Top PDF HBV-related hepatocellular carcinoma susceptibility gene KIF1B is not associated with development of chronic hepatitis B.

HBV-related hepatocellular carcinoma susceptibility gene KIF1B is not associated with development of chronic hepatitis B.

HBV-related hepatocellular carcinoma susceptibility gene KIF1B is not associated with development of chronic hepatitis B.

susceptibility [22], implying that distinct genetic mechanism may contribute to corresponding step of HCV-induced HCC develop- ment . The genome-wide analyses on loss of heterozygosity (LOH) in HCC by Li et al. further support our current result, which suggested the LOH of 1p36.21–36.32 region was significant related to HCC development, but not associated with the progression to CHB [23]. Noteworthy, the new identified KIF1B locus for HCC is located at 1p36 region, which encodes two spliced isoforms of kinesin protein (KIF1Ba and KIF1Bb) involved in the transport of organelles and vesicles [24]. Of these two isoforms, KIF1Bb has been elucidated to act as a tumor suppressor in multiple cancers by acting a variety of inhibitors of cell proliferation and/or activators of apoptotic cell death [25,26]. Moreover, because a non-significant difference test cannot be interpreted as acceptance of the null hypothesis, equivalence-based method that provide the probability of observing a lack of association by chance was conducted to avoid the false-negative results in this study. P-values of nonsuperiority test for rs8019, rs17401966 and rs17401924 is 0.002, 0.050 and 0.017, respec- tively, and the nonexistence of association between KIF1B and
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Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China.

Association of hepatitis B virus pre-S deletions with the development of hepatocellular carcinoma in Qidong, China.

enhances HCC development, and this may be related with the oncogenic properties of this mutant virus [12,26,27]. This suggested the higher oncogenic potential of pre-S2 deletions, compared with that of pre-S1 deletions. Most previous studies on the relationship between pre-S deletion and the risk of HCC were conducted with the use of samples taken either at the baseline of the prospective cohort or after the diagnosis of cancer. Because most HBV mutations are acquired during the course of chronic infection rather than being obtained from an initial infection, it is important to know when or at which stage of the disease the mutations developed [10]. This study was facilitated by the availability of prospectively collected plasma samples from Qidong. To date, there is a lack of longitudinal observation on pre-S deletion over the period of HCC progression. We then recruited a series of serum samples spanning the years before and after HCC diagnosis. Our longitudinal study on patients who carried the pre-S deletion mutations at the stage of HCC also revealed that, in about half of cases, the deletion was indeed absent 5–10 years prior to the occurrence of HCC. The result demonstrated that a gradual occurrence of pre-S deletions during the progression of HCC. This observation provided direct evidence that the pre-S deletions were not acquired at the beginning of infection, but that these mutations arose de novo during the progression of liver disease.
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Serum microRNAs as biomarkers for hepatocellular carcinoma in Chinese patients with chronic hepatitis B virus infection.

Serum microRNAs as biomarkers for hepatocellular carcinoma in Chinese patients with chronic hepatitis B virus infection.

and paraffinembedding, and can be efficiently extracted from and quantified in such specimens [13]. Investigation of cancer-specific miRNAs in the circulation is an emerging and exciting field of study. One of the first studies measuring miRNA levels in serum was reported by Lawrie et al. [14], who showed that sera levels of miR-21 were associated with relapse-free survival in patients with diffuse large B-cell lymphoma. Subsequently, circulating miRNAs have been postulated as novel biomarkers for cancer, and other disease processes [15–27]. To date, there have been no systematical reports on the role of circulating miRNAs in HCC, and it is not fully understood whether serum miRNAs have a clinicopathological influence in HCC. We hypothesized that levels of specific cancer-associated miRNAs in circulation would differ between HCC patients and chronic HBV infection patients without HCC or healthy individuals. If this hypothesis held truth, it would signify a major breakthrough in HCC management, bringing us ever closer to finding a novel, sensitive, and noninvasive biomarker for this common disease.
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GWAS identifies novel susceptibility loci on 6p21.32 and 21q21.3 for hepatocellular carcinoma in chronic hepatitis B virus carriers.

GWAS identifies novel susceptibility loci on 6p21.32 and 21q21.3 for hepatocellular carcinoma in chronic hepatitis B virus carriers.

