronic liver diseases. Excess iron can feed the Fenton reaction to generate unquenchable amounts of free radicals that cause grave cellular and tissue damage and thereby contribute to fibrosis. Moreover, excess iron can induce fibrosis-promoting signals in the parenchymal and non-parenchymal cells, which accelerate disease progression and exacerbate liver pathology. Fibrosis regression is achievable following treatment, but if untreated or unsuccessful, it can progress to the irreversible cirrhotic stage leading to organ failure and hepatocellular carcinoma, where resection or transplantation remain the only curative options. Therefore,understanding the role of iron in liver fibrosis is extremely essential as it can help in formulating iron-related diagnostic, prognostic and treatment strategies. These can be implemented in isolation or in combination with the current approaches to prepone detection, and halt or decelerate fibrosis progression before it reaches the irreparable stage. Thus, this review narrates the role of iron in liver fibrosis. It examines the underlying mechanisms by which excess iron can facilitate fibrotic responses. It describes the role of iron in various clinical pathologies and lastly,highlights the significance and potential of iron-related proteins in the diagnosis and therapeutics of liver fibrosis.

MicroRNAs and liver cancer associated with iron overload:Therapeutic targets unravelled

Primary liver cancer is a global disease that is on the increase.Hepatocellular carcinoma(HCC)accounts for most primary liver cancers and has a notably low survival rate,largely attributable to late diagnosis,resistance to treatment,tumour recurrence and metastasis.MicroRNAs(miRNAs/miRs)are regulatory RNAs that modulate protein synthesis.miRNAs are involved in several biological and pathological processes including the development and progression of HCC.Given the poor outcomes with current HCC treatments,miRNAs represent an important new target for therapeutic intervention.Several studies have demonstrated their role in HCC development and progression.While many risk factors underlie the development of HCC,one process commonly altered is iron homeostasis.Iron overload occurs in several liver diseases associated with the development of HCC including Hepatitis C infection and the importance of miRNAs in iron homeostasis and hepatic iron overload is well characterised.Aberrant miRNA expression in hepatic fibrosis and injury response have been reported,as have dysregulated miRNA expression patterns affecting cell cycle progression,evasion of apoptosis,invasion and metastasis.In2009,miR-26a delivery was shown to prevent HCC progression,highlighting its therapeutic potential.Several studies have since investigated the clinical potential of other miRNAs with one drug,Miravirsen,currently in phaseⅡclinical trials.miRNAs also have potential as biomarkers for the diagnosis of HCC and to evaluate treatment efficacy.Ongoing studies and clinical trials suggest miRNA-based treatments and diagnostic methods will have novel clinical applications for HCC in the coming years,yielding improved HCC survival rates and patient outcomes.

Molecular pathogenesis and clinical conse-quences of iron overload in liver cirrhosis

BACKGROUND: The liver, as the main iron storage compart-ment and the place of hepcidin synthesis, is the central organ involved in maintaining iron homeostasis in the body. Exces-sive accumulation of iron is an important risk factor in liver disease progression to cirrhosis and hepatocellular carcinoma. Here, we review the literature on the molecular pathogenesis of iron overload and its clinical consequences in chronic liver diseases. DATA SOURCES: PubMed was searched for English-language articles on molecular genesis of primary and secondary iron overload, as well as on their association with liver disease pro-gression. We have also included literature on adjuvant thera-peutic interventions aiming to alleviate detrimental effects of excessive body iron load in liver cirrhosis. RESULTS: Excess of free, unbound iron induces oxidative stress, increases cell sensitivity to other detrimental factors, and can directly affect cellular signaling pathways, resulting in accelerated liver disease progression. Diagnosis of liver cirrhosis is, in turn, often associated with the identiifcation of a pathological accumulation of iron, even in the absence of genetic background of hereditary hemochromatosis. Iron depletion and adjuvant therapy with antioxidants are shown to cause signiifcant improvement of liver functions in patients with iron overload. Phlebotomy can have beneifcial effects on liver histology in patients with excessive iron accumulation combined with compensated liver cirrhosis of different etiology. CONCLUSION: Excessive accumulation of body iron in liver cirrhosis is an important predictor of liver failure and avail-able data suggest that it can be considered as target for adju-vant therapy in this condition.

