bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pretreatment alanine transaminase level may not be the most important predictor of HBeAg loss in the older patient
Authors: Lee Jung Il , Park Hyun Joo , Lee Jin Woo , Kim Young Soo , Jeong Seok , Lee Don Haeng , Kim Hyung Gil , Shin Yong Woon , Kwon Kye Sook 
Published: March 2010

AbstractBackground: Elevated pretreatment alanine aminotransferase (ALT) over two times the upper limit of normal reference range has been accepted as a marker for predicting HBeAg loss and an indicator for initiating antiviral therapy. Recently, several opinions argued that in patients aged over 40 years, the treatment should be started if they have elevated serum hepatitis B virus (HBV) DNA without elevated ALT. However, initiating treatment in these patients might be argued against by the concept that the rate of HBeAg loss depends on the pretreatment ALT.Aim: This study was conducted to investigate the usefulness of pretreatment ALT in predicting HBeAg loss in patients aged over 40 years under lamivudine treatment.Methods: We retrospectively analyzed 820 HBeAg‐positive patients treated with lamivudine. The patients with hepatocellular carcinoma at or after initiating the lamivudine treatment and patients with evident liver cirrhosis were excluded. Three hundred fifty‐five patients met the criteria and were divided into two groups: ≤40 years of age (Group 1) and >40 years of age (Group 2).Results: Analysis using the Kaplan–Meier method and the log rank test showed that the cumulative rate of HBeAg loss was not different in the two groups. Multivariate modelling indicated that an elevated pretreatment ALT level was a predictor of HBeAg loss in Group 1 (P<0.05), whereas it failed to act as a predictor in Group 2.Conclusion: Antiviral therapy might not need to be deferred until the ALT level increases in order to enhance the chance of HbeAg loss in HBV DNA‐(+) patients aged over 40 years.
Budd‐Chiari syndrome in Sweden: epidemiology, clinical characteristics and survival – an 18‐year experience
Authors: Rajani Rupesh , Melin Tor , Björnsson Einar , Broomé Ulrika , Sangfelt Per , Danielsson Åke , Gustavsson Anders , Grip Olof , Svensson Hans , Lööf Lars , Wallerstedt Sven , Almer Sven HC 
Published: March 2010

AbstractBackground: The exact incidence and prevalence of Budd‐Chiari syndrome (BCS) is unknown in the general population. Published reports differ in terms of the clinical characteristics, effects of therapy and survival.Aims: To investigate the epidemiology, clinical presentation and survival in patients with BCS.Methods: Retrospective multicentre study in Sweden reviewing the medical records of all patients with BCS 1986–2003, identified from the computerised diagnosis database of 11 hospitals, including all university hospitals and liver transplantation centres.Results: Forty‐three patients with BCS were identified, of whom nine (21%) had concomitant portal vein thrombosis. The mean age‐standardised incidence and prevalence rates in 1990–2001 were calculated to be 0.8 per million per year and 1.4 per million inhabitants respectively. Myeloproliferative disorders (38%), thrombophilic factors (31%) and oral contraceptives (30%) were common aetiological factors. Two or more risk factors were present in 44%. In 23%, no risk factor was evident. The median follow‐up time was 2.7 years. Seventy‐two percent were on anticoagulant therapy during follow‐up. Transjugular intrahepatic portosystemic shunting, surgical shunting procedures and liver transplantation were performed in 4, 6 and 18 patients respectively. Nineteen patients died. The overall transplantation‐free survival at 1, 5 and 10 years was 47, 28 and 17% respectively.Conclusions: Budd‐Chiari syndrome is a rare disorder; the mean age‐standardised incidence and prevalence rates in Sweden in 1990–2001 were calculated to be 0.8 per million per year and 1.4 per million inhabitants respectively. The presence of a myeloproliferative disorder was a common aetiological factor in our cohort and about half of the patients had a multifactorial aetiology. The transplantation‐free survival was poor.
Integrin alpha V polymorphisms and haplotypes in a Korean population are associated with susceptibility to chronic hepatitis and hepatocellular carcinoma
Authors: Lee Seung Ku , Kim Min‐Ho , Cheong Jae Youn , Cho Sung Won , Yang Song‐Ju , Kwack KyuBum 
Published: March 2010