HBV-related HCC. SNP imputation of the region did not reveal any SNPs that showed stronger association than rs455804. GRIK1 encodes CLUR5, which is involved in the glutamate signaling, as one of the ionotropic glutamate receptor, kainite 1 protein (GLUR5), a subunit of ligand-activated channels and involved in glutamate signaling. Our discovery of the association of GRIK1 with HCC has enhanced the emerging evidences for the important role of glutamate signaling pathway in cancer development. Glutamate has been shown to play a central role in the malignant phenotype of gliomas through multiple molecular mechanisms [20]. Inhibition of glutamate release and/or glutamate receptor activity can inhibit the proliferation and/or invasion of tumor cells in breast cancer [21], laryngeal cancer [22], and pancreatic cancer [23], and ionotrpic glutamate receptor (GLUR6) was also suggested to play a tumor-suppressor role in gastric cancer [24]. Recently, the exome sequencing analysis revealed that GRIN2A (encoding the ionotrpic glutamate receptor (N-methyl D-aspartate) subunit 2A) was mutated in 33% of melanoma tumors, clearly indicating the involvement of glutamate signaling in melanoma development. Finally, SNPs within GRIK1 have also been found significantly associated with paclitaxel response in NCI60 cancer cell lines, and may play a role in the cellular response to paclitaxel treatment in cancer [25]. Consistent with the previous observa- tions, our discovery of GRIK1 as a HBV-related HCC suscepti- bility gene has suggested the importance of glutamate signaling in HBV-related HCC development, and, although still speculative, has highlighted the glutamate signaling pathway as a potentially novel target for the treatment of HCC.
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Comparison of clinical manifestations and outcomes between hepatitis B virus- and hepatitis C virus-related hepatocellular carcinoma: analysis of a nationwide cohort.

Comparison of clinical manifestations and outcomes between hepatitis B virus- and hepatitis C virus-related hepatocellular carcinoma: analysis of a nationwide cohort.

HBV infection, in addition to chronic inflammation, the integration of HBV DNA into the host hepatocyte DNA and the expression of viral proteins, which transactivate human oncogenes, may play a role in hepatocarcinogenesis, while in HCV infection, chronic inflammation seems to play a main role in oncogenesis [13–15]. Thus, cirrhosis almost always accompanies HCV-related HCC [16], but not in HBV-related HCC [17,18]. HBV infection usually occurs in the perinatal period in an endemic area, while the immune status of the host is still immature [8]. Meanwhile, HCV infection occurs in adults with a fully matured immune system [19]. A combination of virus-specific, host genetic, environmental, and immune-related factors will affect the HCC manifestations, thus these differences in hepatocarcinogenesis may affect clinical manifestations as well as patients outcome. Indeed, several previous studies have assessed the impact of viral etiology on clinical manifestation and long-term outcome [20–22]. However, still controversies exist whether different HCC surveil- lance and management strategies according to the viral etiologies are needed. This question has not been answered, in part, because most studies were performed on a single hospital base which inevitably has a selection bias, with limited sample size and limited follow-up period. The sample sizes were 205, 359 and 127 in reports by Shiratori et al.’s [20], Tanabe et al.’s [21], and Hiotis et al.’s [22], respectively. Therefore, in this study, we used data from population-based nationwide cancer registry which has less selection bias, with large study sample and long-term follow-up period, and assessed whether true differences exist in clinical manifestations and long-term outcomes of HCC patients between the two viral etiologies.
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Development of a highly sensitive glycan microarray for quantifying AFP-L3 for early prediction of hepatitis B virus-related hepatocellular carcinoma.

Development of a highly sensitive glycan microarray for quantifying AFP-L3 for early prediction of hepatitis B virus-related hepatocellular carcinoma.

It is well known that AFP-L3 concentration correlates well with AFP; however, AFP-L3% is not correlated with AFP [25,26]. AFP-L3% is a marker that is independent of AFP. We found that the levels of AFP-L3–specific IgG were significantly higher in HCC patients than in CHB patients. Additionally, consistent with previous studies [25], elevation of the AFP-L3 ratio was independent of increases in total AFP in HCC patients. Although prolonged observations will be required to clarify whether the AFP-L3 ratio is useful for predicting HCC, our findings suggest that this ratio is useful for early detection of HCC compared with CHB, even in subjects with serum AFP serum levels ,20 ng/mL. Taketa et al. [25] have reported that AFP-L3 values elevated above the cutoff value of 15% with an average of 4.064.9 months before the detection of HCC by imaging techniques. Sato et al. [27] also have demonstrated that lectin-reactive AFP elevated 3– 18 months before the detection. Also, an increase in the AFP-L3 ratio prior to detection of HCC by various advanced imaging modalities may contribute to the more precise identification of chronic liver disease in patients with a relatively high risk of HCC [28]. In this study, we demonstrated that the glycan microarray assay has great clinical utility for detecting HCC changes in patients with low total AFP concentrations after treatment for HCC.
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A Non-Synonymous Single Nucleotide Polymorphism in the HJURP Gene Associated with Susceptibility to Hepatocellular Carcinoma among Chinese.

