单源双能CT成像碘(水)浓度值评估脂肪肝和肝岛血供的价值

目的:探讨单源双能CT能谱成像的碘(水)浓度值评估脂肪肝和肝岛血供的价值。方法:搜集行能谱CT扫描且诊断为脂肪肝及肝岛的20例患者。由两位放射科医生分别测量同一患者脂肪肝背景和肝岛的平扫及三期增强扫描的混合能量CT值及碘(水)浓度值,计算混合能量CT值及碘(水)浓度值的三期增强率。使用Bland-Altman图、直线回归分析及组内相关系数(ICC)检验两位观察者所测数据的一致性。比较脂肪肝与肝岛平扫、三期增强扫描的混合能量CT值及碘(水)浓度值的差异,比较脂肪肝与肝岛混合能量CT值及碘(水)浓度值三期增强率的差异。结果:两位观察者所测数据的一致性很好(ICC>0.75)。平扫及三期增强扫描中,肝岛的混合能量CT值和碘(水)浓度值均高于脂肪肝背景(P值均<0.001);脂肪肝与肝岛的混合能量CT值三期增强率差异均有统计学意义(P=0.006、P<0.001、P<0.001);脂肪肝与肝岛的碘(水)浓度值三期增强率差异均无统计学意义(P=0.455、P=0.279、P=0.279)。结论:单源双能CT能谱成像碘(水)值增强率评估脂肪肝与肝岛血供更可靠,证实肝岛与脂肪肝血供状态一致,为临床上鉴别肝岛与不典型乏血供肝脏肿瘤提供了相关依据。

超声检测脂肪肝患者胆囊床附近肝岛的发生率及临床意义

目的：研究脂肪肝患者胆囊床附近肝岛的发生率及临床意义。方法：搜集经超声诊断为脂肪肝的患者5／13例，其中男310例，女233例，年龄13～69岁，平均45．6岁。由同一超声科医生对所有患者进行腹部脏器常规超声检查，重点扫查胆囊床处肝组织。结果：81．9％的脂肪肝患者胆囊床处出现肝岛，轻度脂肪肝患者与中～重度脂肪肝患者胆囊床处肝岛的发生率分别为81．2％、87．1％，脂肪肝严重程度与肝岛的发生率无相关性（x2值为1．464，P值为0．226）。男性脂肪肝患者与女性脂肪肝患者胆囊床处肝岛发生率分别为83．5％、79．8％，性别与肝岛的发生率无相关性（x2值为1．245，P值为0．265）。结论：弥漫性脂肪肝患者胆囊床附近肝岛具有较高的发生率，在与肝内占位性病变及胆囊病变侵及肝脏的鉴别诊断中应予以考虑。

CT与MRI在诊断球形肝岛及局灶性脂肪变性中价值和意义

目的:探讨CT、MRI在诊断球形肝岛及局灶性脂肪变性中价值及临床意义。方法:回顾分析78例经CT或MRI复查证实的球形肝岛及局灶性脂肪变性完整病例资料。结果:脂肪肝中的正常肝岛56例,其中单发圆形或椭圆形肝岛15例、多发圆形或椭圆形的41例。正常肝内局灶性脂肪变性22例,均为单发圆形或团块状病灶。增强前、后CT显示正常肝岛保持正常肝组织与脾脏密度关系;肝组织局灶脂肪变性呈相对低密度。MRI SE T1、T2WI及梯度回波同相位T1WI显示正常肝岛相对低信号区;局灶脂肪变性区呈稍高信号。梯度回波反相位T1WI正常肝岛呈高信号;局灶脂肪变性区呈低信号。脂肪抑制T2WI均呈等信号。结论:MRI比CT在诊断球形肝岛及局灶性脂肪变性中更有优势,在CT上与肝占位鉴别困难时应做MRI确定。

能谱CT碘浓度增强率在评估脂肪肝合并肝岛血供方面的优势

研究能谱CT碘水浓度增强率在评估脂肪肝和肝岛血供方面的价值。方法 收集60例脂肪肝合并肝岛的病例,对平扫、三期增强的混合能量CT值和碘水浓度值进行统计和分析。结果 肝岛的数据均显著大于脂肪肝,且脂肪肝和肝岛在混合能量CT值的增强率中具有显著性差异。在碘水浓度增强率方面,脂肪肝和肝岛无显著性差异。结论 能谱CT的碘水浓度增强率可用于评估脂肪肝和肝岛血供,对于鉴别乏血供非典型肿瘤具有显著优势。