Iron overload and HFE gene mutations in Polish patients with liver cirrhosis

BACKGROUND:Increased liver iron stores may contribute to the progression of liver injury and fibrosis,and are associated with a higher risk of hepatocellular carcinoma development.Pre-transplant symptoms of iron overload in patients with liver cirrhosis are associated with higher risk of infectious and malignant complications in liver transplant recipients.HFE gene mutations may be involved in the pathogenesis of liver iron overload and influence the progression of chronic liver diseases of different origins.This study was designed to determine the prevalence of iron overload in relation to HFE gene mutations among Polish patients with liver cirrhosis.METHODS:Sixty-one patients with liver cirrhosis included in the study were compared with a control group of 42 consecutive patients subjected to liver biopsy because of chronic liver diseases.Liver function tests and serum iron markers were assessed in both groups.All patients were screened for HFE mutations (C282Y,H63D,S65C).Thirty-six of 61 patients from the study group and all controls had liver biopsy performed with semiquantitative assessment of iron deposits in hepatocytes.RESULTS:The biochemical markers of iron overload and iron deposits in the liver were detected with a higher frequency (70% and 47% respectively) in patients with liver cirrhosis.There were no differences in the prevalence of all HFE mutations in both groups.In patients with a diagnosis of hepatocellular carcinoma,no significant associations with iron disorders and HFE gene mutations were found.CONCLUSIONS:Iron disorders were detected in patients with liver cirrhosis frequently but without significant association with HFE gene mutations.Only the homozygous C282Y mutation seems to occur more frequently in the selected population of patients with liver cirrhosis.As elevated biochemical iron indices accompanied liver iron deposits more frequently in liver cirrhosis compared to controls with chronic liver disease,there is a need for more extensive studies searching for the possible influence of non-HFE iron homeostasis regulators and their modulation on the course of chronic liver disease and liver cirrhosis.

Iron and non-alcoholic fatty liver disease

The mechanisms that promote liver injury in non-alcoholic fatty liver disease(NAFLD) are yet to be thoroughly elucidated. As such, effective treatment strategies are lacking and novel therapeutic targets are required. Iron has been widely implicated in the pathogenesis of NAFLD and represents a potential target for treatment. Relationships between serum ferritin concentration and NAFLD are noted in a majority of studies, although serum ferritin is an imprecise measure of iron loading. Numerous mechanisms for a pathogenic role of hepatic iron in NAFLD have been demonstrated in animal and cell culture models. However, the human data linking hepatic iron to liver injury in NAFLD is less clear, with seemingly conflicting evidence, supporting either an effect of iron in hepatocytes or within reticulo-endothelial cells. Adipose tissue has emerged as a key site at which iron may have a pathogenic role in NAFLD. Evidence for this comes indirectly from studies that have evaluated the role of adipose tissue iron with respect to insulin resistance. Adding further complexity, multiple strands of evidence support an effect of NAFLD itself on iron metabolism. In this review, we summarise the human and basic science data that has evaluated the role of iron in NAFLD pathogenesis.