A Non-Synonymous Single Nucleotide Polymorphism in the HJURP Gene Associated with Susceptibility to Hepatocellular Carcinoma among Chinese.

HCC was made by either positive histologic findings or an elevated serum α-fetoprotein level ( 400 ng/mL) combined with at least one positive image on angiography, sonography, and/or high-resolution contrast computed tomography. The controls were also chronic HBV carriers, and the selection criteria for them included no individual history of cancer and frequency matching to the cases on sex and age (± 5 years). The HBV carriers are subjects positive for both hepatitis B surface antigen (HBsAg) and antibody immunoglobulin G to hepatitis B core antigen (anti-HBcAg) for at least 6 months. Subjects were considered smokers if they smoked up to 1 year before the date of cancer diagnosis for cases or up to the date of interview for con- trols. Information was collected on the number of cigarettes smoked per day, the age at which the subjects started smoking, and the age at which ex-smokers stopped smoking. An alcohol drinker was defined as someone who consumed alcoholic beverages at least once per week for  6 months. All subjects included in this study were negative for antibodies to HCV, hepatitis D virus, or human immunodeficiency virus; and had no other types of liver disease, such as autoimmune hepatitis, toxic hepatitis, and primary biliary cirrhosis or Budd—Chiari syndrome.
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The emergence of YMDD mutants precedes biochemical flare by 19 weeks in lamivudine-treated chronic hepatitis B patients: an opportunity for therapy reevaluation

The emergence of YMDD mutants precedes biochemical flare by 19 weeks in lamivudine-treated chronic hepatitis B patients: an opportunity for therapy reevaluation

Given the loss of therapeutic efficacy associated with the development of resistance to lamivudine (LMV) and the availability of new alterna- tive treatments for chronic hepatitis B patients, early detection of viral genotypic resistance could allow the clinician to consider therapy modification before viral breakthrough and biochemical relapse oc- cur. To this end, 28 LMV-treated patients (44 ± 12 years; 24 men), on their first therapy schedule, were monitored monthly at four Brazilian centers for the emergence of drug resistance using the reverse hybrid- ization-based INNO-LiPA HBV DR assay and occasionally sequenc- ing (two cases). Positive viral responses (HBV DNA clearance) after 6, 12, and 18 months of therapy were achieved by 57, 68, and 53% of patients, while biochemical responses (serum alanine aminotrans- ferase normalization) were observed in 82, 82, and 53% of cases. All viral breakthrough cases (N = 8) were related to the emergence of YMDD variants observed in 7, 21, and 35% of patients at 6, 12, and 18 months, respectively. The emergence of these variants was not associ- ated with viral genotype, HBeAg expression status, or pretreatment serum alanine aminotransferase levels. The detection of resistance- associated mutations was observed before the corresponding bio- chemical flare (41 ± 14 and 60 ± 15 weeks) in the same individuals. Then, if highly sensitive LMV drug resistance testing is carried out at frequent and regular intervals, the relatively long period (19 ± 2 weeks) between the emergence of viral resistance and the onset of biochemical relapse can provide clinicians with ample time to re- evaluate drug therapy.
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Predictability of liver-related seromarkers for the risk of hepatocellular carcinoma in chronic hepatitis B patients.

Predictability of liver-related seromarkers for the risk of hepatocellular carcinoma in chronic hepatitis B patients.

All of the liver-related seromarkers we analyzed are associated with liver diseases such as fibrosis, cirrhosis, jaundice, and fatty liver. They may reflect the status of the liver, such as liver cells injury, inflammation, necroinflammation, or proliferation, at the time of examination. AAR has been suggested as a fibrosis marker. By analyzing these 13 liver-related seromarkers along with the AAR, we first tried to find out candidate predictors that had significant associations with HCC. Then, we further selected predictors according to the results of multivariate analysis and biological rationale. Finally, liver-related seromarkers included in the models were ALT, AAR, AFP, GGT, albumin, and alpha-1 globulin. All of them were significantly associated with HCC in multivariate analyses. Among the six predictors, ALT, AAR, AFP, GGT, and albumin are widely used. Although Alpha-1 globulin is not commonly used, it had an independent and significant association with HCC in this study, and is also available in clinical practice. In addition, both ALT and albumin have been found to be HCC predictors in chronic hepatitis B patients. [12– 14] AFP is a well-known HCC seromarker, and AAR is a cirrhotic marker that may reflect progressive liver functional impairment if it equals 1 or higher. [22] Serum GGT mostly comes from liver; it has been found to be useful for the diagnosis of HCC in patients with low AFP levels or at a relatively early stage. [27] The deficiency of alpha-1-antitrypsin, the main (,90%) protein of the alpha-1 globulins, has been found to be associated with an increased risk for liver damage, cirrhosis and HCC. [28].
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Pre-S deletion and complex mutations of hepatitis B virus related to young age hepatocellular carcinoma in Qidong, China.