超声造影对脂肪肝低脂灶诊断的应用价值

目的:探讨实时超声造影技术对脂肪肝中低脂灶诊断价值。方法:对58例脂肪肝患者中肝内65个低脂灶进行超声造影检查,实时观察病灶的增强模式。结果:常规超声44个(67.7%)病灶诊断为低脂灶,呈低回声;超声造影检查63个(96.9%)病灶诊断为低脂灶,表现为动脉期、门脉期及延迟期呈等增强;2个(3.1%)病灶诊断为良性病变,考虑为低脂灶的可能性大,动脉早期呈一过性高增强,动脉期和门脉期呈等增强。常规超声诊断低脂灶符合率为67.7%,超声造影为96.9%。结论:超声造影有助于低脂灶的诊断和鉴别诊断,是除增强CT、MRI以外的可行的诊断方法。

MRI检查对肝脏Ⅰ、Ⅳ段CT上不典型脂肪肝诊断的影像研究

目的:探讨MRI检查对肝脏Ⅰ、Ⅳ段CT上不典型脂肪肝诊断的影像。方法:将2018年2月到2019年9月我院收治的45例肝脏Ⅰ、Ⅳ段CT上不典型脂肪肝患者作为研究对象,对其予以CT与MRI扫描检查,对患者的病灶类型及其病灶分布情况、CT表现与MRI表现进行观察。结果:①15例患者为局灶性脂肪肝类型,共18个病灶,其中12例患者为单发,3例患者为双发;在病灶位置方面,Ⅰ段患者共3例,共3个病灶,Ⅳ段患者共12例,共15个病灶。②30例患者肝岛类型,共36个病灶,其中23例患者为单发,7例患者为双发;在病灶位置方面,Ⅰ段患者共5例,共5个病灶,Ⅳ段患者共25例,共31个病灶。经CT检查并未能够对患者进行确诊;在MRI常规扫描中仅能够对少数具有较多脂肪含量的病灶进行辨认;与反相位像上的信号强度及周围肝组织病变相比,18个局灶性脂肪肝病灶在同相位像上的信号具有更高的强度表现;在反相位像上,36个肝岛病灶均表现出较强的信号分布特点,而周围肝组织的信号强度则较低,从而明确肝岛与正常肝组织界限。结论:MRI检查对肝脏Ⅰ、Ⅳ段CT上不典型脂肪肝诊断具有积极影响,不仅能够明确患者的疾病类型,同时能够明确病灶位置。

Non-invasive means of measuring hepatic fat content

Hepatic steatosis affects 20% to 30% of the general adult population in the western world. Currently, the technique of choice for determining hepatic fat deposition and the stage of fibrosis is liver biopsy. However, it is an invasive procedure and its use is limited, particularly in children. It may also be subject to sampling error. Non-invasive techniques such as ultrasound, computerised tomography (CT), magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (1H MRS) can detect hepatic steatosis, but currently cannot distinguish between simple steatosis and steatohepatitis, or stage the degree of fibrosis accurately. Ultrasound is widely used to detect hepatic steatosis, but its sensitivity is reduced in the morbidly obese and also in those with small amounts of fatty infiltration. It has been used to grade hepatic fat content, but this is subjective. CT can detect hepatic steatosis, but exposes subjects to ionising radiation, thus limiting its use in longitudinal studies and in children. Recently, magnetic resonance (MR) techniques using chemical shift imaging have provided a quantitative assessment of the degree of hepatic fatty infiltration, which correlates well with liver biopsy results in the same patients. Similarly, in vivo 1H MRS is a fast, safe, non-invasive method forthe quantification of intrahepatocellular lipid (IHCL) levels. Both techniques will be useful tools in future longitudinal clinical studies, either in examining the natural history of conditions causing hepatic steatosis (e.g. non-alcoholic fatty liver disease), or in testing new treatments for these conditions.

Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD)in rats

Objective： The prevalence of non-alcoholic fatty liver disease （NAFLD） has markedly increased. Insulin resistance has been implicated in the pathogenesis of NAFLD. This study was aimed at observing the relationship between insulin resistance and NAFLD, and evaluating the role of pioglitazone （PGZ） acting as insulin-sensitizing agents in the prevention and treatment of rat fatty liver induced by high fat feeding. Methods： The rats were separated randomly into 6 groups： model group Ⅰ were fed high fat diet for 8 weeks, PGZ prevention group were given PGZ 4 mg/（kg.d） simultaneously, while control group Ⅰ were fed normal food for 8 weeks; model group Ⅱ were fed high fat diet for 16 weeks, PGZ treatment group were given PGZ 4 mg/（kg.d） orally simultaneous with high fat diet for 8 weeks after high fat feeding for 8 weeks, control group Ⅱ were fed normal food for 16 weeks. The rats were sacrificed after 8 weeks and 16 weeks respectively. Liver weight, body weight, serum activities of alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, alkaline phosphatase （ALP）, tumor necrosis factor alpha （TNF-α）, fasting blood glucose （FBG）, fasting plasma insulin （FINS）, HOMA （homeostasis model assessment） insulin resistance index （HOMA-IR）, and the liver histology of rats of all groups were assayed. Results： After 8 weeks, the liver in model group Ⅰ showed typical steatosis, accompanied with mild to moderate lobular inflammatory cell infiltration, liver indexes and serum levels of ALT, AST, ALP, TNF-α were significantly increased （P〈0.05） compared with control group Ⅰ. Whereas, the degree of hepatic injury was attenuated in PGZ prevention group, liver indexes and serum levels of ALT, ALP were significantly decreased （P〈0.05） compared with model group Ⅰ. After 16 weeks, notable steatosis, and lobular inflammation were observed in model group Ⅱ rat liver, while the degree of hepatic injury was attenuated in the PGZ treatment group. Liver index, serum levels ofALT, AST, ALP, FINS and HOMA-IR were significantly increased （P〈0.05） in model group Ⅱ compared with control group Ⅱ. Whereas, in PGZ treatment group, serum levels of AST and FINS showed decreasing tendency, liver indexes, serum levels of ALT, ALP, TNF-α and HOMA-IR were significantly decreased compared with model group Ⅱ. Conclusion： Insulin resistance plays a role in the pathogenesis of NAFLD in rats. Pioglitazone can attenuate insulin resistance and biochemical and histological injury in high fat-induced fatty liver in rats.

Visceral fat and insulin resistance as predictors of non-alcoholic steatohepatitis

AIM： To examine whether visceral fat is associated with non-alcoholic steatohepatitis （NASH）, to assess for parameters associated with visceral adiposity and to investigate for factors associated with fibrotic severity in NASH. METHODS： Thirty NASH and 30 control subjects underwent biochemical tests, anthropometric assessment, bioelectrical impedance, dual energy X-ray absorptiometry and abdominal fat study by CT scan. Liver biopsies were graded according to the Brunt criteria. RESULTS： NASH subjects had elevated blood pressure, body mass index, waist circumference and waist-to-hip ratio. A greater number of diabetes rnellitus, impaired glucose tolerance test and HOMA-IR 〉 3.5 were found in NASH patients. HOMA-IR 〉 2.8 （OR 20.98, 95% CI 3.22-136.62; P 〈 0.001） and visceral fat area 〉 158 cm^2 （OR 18.55, 95% CI 1.60-214.67; P = 0.019） were independent predictors for NASH. Advanced stage of NASH was found in 15 （50%） patients. HOMA-IR 〉 3.5 （OR 23.12, 95% CI 2.00-266.23; P = 0.012） and grading of portal inflammation （OR 7.15, 95% CI 1.63-31.20; P = 0.009） were determined as independent risk factors for advanced stage of NASH. CONCLUSION： Obesity （especially central obesity） and metabolic syndrome are common in Thai NASH. Insulin resistance and elevated visceral fat are risk factors for the presence of NASH. The advanced stage of thedisease is related to insulin resistance.

Iron overload and cofactors with special reference to alcohol,hepatitis C virus infection and steatosis/insulin resistance

There are several cofactors which affect body iron metabolism and accelerate iron overload. Alcohol and hepatic viral infections are the most typical examples for clarifying the role of cofactors in iron overload. In these conditions, iron is deposited in hepatocytes and Kupffer cells and reactive oxygen species （ROS） produced through Fenton reaction have key role to facilitate cellular uptake of transferrin-bound iron. Furthermore, hepcidin, antimicrobial peptide produced mainly in the liver is also responsible for intestinal iron absorption and reticuloendothelial iron release. In patients with ceruloplasmin deficiency, anemia and secondary iron overload in liver and neurodegeneration are reported. Furthermore, there is accumulating evidence that fatty acid accumulation without alcohol and obesity itself modifies iron overload states. Ineffective erythropoiesis is also an important factor to accelerate iron overload, which is associated with diseases such as thalassemia and myelodysplastic syndrome. When this condition persists, the dietary iron absorption is increased due to the increment of bone marrow erythropoiesis and tissue iron overload will thereafter occurs. In porphyria cutanea tarda, iron is secondarily accumulated in the liver.