Iron metabolism disorders in patients with hepatitis B-related liver diseases

AIM To investigate the relationship between levels of iron metabolism markers and hepatitis B virus(HBV)-related chronic liver diseases.METHODS This case-control study with 318 participants included 78 cases of chronic hepatitis B, 85 cases of HBV-related liver cirrhosis, 77 cases of HBV-related hepatocellular carcinoma, and 78 healthy controls. Markers of iron metabolism were detected in participants. Hematological and biochemical parameters and HBV-DNA were assessed. Child-Pugh grade and Barcelona Clinic Liver Cancer stage were determined for each hepatocellular carcinoma patient. Perls' staining was performed on liver sections. The SPSS program was used for all statistical analyses, and statistical significance was considered if a P-value < 0.05.RESULTS Significantly higher serum ferritin and lower serum hepcidin levels were detected in all groups of HBV-infected patients compared with healthy controls. Serum iron, total iron binding capacity, and serum transferrin levels were significantly lower in patients with cirrhosis and hepatocellular carcinoma, whereas the hepcidin level was higher than that in chronic hepatitis B patients. Correlation analysis indicated that serum hepcidin was negatively correlated with HBV-DNA load(P < 0.01). Serum ferritin and transferrin saturation levels increased proportionally to the extent of liver cirrhosis and poorer Child-Pugh scores(P < 0.05). The decreased serum iron and transferrin saturation levels were significantly correlated with a smaller hepatocellular carcinoma tumor burden according to Barcelona Clinic Liver Cancer staging. Liver histology showed a clearly increasing trend in iron deposition in the liver tissues with increased fibrosis, which became prominent at stages 3(severe liver fibrosis) and 4(cirrhosis). CONCLUSION Iron metabolism disorders occur in patients with HBVrelated liver diseases. The serum markers of iron metabolism disorders vary in different stages of HBV-related liver diseases.

Current status of superparamagnetic iron oxide contrast agents for liver magnetic resonance imaging

Five types of superparamagnetic iron oxide （SPIO）,i.e. Ferumoxides （Feridex？ Ⅳ, Berlex Laboratories）,Fe r u c a r b o t ra n （ Re s ov i s t？, B aye r H e a l t h c a re ） ,Ferumoxtran-10 （AMI-227 or Code-7227, Combidex？, AMAG Pharma; Sinerem？, Guerbet）, NC100150（Clariscan？, Nycomed,） and （VSOP C184, Ferropharm）have been designed and clinically tested as magneticresonance contrast agents. However, until nowResovist？ is current available in only a few countries.The other four agents have been stopped for furtherdevelopment or withdrawn from the market. AnotherSPIO agent Ferumoxytol （Feraheme） is approved forthe treatment of iron deficiency in adult chronic kidneydisease patients. Ferumoxytol is comprised of ironoxide particles surrounded by a carbohydrate coat, andit is being explored as a potential imaging approach forevaluating lymph nodes and certain liver tumors.

Liver steatosis correlates with iron overload but not with HFE gene mutations in chronic hepatitis C

BACKGROUND: Liver steatosis and iron overload, which are frequently observed in chronic hepatitis C (CHC), may contribute to the progression of liver injury. This study aimed to evaluate the correlation between liver steatosis and iron overload in Polish patients with CHC compared to non- alcoholic fatty liver disease (NAFLD) and HFE-hereditary hemochromatosis (HH) patients. METHODS: A total of 191 CHC patients were compared with 67 NAFLD and 21 HH patients. Liver function tests, serum markers of iron metabolism, cholesterol and triglycerides were assayed. The inflammatory activity, fibrosis, iron deposits and steatosis stages were assessed in liver specimens. HFE gene polymorphisms were investigated by PCR-RFLP. RESULTS: Liver steatosis was associated with obesity and diabetes mellitus. This disease was confirmed in 76/174 (44%) CHC patients, most of whom were infected with genotype 1. The average grade of steatosis was higher in NAFLD patients. CHC patients had significantly higher iron concentrations and transferrin saturations than NAFLD patients. Compared with CHC patients, HH patients had higher values of serum iron parameters and more intensive hepatocyte iron deposits without differences in the prevalence and intensity of liver steatosis. In the CHC group, lipids accumulation in hepatocytes was significantly associated with the presence of serummarkers of iron overload. No correlation between the HFE gene polymorphism and liver steatosis in CHC patients was found. CONCLUSIONS: Liver steatosis was diagnosed in nearly half of CHC patients, most of whom were infected with genotype 1. The intensity of steatosis was lower in CHC patients than that in NAFLD patients because of a less frequent diagnosis of metabolic syndrome. Only in CHC patients were biochemical markers of iron accumulation positively correlated with liver steatosis; these findings were independent of HFE gene mutations.