AbstractBackground/Aims: Integrins are cell surface receptors for extracellular matrix (ECM) proteins that initiate signalling pathways that modulate proliferation, survival, invasion or metastasis. Consequently, integrins are potential targets for the treatment of cancer. In this study, we investigated whether single nucleotide polymorphisms (SNPs) in integrin αV (ITGAV) in a Korean population were associated with chronic hepatitis B virus (HBV) infection and HBV‐infected hepatocellular carcinoma (HCC).Patients and Methods: Thirteen ITGAV SNPs in 111 cases of chronic HBV infection, 86 cases of HBV‐infected HCC and 107 cases of acute self‐limited HBV infection were genotyped using Illumina's Sentrix array matrix (SAM) chip.Results: The ITGAV intron SNPs rs9333289 and rs11685758, the 3′‐untranslated region SNP rs1839123 and haplotype 3 (T–T–A) were associated with enhanced susceptibility to HBV‐infected HCC (OR=1.75–2.42; P=0.02–0.05), while the intron SNP rs2290083 was associated with both chronic infection and HBV‐infected HCC (OR=1.73–2.01; P=0.01–0.04). In addition, both rs2290083 and ht1 (C–C–G) were associated with the age at which chronic infection occurred, as determined by Cox relative hazard analysis (RH=1.39–1.62, P=0.04–0.01)Conclusion: ITGAV SNPs and haplotypes may be genetic factors that increase the susceptibility of Koreans to chronic HBV infection and HBV‐infected HCC.
Hepatitis C virus infection enhances insulin resistance induced by visceral fat accumulation
Authors: Eguchi Yuichiro , Mizuta Toshihiko , Ishibashi Eriko , Kitajima Yoichiro , Oza Noriko , Nakashita Shunya , Hara Megumi , Iwane Shinji , Takahashi Hirokazu , Akiyama Takumi , Ario Keisuke , Kawaguchi Yasunori , Yasutake Tsutomu , Iwakiri Ryuichi , Ozaki Iwata , Hisatomi Akitaka , Eguchi Takahisa , Ono Naofumi , Fujimoto Kazuma 
Published: March 2010

AbstractBackground/Aims: To clarify the impact of visceral obesity on hepatitis C virus (HCV)‐infected patients, we examined the relationship between insulin resistance development and visceral fat accumulation.Methods: We analyzed 87 HCV‐infected patients with mild fibrosis (stage 1 or 2) in comparison with 125 sex‐ and age‐matched patients with non‐alcoholic fatty liver disease (NAFLD). The degree of visceral fat area (VFA; cm2) at the umbilical level was measured by abdominal computed tomography and divided into two grades: no visceral obesity, VFA<100 and visceral obesity, VFA≥100. Insulin resistance was evaluated by homeostasis model assessment of insulin resistance (HOMA‐IR) and the quantitative insulin sensitivity check index (QUICKI). Pancreatic β‐cell function was evaluated by homeostasis model assessment of β‐cell function (HOMA‐β). Serum soluble tumour necrosis factor (TNF)‐receptors 1 and 2 and adiponectin were measured.Results: Insulin resistance evaluated by HOMA‐IR and QUICKI was correlated with visceral fat accumulation, and was higher in HCV patients than in NAFLD patients with visceral obesity. HOMA‐β was higher in HCV patients than in NAFLD patients for each VFA grade. Serum‐soluble TNF‐receptors 1 and 2 were higher in HCV patients than in NAFLD patients with visceral obesity.Conclusions: Hepatitis C virus infection is a risk factor for development of insulin resistance, particularly in patients with visceral obesity.
Phosphorylation of extracellular signal‐regulated kinase 1/2, p38 mitogen‐activated protein kinase and nuclear translocation of nuclear factor‐κB are involved in upregulation of matrix metalloproteinase‐9 by tumour necrosis factor‐α
Authors: Itatsu Keita , Sasaki Motoko , Harada Kenichi , Yamaguchi Junpei , Ikeda Hiroko , Sato Yasunori , Ohta Tetsuo , Sato Hiroshi , Nagino Masato , Nimura Yuji , Nakanuma Yasuni 
Published: March 2010