Hepatic steatosis:A benign disease or a silent killer

Steatosis is a common feature of many liver diseases,namely non-alcoholic steatohepatitis(NASH) and hepatitis C virus(HCV) infection,but the pathogenic mechanisms differ.Insulin resistance(IR),a key feature of metabolic syndrome,is crucial for NASH development,associated with many underlying genetically determined or acquired mitochondrial and metabolic defects and culminates to inflammation and progression to fibrosis.This may have potential implications for new drug therapy.In HCV-related disease,steatosis impacts both fibrosis progression and response to treatment.Steatosis in HCV-related disease relates to both viral factors(HCV genotype 3),and host factors(alcohol consumption,overweight,hyperlipidemia,diabetes).Among others,IR is a recognized factor.Hepatic steatosis is reported to be associated with disturbance in the signaling cascade of interferon and downregulation of its receptors.Thus,hepatic steatosis should not be considered a benign feature,but rather a silent killer.

The blind men 'see' the elephant-the many faces of fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is a group of diseases with excess fat in liver in the absence of a poorly defined limit of alcohol consumption. Most common variety, a universal public health problem, is associated with insulin resistance caused by a host of genetic and epigenetic defects modulated by life style and environmental factors. In fact the term NAFLD is loose to incorporate so many etiologies except alcoholism and few other etiologies, presenting as fat in liver. However as a sign fatty liver is very important in predicting the risk of diabetes, cardiovascular disease, stroke, cirrhosis and cancer. Abnormal fat accumulation can result from several defects in nuclear receptors associated with lipid sensing, synthesis and oxidation like LXR, FXR, SREBP, ChREBP and PPAR; defects in the lipid influx-efflux channels, insulin signaling, proteins involved in fatty acid catabolism, defects in adipose tissue development and function, inappropriate nutrition and finally defects in neural regulatory mechanisms. The progress of the disease is determined by the basic defects which results in fat accumulation, an individual’s immunological response to the accumulated fat and its derivatives and the oxidant stress response. Congregation of unrelated genetic defects under same diagnosis ‘NAFLD’ can result in inefficient patient management. Further studies are required to understand the molecular basis of fatty liver to enable a personalized management of diseases presenting as fatty liver in the absence of alcohol abuse.

Diabetes mellitus, insulin resistance and hepatitis C virus infection: A contemporary review

To summarise the literature data on hepatitis C virus (HCV)-infected patients concerning the prevalence of glucose abnormalities and associated risk.METHODSWe conducted a PubMed search and selected all studies found with the key words 'HCV' or 'hepatitis C virus' and 'diabetes' or 'insulin resistance'. We included only comparative studies written in English or in French, published from January 2000 to April 2015. We collected the literature data on HCV-infected patients concerning the prevalence of glucose abnormalities [diabetes mellitus (DM) and insulin resistance (IR)] and associated risk [i.e., severe liver fibrosis, response to antivirals, and the occurrence of hepatocellular carcinoma (HCC)].RESULTSHCV infection is significantly associated with DM/IR compared with healthy volunteers and patients with hepatitis B virus infection. Glucose abnormalities were associated with advanced liver fibrosis, lack of sustained virologic response to interferon alfa-based treatment and with a higher risk of HCC development. As new antiviral therapies may offer a cure for HCV infection, such data should be taken into account, from a therapeutic and preventive point of view, for liver and non-liver consequences of HCV disease. The efficacy of antidiabetic treatment in improving the response to antiviral treatment and in decreasing the risk of HCC has been reported by some studies but not by others. Thus, the effects of glucose abnormalities correction in reducing liver events need further studies.CONCLUSIONGlucose abnormalities are strongly associated with HCV infection and show a negative impact on the main liver related outcomes.