Recent advances in liver preconditioning: Thyroid hormone, n-3 long-chain polyunsaturated fatty acids and iron

Liver preconditioning (PC), defined as an enhanced tolerance to injuring stimuli induced by previous specific maneuvers triggering beneficial functional and molecular changes, is of crucial importance in human liver transplantation and major hepatic resection. For these reasons, numerous PC strategies have been evaluated in experimental models of ischemia-reperfusion liver injury, which have not been transferred to clinical application due to side effects, toxicity and difficulties in implementation, with the exception of the controversial ischemic PC. In recent years, our group has undertaken the assessment of alternate experimental liver PC protocols that might have application in the clinical setting. These include thyroid hormone (T3), n-3 long-chain polyunsaturated fatty acids (n-3 LCPUFA), or iron, which suppressed liver damage due to the 1 h ischemia-20 h reperfusion protocol. T3, n-3 LCPUFA and iron are hormetic agents that trigger biologically beneficial effects in the low-dose range, whose multifactorial mechanisms of action are discussed in the work.

铁死亡在非酒精性脂肪性肝病发病中作用的研究进展

铁死亡是近年提出的一种新型细胞死亡方式,其主要特征为铁过载及脂质过氧化。铁死亡参与非酒精性脂肪性肝病的发生发展。铁过载可通过芬顿反应产生大量活性氧,在脂氧合酶的作用下,肝细胞膜上的不饱和脂肪酸发生脂质过氧化,从而诱导肝细胞死亡,导致非酒精性脂肪性肝病/非酒精性脂肪性肝炎的发生。阻断铁死亡可能成为保护肝细胞的治疗策略之一。

铁过载对不同类型高脂膳食所致肝损伤的影响

目的:探究铁过载联合不同类型高脂膳食对小鼠肝损伤的影响。方法:将48只SPF级雄性C57BL/6J小鼠按体重随机分为6组,每组8只,普通对照组(ND)、高铁对照组(NDFe)给予基础饲料,棕榈油高脂组(PHFD)、棕榈油高脂高铁组(PHFDFe)、大豆油高脂组(SHFD)和大豆油高脂高铁组(SHFDFe)分别给予对应高脂饲料。从第10周开始,NDFe、PHFDFe和SHFDFe组连续8周每周两次肌肉注射右旋糖酐铁100 mg/kg·bw,其余组注射等剂量生理盐水至第17周。麻醉后取血和肝脏,测定小鼠血清和肝脏生化指标、肝脏病理改变及铁代谢和脂代谢相关基因表达。结果:与对应高脂组相比,铁过载联合高脂膳食可使血清总胆固醇(Total cholesterol,TC)、肝脏甘油三酯(Triglyceride,TG)和谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-Px)水平显著下降(P<0.05),血清TG和谷丙转氨酶(Alanine aminotransferase,ALT)水平、肝脏系数、肝脏铁含量和丙二醛(Malondialdehyde,MDA)水平显著升高(P<0.05),SHFDFe组肝脏MDA水平显著高于PHFDFe组(P<0.05)。PHFDFe组二价金属转运蛋白1(Divalentmetal-iontransporter-1,DMT-1)和膜铁转运蛋白(Ferroportin,FPN)mRNA表达量显著高于PHFD组(P<0.05);SHFDFe组FPN mRNA表达量显著高于与NDFe、PHFDFe和SHFD组(P<0.05),乙酰CoA羧化酶1(acetyl-Coenzyme A carboxylase alpha 1,ACC1)和脂肪酸合酶(Fatty Acid Synthase,FASN)mRNA表达量显著低于SHFD组(P<0.05)。结论:铁过载联合高脂膳食会加重脂质代谢紊乱和氧化应激,铁过载联合大豆油高脂饲料喂养导致的肝损伤高于联合棕榈油高脂饲料喂养。