AbstractBackground: Upregulation of matrix metalloproteinase‐9 (MMP‐9) induced by tumour necrosis factor‐α (TNF‐α) is reportedly involved in a variety of non‐neoplastic and neoplastic diseases. In this study, we examined which signalling pathways are involved in TNF‐α‐induced MMP‐9 upregulation in cholangiocarcinoma (CC).Methods: We used two CC cell lines: HuCCT‐1 and CCKS‐1.Results: In an ex vivo study using HuCCT‐1 and CCKS‐1 cells, TNF‐α treatment induced MMP‐9 production and activation via interaction with TNF receptor‐1 (TNF‐R1) but not with TNF receptor‐2 (TNF‐R2), shown by zymography, and increased MMP‐9 promoter activity (luciferase assay). As for the signalling pathway, TNF‐α stimulation led to the phosphorylation of extracellular signal‐regulated kinase 1/2 (Erk1/2) and p38 mitogen‐activated protein kinase (p38MAPK) and translocation of nuclear factor κB (NF‐κB) (p65) into the nuclei. Inhibition studies using SB203580 (inhibitor of p38MAPK), U0126 (inhibitor of mitogen‐activated or extracellular signal‐regulated protein kinase 1/2) and MG132 (inhibitor of NF‐κB) showed that the phosphorylation of Erk1/2 and p38MAPK with activation of NF‐κB was closely related to MMP‐9 upregulation in both cell lines.Conclusion: These data suggest that TNF‐α/TNF‐R1 interaction leads to the phosphorylation of Erk1/2 and p38MAPK and nuclear translocation of NF‐κB, which is closely associated with the production and activation of MMP‐9 in cultured CC cells of HuCTT‐1 and CCKS‐1. Upregulation of MMP‐9 with NF‐κB activation may be involved in the tumour invasion of CC.
Hepatic steatosis in patients with chronic hepatitis C virus genotype 2 or 3 does not affect viral response in patients treated with peginterferon α‐2a (40KD) (PEGASYS®) plus ribavirin (COPEGUS®) for 16 or 24 weeks
Authors: Rodriguez‐Torres Maribel , Govindarajan Sugantha , Diago Moises , Morgan Thomas , Anand Bhupinderjit , Barange Karl , Suter Frank , Lin Amy , Hooper Gregory , Shiffman Mitchell 
Published: March 2010

AbstractBackground: Hepatic steatosis is common in patients infected with hepatitis C virus (HCV). The effect of steatosis on anti‐HCV therapy efficacy is unclear.Methods: We studied host and viral factors associated with steatosis and the effect of steatosis on treatment efficacy using the database of a large prospective trial in patients with HCV genotypes 2 and 3.Results: Out of 885 patients assessed for steatosis, a total of 614 patients or 69% had steatosis. Patients with genotype 3 were more likely to have steatosis than those with genotype 2 (79 vs. 59%, P<0.001). Using the logistic regression model, steatosis was associated with genotype 3 (P<0.0001), older age (P=0.0025), heavier weight (P<0.0001), higher HCV RNA (P<0.0001), and higher ALT levels (P=0.015). By univariate analysis, steatosis was associated with lower sustained virological response (SVR) in patients with genotype 3, but not in patients with genotype 2. When all factors associated with steatosis and SVR were evaluated by logistic regression analysis; genotype, age, bodyweight, histological diagnosis, ALT quotient, baseline HCV RNA and treatment duration were associated with the probability of SVR, but gender, race and steatosis were not. Further analysis showed that steatosis remained a non‐significant factor while baseline viral load was significantly associated with the probability of an SVR.Conclusions: Steatosis did not influence the efficacy of treatment in our study population. Baseline viral load is a confounding factor, particularly in patients infected with genotype 3 and once baseline viral load was accounted for, the association between steatosis and SVR was not relevant.
Caveolin‐1 and Rac regulate endothelial capillary‐like tubular formation and fenestral contraction in sinusoidal endothelial cells
Authors: Yokomori Hiroaki , Oda Masaya , Yoshimura Kazunori , Nagai Toshihiro , Fujimaki Kayo , Watanabe Shuichi , Hibi Toshifumi 
Published: March 2010