Effect of Breathwalk on body composition,metabolic and mood state in chronic hepatitis C patients with insulin resistance syndrome

AIM： To identify the anthropometric, metabolic and mood state in hepatitis C virus （HCV）-infected patients from the west of Mexico and to evaluate the effect of 13reathwalk （13W）, a combination of walking, synchronized breathing and focussed attention, on those patients. METHODS： In an experimental study, 17 patients with serological and molecular diagnosis of HCV, not receiving pharmacological treatment, were studied. One hour sessions of 13W were practiced 3 times at week for six months. Body composition was assessed by electric impedance. Biochemical profiles and insulin resistance （IR） risk was assessed by conventional methods. Mood state was evaluated with specific and open questions at the beginning and at the end of the program. RESULTS： Seventy percent of patients were overweight or obese, and 77% of the patients presented with IR at the beginning of the study. Improvements were observed at the 3^rd mo, and statistically significant differences were recorded at the 6^th mo using the fitness score （76 vs 83, P 〈 0.01）, in alanine aminotransferase （ALT）（106±93 U/L vs 59 ± 32 U/L, P 〈 0.01）, total bilirubin （0.09 ± 1 mg/dL vs 0.62 ± 0.2 mg/dL, P 〈 0.01）, ALT/ AST ratio （1.04 vs 0.70, P 〈 0.01）, triglycerides （165 ± 86 mg/dL vs 124 ± 49 mg/dL, P 〈 0.01） and the IR risk （4.0 vs 2.7）. Most patients （88%） indicated to feel better at the end of BW （P 〈 0.01）.CONCLUSION： Breathwalk has an important effect on body composition, lipid profile and liver enzymes. It is also easy, inexpensive and has a beneficial effect on metabolic and mood state in HCV patients.

CpG island methylator phenotype in plasma is associated with hepatocellular carcinoma prognosis

AIM： To evaluate the clinical significance of CpG island methylator phenotype （CIMP） in plasma and its association with hepatocellular carcinoma （HCC） progress. METHODS： CIMP status of 108 HCC patients was analyzed using a methylation marker panel in tumor tissues and plasma with methylation-specific polymerase chain reaction. Fifteen samples of non-neoplastic liver tissues and 60 of plasma from healthy persons were examined simultaneously. Examined genes included APC, WIF-1, RUNX-3, DI C-1, SFRP-1, DKK and E-cad.26/108, 24.07% in plasma; WIF-1, 53/108, 49.07% in tissue and 35/108, 32.41% in plasma; RUNX-3, 52/108, 48.14% in tissue and 42/108, 38.89% in plasma; DIC-1, 38/108, 35.18% in tissue and 23/108, 21.30% in plasma; SFRP-1, 40/108, 37.04% in tissue and 31/108, 28.7% in plasma; DKK, 39/108, 36.1% in tis- sue and 25/108, 23.14% in plasma; and E-cad, 37/108, 34.3% in tissue and 18/108, 16.67% in plasma. CIMP＋ （≥3 methylated genes） was detected in 68 （60.2%） tumor tissue samples and 62 （57.4%） plasma samples. CIMP was not detected in non-neoplastic liver tissues or plasma of healthy persons. CIMP status in tumor tissues differed significantly in gender, hepatitis B surface antigen, alpha-fetoprotein, and tumor-node- metastasis stage （P 〈 0.05）. Similar results were obtained with plasma samples （P 〈 0.05）. There was no difference in CIMP status in age, presence of hepatitis C virus antibody, cirrhosis, number of nodes, number of tumors, tumor size, or Edmondson-Steiner stage. A one-year follow-up found that the metastatic rate and recurrence rate in the CIMP＋ group were significantly higher than in the CIMP- group as assessed with plasma samples （P 〈 0.05）. CONCLUSION： Plasma DNA can be a reliable sample source for CIMP analysis. CIMP in plasma may serve as a molecular marker of late-stage and poor-prognosis HCC.

Adiponectin,a key adipokine in obesity related liver diseases

Non-alcoholic fatty liver disease (NAFLD) comprising hepatic steatosis,non-alcoholic steatohepatitis (NASH),and progressive liver fibrosis is considered the most common liver disease in western countries.Fatty liver is more prevalent in overweight than normal-weight people and liver fat positively correlates with hepatic insulin resistance.Hepatic steatosis is regarded as a benign stage of NAFLD but may progress to NASH in a subgroup of patients.Besides liver biopsy no diagnostic tools to identify patients with NASH are available,and no effective treatment has been established.Visceral obesity is a main risk factor for NAFLD and inappropriate storage of triglycerides in adipocytes and higher concentrations of free fatty acids may add to increased hepatic lipid storage,insulin resistance,and progressive liver damage.Most of the adipose tissue-derived proteins are elevated in obesity and may contribute to systemic inflammation and liver damage.Adiponectin is highly abundant in human serum but its levels are reduced in obesity and are even lower in patients with hepatic steatosis or NASH.Adiponectin antagonizes excess lipid storage in the liver and protects from inflammation and fibrosis.This review aims to give a short survey on NAFLD and the hepatoprotective effects of adiponectin.