磁共振IDEAL-IQ序列对非酒精性脂肪性肝病患者肝脏脂肪及铁沉积的诊断价值

目的探讨磁共振IDEAL-IQ序列在非酒精性脂肪性肝病(NAFLD)定量评估中的价值。方法回顾性分析50例临床诊断为NAFLD患者的临床资料,收集年龄、性别、血糖、血脂、尿酸、肝功能等临床及实验室指标。所有患者均接受肝脏磁共振IDEAL-IQ序列扫描并通过测量获得肝脏脂肪分数(PDFF)及铁沉积(R2^(*))值,其中22例患者行肝脏活检并获得肝脏脂肪变性的病理学分级(S0~3级)。采用相关性分析评价PDFF及R2^(*)值与临床、实验室指标的相关性。采用ROC曲线分析PDFF值对不同程度脂肪肝的诊断效能,采用约登指数确定最佳截断值。结果PDFF值与UA、AST、ALT、HDL-C相关(r=0.425,P<0.01;r=0.584,P<0.01;r=0.505,P<0.01;r=-0.296,P<0.05);R2^(*)值与各临床及实验室指标无明显相关性(P>0.05);PDFF评估轻度(S1)、中度(S2)及重度(S3)脂肪肝的AUC值0.972(95%CI:0.905~1.000)、0.902(95%CI:0.765~1.000)、0.825(95%CI:0.528~1.000),P<0.05。结论PDFF值与多项生化指标相关,可作为补充指标定量评价NAFLD;与金标准比较,PDFF值对不同程度脂肪肝展现出良好的诊断效能。

中药基于铁死亡机制防治肝癌研究进展

肝癌是各种慢性肝脏疾病的终末阶段,在我国的发病率及病死率均较高。铁死亡是一种调节性细胞死亡(RCD)的现象,其机制与细胞内铁元素的代谢紊乱和过氧化物堆积有关。近年来对铁死亡相关通路的研究发现,铁死亡与肝癌的防治密切相关。中医认为“肝藏血”,而铁死亡发生的过程与血细胞中的铁存在相关性,积极探索中药调控铁死亡的机制,挖掘并提取传统中药的活性成分,对中药的现代化发展颇有裨益。现通过简单阐述铁死亡发生的机制,对中药如何通过各种通路调节干预肝癌细胞的活性和增殖、诱导肝癌细胞铁死亡进行综述,以期为中药防治该疾病开辟新思路。

铁死亡在不同肝脏疾病的研究进展

长期以来,肝脏疾病造成的死亡率一直偏高,已成为一个全球性的健康问题。肝细胞损伤促进了各种肝脏疾病的进展,故了解肝细胞是如何死亡的成为一个关键的研究领域。铁死亡是一种新发现的非凋亡形式的细胞死亡,其特征是铁依赖性脂质过氧化。近来研究发现,铁死亡在许多疾病的发生和发展中起着重要的调节作用,特别是肝脏疾病。对铁死亡的研究可能为各种肝脏疾病发病机制提供新的认识,并显示了铁死亡靶向治疗肝脏疾病的巨大潜力。本文简述了铁死亡的概念和启动机制,并讨论了铁死亡在各种肝脏疾病中的诱导或抑制作用。

Metabolically based liver damage pathophysiology in patients with urea cycle disorders-A new hypothesis