AbstractBackground/Aims: Rho guanidine triphosphatases (GTPases) are major regulators of cell migration. We investigated the cytoskeleton and Rho GTPases during cell migration and morphogenesis processes in isolated rat liver sinusoidal endothelial cells (LSECs) cultured on Matrigel while stimulated by the vascular endothelial growth factor (VEGF).Methods: To obtain primary monolayers, LSECs were cultured on Matrigel for 5–17 h with or without VEGF. Sinusoidal endothelial fenestrae (SEF) morphology was observed using scanning electron microscopy and transmission electron microscopy. RhoA, Rac1 and phosphorylated myosin light‐chain kinase, Rho‐binding domain of Rhotekin and the p21‐binding domain of p21‐activated protein kinase were analysed using Western blotting.Results: The LSECs showed cellular protrusions and or cords of aligned cells resembling primitive capillary‐like structures, with SEF contraction. Time course analyses of Rac1 activation matched specific morphological changes. Rac1 activity increased progressively to 17 h in cells cultured without VEGF, but markedly increased at 7 h in the presence of VEGF. RhoA activity was slightly elevated at 5 h. The levels of endogenous caveolin‐1 (CAV‐1) expression increased in a time‐dependent manner, reaching a peak at 7 h. CAV‐1 expression occurred immediately before the formation of the capillary‐like tube. Moreover, treatment with VEGF regulated CAV‐1 expression in LSECs.Conclusions: Spatial activation of Rac1 is involved in the formation of a capillary‐like tubular network accompanying SEF contraction in LSECs, implying that endothelial migration and adhesion are necessary for LSECs tubular formation in the liver. CAV‐1 might play an important positive role in the regulation of LSEC tubular formation.
Management of the Diabetic Patient with Advanced Chronic Kidney Disease
Authors: Alicic Radica Z. , Tuttle Katherine R. 
Published: March 2010

AbstractDiabetic kidney disease (DKD) is the leading cause of end‐stage renal disease (ESRD), and one of the most prevalent microvascular complications of both type 1 and type 2 diabetes. Additionally, risk of death is increased at all stages of DKD. As early as the microalbuminuric stage, the death rate approaches 20% per year. Therefore, management strategies should address reducing risk of mortality as well as progression to ESRD. DKD is associated with multiple co‐morbidities including hypertension, dyslipidemia, cardiovascular disease, anemia, and bone and mineral metabolism disorders (BMD). Anemia and BMD often occur earlier in the course of DKD than with other forms of chronic kidney disease. Pharmacological and dietary management of hyperglycemia, hypertension, dyslipidemia, anemia, and BMD pose specific challenges in DKD. However, with heightened awareness of risks and a multifactorial management approach, the impact of DKD on micro‐ and macrovascular complications and death can be reduced.
Glycemic Control and Burnt‐Out Diabetes in ESRD
Authors: Kovesdy Csaba P. , Park Jong C. , Kalantar‐Zadeh Kamyar 
Published: March 2010

AbstractTreatment of early diabetes mellitus, the most common cause of chronic kidney disease (CKD), may prevent or slow the progression of diabetic nephropathy and lower mortality and the incidence of cardiovascular disease in the general diabetic population and in patients with early stages of CKD. It is unclear whether glycemic control in patients with advanced CKD, including those with end‐stage renal disease (ESRD) who undergo maintenance dialysis treatment is beneficial. Aside from the uncertain benefits of treatment in ESRD, hypoglycemic interventions in this population are also complicated by the complex changes in glucose homeostasis related to decreased kidney function and to dialytic therapies, occasionally leading to spontaneous resolution of hyperglycemia and normalization of hemoglobin A1c levels, a condition which might be termed “burnt‐out diabetes.” Further difficulties in ESRD are posed by the complicated pharmacokinetics of antidiabetic medications and the serious flaws in our available diagnostic tools used for monitoring long‐term glycemic control. We review the physiology and pathophysiology of glucose homeostasis in advanced CKD and ESRD, the available antidiabetic medications and their specifics related to kidney function, and the diagnostic tools used to monitor the severity of hyperglycemia and the therapeutic effects of available treatments, along with their deficiencies in ESRD. We also review the concept of burnt‐out diabetes and summarize the findings of studies that examined outcomes related to glycemic control in diabetic ESRD patients, and emphasize areas in need of further research.
Characteristics of Elderly Patients with Diabetes and End‐Stage Renal Disease
Authors: Goldfarb‐Rumyantzev Alexander S. , Rout Preeti 
Published: March 2010