Adiponectin as a protective factor in hepatic steatosis

AIM: Obesity and insulin resistance (IR) are closely related to hepatic steatosis (HS), and adiponectin is a hepatic insulin sensitizer that has important effects in liver function. This study aims at investigating the relationship between serum adiponectin concentration and the presence of HS. METHODS: We carried out a cross-sectional study in a check-up unit of a University Hospital in Mexico City. We enrolled 196 subjects, comprising 98 subjects with HS (27 women, 71 men) and 98 controls (37 women and 61 men). Anthropometric, metabolic and biochemical variables were measured in the two groups. Serum adiponectin and leptin concentrations were determined, their association with grade of HS tested, and concentrations, according to quartiles, compared between cases and controls. X2 analysis for linear trends was used to test for a dose-response relationship and logistic regression analysis was conducted to test for a protective effect of adiponectin. RESULTS: The HS subjects were older and more obese than controls, with a central obesity pattern. In the fourth quartile of adiponectin concentrations, HS was less common and severe. In a multivariate model of the fourth quartile of the adiponectin concentrations, we observed a protective effect (OR = 0.17, 95%CI: 0.04-0.67, P= 0.01). In subjects with more severe HS, we observed higher leptin concentrations, and caloric intakes, total fat and iron consumption were higher than in controls. CONCLUSION: The results of the present study suggest that a high serum concentration of adiponectin is associated with a protective effect against HS.

Insulin and heparin in treatment of hypertriglyceridemia-induced pancreatitis

TO THE EDITOR We read with great interest the case report, “Hypertriglyceridernia -induced pancreatitis： A case-based review” by Gan eta]11 in the November 2006 issue of World Journal of Gastroenterology. We agree that in acute setting, pancreatitis due to hyper- triglyceridemia （HTG） should be ruled out as it is a treat-able and preventable condition. It needs to be treated conservatively along with measures to lower the triglyceride level. The various modalities to treat hypertriglyceridemia are plasmapheresis, insulin and heparin, purified apo C Ⅱ, and fibric acid derivatives^[2-5]. Plasmapheresis and purified apo C Ⅱ infusion are not easily available. There is limited literature about the efficacy of intravenous insulin and heparin, both of which can enhance lipoprotein lipase activity.

Insulin resistance in H pylori infection and its association with oxidative stress

AIM: To determine the insulin resistance (IR) and oxidative status in H pylori infection and to find out if there is any relationship between these parameters and insulin resistance. METHODS: Fifty-five H pylori positive and 48 H pylori negative patients were enrolled. The homeostasis model assessment (HOMA) was used to assess insulin resistance. Serum total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) were determined in all subjects. RESULTS: The total antioxidant capacity was significantly lower in H pylori positive group than in H pylori negative group (1.36 ± 0.33 and 1.70 ± 0.50, respectively; P < 0.001), while the total oxidant status and oxidative stress index were significantly higher in H pylori positive group than in H pylori negative group (6.79 ± 3.40 and 5.08 ± 0.95, and 5.42 ± 3.40 and 3.10 ± 0.92, respectively; P < 0.001). Insulin resistance was significantly higher in H pylori positive group than in H pylori negative group (6.92 ± 3.86 and 3.61 ± 1.67, res- pectively; P < 0.001). Insulin resistance was found to be significantly correlated with total antioxidant capacity (r = -0.251, P < 0.05), total oxidant status (r = 0.365, P < 0.05), and oxidative stress index (r = 0.267, P < 0.05). CONCLUSION: Insulin resistance seems to be associated with increased oxidative stress in H pylori infection. Further studies are needed to clarify the mechanisms underlying this association and elucidate the effectof adding antioxidant vitamins to H pylori eradication therapy on insulin resistance during H pylori infection.

Impact of liver diseases on the development of type 2 diabetes mellitus

The prevalence of type 2 diabetes mellitus （T2DM） is higher in patients who have liver diseases such as nonalcoholic fatty liver disease, chronic viral hepatitis, hemochromatosis, alcoholic liver disease and cirrhosis. It is suggested that there is a pathogenic link between the presence of T2DM and the severity of liver injury. However, evidence related to the impact of hepatic inflammation on the development of T2DM has not yet emerged. This article provides an overview of the evidence for an increased prevalence of diabetes in a range of liver diseases, the impact of liver diseases on insulin resistance and 13 cell dysfunction, and the potential mechanisms whereby coexistent liver diseases exacerbate the development of T2DM.