The underlying pathophysiology of liver dysfunction in urea cycle disorders(UCDs) is still largely elusive. There is some evidence that the accumulation of urea cycle(UC) intermediates are toxic for hepatocyte mitochondria. It is possible that liver injury is directly caused by the toxicity of ammonia. The rarity of UCDs, the lack of checking of iron level in these patients, superficial knowledge of UC and an underestimation of the metabolic role of fumaric acid, are the main reasons that are responsible for the incomprehension of the mechanism of liver injury in patients suffering from UCDs. Owing to our routine clinical practice to screen for iron overload in severely ill neonates, with the focus on the newborns suffering from acute liver failure, we report a case of citrullinemia with neonatal liver failure and high blood parameters of iron overload. We hypothesize that the key is in the decreased-deficient fumaric acid production in the course of UC in UCDs that causes several sequentially intertwined metabolic disturbances with final result of liver iron overload. The presented hypothesis could be easily tested by examining the patients suffering from UCDs, for liver iron overload. This could be easily performed in countries with a high population and comprehensive national register for inborn errors of metabolism. Conclusion: Providing the hypothesis is correct, neonatal liver damage in patients having UCD can be prevented by the supplementation of pregnant women with fumaric or succinic acid, prepared in the form of iron supplementation pills. After birth, liverdamage in patients having UCDs can be prevented by supplementation of these patients with zinc fumarate or zinc succinylate, as well.

MRI R2^(*)值鉴别肝细胞癌与肝内肿块型胆管癌

目的观察MRI定量R2^(*)值鉴别肝细胞癌(HCC)与肝内肿块型胆管癌(IMCC)的价值。方法回顾性分析106例HCC(HCC组)及49例IMCC(IMCC组)患者临床和上腹部MRI(包括2D多回波快速梯度回波序列R2^(*)Map图像)资料,比较2组肿瘤R2^(*)值、T2^(*)值、表观弥散系数(ADC)值、肿瘤近旁及远旁肝实质R2^(*)值、竖脊肌R2^(*)值,以及肿瘤与肝实质R2^(*)比值(T/L-R2^(*))和肿瘤与竖脊肌R2^(*)比值(T/M-R2^(*));绘制受试者工作特征曲线,计算曲线下面积(AUC),比较各参数鉴别HCC与IMCC的效能。结果相比IMCC组,HCC组男性、甲胎蛋白≥9 ng/ml、伴肝硬化、有假包膜、瘤内出血、动脉晚期非环形强化及门静脉期非环形廓清者占比均较高,而淋巴结转移者占比较低(P均<0.05)。HCC平均R2^(*)值为(32.58±9.52)Hz,高于IMCC[(21.64±6.64)Hz,P<0.05]。以肿瘤R2^(*)值、T/L-R2^(*)、T/M-R2^(*)及肿瘤T2^(*)值鉴别HCC与IMCC的效能差异均无统计学意义(P均>0.05)而均高于ADC值(P均<0.05)。肿瘤R2^(*)值的AUC为0.848;以25.79 Hz为最佳截断值,其鉴别HCC与IMCC的敏感度为77.36%、特异度为85.71%。结论MRI定量R2^(*)值可用于鉴别HCC与IMCC。

铁沉积对非酒精性脂肪性肝炎兔模型肝脏质子密度脂肪分数的影响

目的建立兔非酒精性脂肪性肝炎(NASH)模型,观察铁沉积对肝脏质子密度脂肪分数(PDFF)的影响。方法将70只新西兰大白兔随机分为单纯高脂组(A组,n=35)及高脂联合铁剂组(B组,n=35);再将B组分为1、2、3、4、8、12及16 ml共7个亚组,每组5只。对A组以高脂饲料饲养,对B组以高脂饲料饲养并经耳缘静脉注射右旋糖酐铁溶液(含铁100 mg/ml),建立NASH模型;行MRI及病理学检查,观察基于MRI所测PDFF与基于病理所测脂肪分数(FF)的相关性。结果建模结束时A、B组兔存活率分别为91.43%和74.29%,建模用时分别为(7.27±1.01)周和(5.07±1.27)周。B组各亚组中,随注射铁含量增加,MRI显示肝脏信号逐渐减低、胆囊及大血管显示欠清,其中1及2 ml亚组拟合优度分数均<5%、其余各亚组均≥5%,且仅1及2 ml亚组PDFF与FF相关(r=0.961、0.893,P=0.039、0.041)。结论NASH模型兔肝脏铁沉积增加将影响MRI测量肝脏PDFF的准确性。