AbstractBecause of a combination of demographic and social factors, such as the aging of the population in general, increased incidence of diabetes, and more liberal criteria for renal replacement therapy initiation, the proportion of the end‐stage renal disease (ESRD) patients with diabetes who are considered elderly is currently the fastest growing segment of incident ESRD population. Despite the fast growth of this group, it is poorly characterized in current literature. In this review, we attempt to summarize the data available to date regarding demographic composition, outcomes, choice of renal replacement therapy, and other management issues including renal transplantation. There is significant evidence that the elderly diabetic patients might differ from the general dialysis population regarding renal replacement modality, vascular access for dialysis, and that guidelines addressing chronic kidney disease (CKD) issues such as nutrition and blood pressure may need modification in this ESRD subgroup. At the same time, other areas such as anemia and bone mineral metabolism have not been adequately studied. Lastly, despite lower rates of kidney transplantation in this population, it confers significant survival advantages, similar to that seen in younger populations. As the fastest growing group in the incident ESRD population, these patients have issues related to clinical management, which represent very important areas for future research.
Transplantation in Diabetic Kidney Failure Patients: Modalities, Outcomes, and Clinical Management
Authors: Luan Fu L. , Samaniego Millie 
Published: March 2010

AbstractDiabetes mellitus (DM) is a common and devastating disease, affecting up to 19.3 million Americans. It is the leading cause of chronic kidney disease (CKD) and end‐stage renal disease (ESRD) in the United States. Diabetic patients with ESRD have a high incidence of cardiovascular disease and death. For those kidney transplant patients with no history of DM prior to transplantation, the development of new onset diabetes after transplantation (NODAT) also poses a serious threat to both graft and patient survival. Kidney transplantation is the best renal replacement option for diabetic ESRD and has the potential to halt the progression of cardiovascular diseases. Early referral for transplant evaluation is essential for pre‐emptive or early kidney transplantation in this cohort of patients. In type 1 DM patients with ESRD, simultaneous pancreas and kidney transplantation (SPK) should be encouraged; and in patients facing prolonged waiting time for SPK transplantation but with an available living donor, living donor kidney transplantation followed by pancreas after kidney transplantation (PAK) is a suitable alternative. Islet transplantation in type 1 diabetics is deemed experimental by Medicare, and easy access to this modality remains restricted to qualified patients enrolled in clinical trials or with private insurance. The optimal management of kidney transplant patients with pre‐existent DM or NODAT involves a multi‐pronged approach consisting of pharmacological and nonpharmacological intervention to address all potential cardiovascular risk factors such as glycemic and lipid control, blood pressure control, weight loss, and smoking cessation. Finally, re‐transplantation should be recommended in suitable kidney transplant patients when the kidney allograft demonstrates continuous and progressive decline in function.
Outcomes of Arteriovenous Fistulae Created by a U.S. Interventional Nephrologist
Authors: Mishler Rick , Yevzlin Alexander S. 
Published: March 2010

AbstractArteriovenous fistulae (AVF) outcomes in the United States continue to fall short of expectations and continue to compare disfavorably to European AVF outcomes. This study presents the early experience of nephrologist created AVF outcomes in the U.S. hemodialysis population. A retrospective analysis of a prospectively collected vascular access database was performed. All patients who were referred for vascular access placement over a 1‐year period were eligible for inclusion. One hundred five (n = 105) patients were initially included in the database. An AVF was placed in 100% of patients referred for vascular access. Two complications were identified (one steal syndrome and one infection) for a rate of 1.9%. The patient demographics included 38.7% female, age 63.6±14.8, 50.0% diabetic, 66.0% hypertensive, with 65.1% of patients in stage 5 chronic kidney disease at the time of AVF placement. Average target artery diameter was 4.09 ± 1.16 mm while average target vein diameter was 3.66 ± 1.20. Twenty‐one AVF were placed in the forearm (19.8%) with the remainder being placed in the upper arm vessels. Eighteen patients (18.56%) failed to mature at 6 weeks. Sixty‐four patients (65.98%) required revision or intervention of their AVF between 12 weeks postoperatively and the endpoint of the study. Eighty patients (84.21%) had patent AVF at an average follow‐up of 286.2 ± 98.14 days. No identifiable risk factors among those listed above were associated with a significant impact on AVF outcomes. AVF outcomes that compare favorably to those of Europe can be achieved by U.S. interventional nephrologists. Furthermore, the dictum that distal is better needs to be re‐examined if the United States hopes to achieve the goal of 66% AVF prevalence.