Pre-S deletion and complex mutations of hepatitis B virus related to young age hepatocellular carcinoma in Qidong, China.

The strengths of this study include the sequence analysis of a series of serum samples from a community-based cohort study, repeated sequence analysis provides data on the long-term stability of viral sequence and helps clarify the temporal relationship between a sequence mutation and the occurrence of HCC. Furthermore, this association between viral factors and HCC is unlikely to be biased by the effect of antiviral therapy because the proportion of participants in this cohort who received such therapy was very low ( ,1%) and no participants with a history of such therapy were included in the analysis. There are also several limitations in this study. First, although CH patients in the control group were age matched with those in the HCC group, the possibility of developing malignancy in the future cannot be denied. Second, the generalizability of the results is limited because all the study subjects were males, a larger cohort and a longer follow-up time are needed for a similar study in females. In conclusion, this current study further supports the view that Chronic HBV carriers below 40 years of age should not be neglected and should be included surveillance programs for HCC, especially those high risk subjects infected with HBV of complex sequence mutations. These HBV mutations may serve as useful biomarkers for predicting the clinical outcomes of young patients with chronic hepatitis B. Modifications of regular HCC screening guidelines could be expected to result in earlier disease detection and improved prognosis in young patients.
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A 3' UTR SNP in COL18A1 is associated with susceptibility to HBV related hepatocellular carcinoma in Chinese: three independent case-control studies.

A 3' UTR SNP in COL18A1 is associated with susceptibility to HBV related hepatocellular carcinoma in Chinese: three independent case-control studies.

Hepatocellular carcinoma (HCC) is one of the most common malignancy and ranks fifth in men and eighth in women among causes of cancer mortality worldwide. It is estimated that about 564,000 new cases of HCC are reported throughout the world each year [1]. Eastern Asia is the geographic area at highest risk of HCC [1]. The cause of HCC is a complex interplay between multiple genetic and environmental factors [2]. Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the main viral factors of HCC, while in China, HBV related HCC is the most frequent. On the other hand, accumulated evidences in molecular genetics indicate that single nucleotide polymorphisms (SNP) in immune response, angiogenesis and tumorigenesis related genes are associated with susceptibility to HCC [3,4,5,6]. Recent progress in genome-wide association study (GWAS) also have identified new susceptibility loci for HCC [7,8].
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Rev. Bras. Reumatol.  vol.52 número4 en v52n4a15

Rev. Bras. Reumatol. vol.52 número4 en v52n4a15

Anti-TNF- α agents have emerged as a potent treatment for patients with rheumatoid arthritis unresponsive to conven- tional disease-modifying antirheumatic drugs. Increased susceptibility to infections induced by these drugs is the main complication of their use. Reactivation of hepatitis B virus (HBV) is one of the most worrisome side effects in patients with HBV infection receiving anti-TNF- α. We report the case of a 56-year-old male patient with stable hepatitis B and good response to the antiviral combination of lamivudine and tenofovir when infl iximab was started. The patient went into remission. During the 30-month treatment with the biologic, his liver function remained stable, with no HBV reactivation.
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Occult HBV Infection Reactivation in Non-Hodgkin’s Lymphoma: An Update on Prevalence and Management

Occult HBV Infection Reactivation in Non-Hodgkin’s Lymphoma: An Update on Prevalence and Management

between these patients is not negligible. Therefore, in our view, the reports that analyse all HBsAg negative patients may be considered more reliable on assessing this issue. The methods to diagnose HBV reactivation varied widely across the diferent studies and thus also the deinition of OBI reactivation. In the majority of the studies, especially those in a small population, a ‘pre-clinical HBV reactivation’ is considered, that is deined as the reappearance of detectable HBV DNA in the serum, even without an abnormal ALT level. On the contrary, large population studies very often use a ‘clinical reactivation’ deinition, usually described as the derangement of ALT/aspartate transaminase (at least 2/3 times upper normal values), with HBsAg and HBV DNA detectable in the serum. Finally, among the reviewed studies, only a few papers reported that an analysis of DNA extracts from liver tissues was performed, thus assessing the ‘true prevalence of OBI’. 37 As previously said, after
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Virus analysis of hepatocellular carcinoma "non-A, non-C" and hepatitis B virus.

Virus analysis of hepatocellular carcinoma "non-A, non-C" and hepatitis B virus.

Este estudo mostra que no Japão, a implicação do HBV nos pacientes portadores de CHC qualificados de “não-B, não- C”, é freqüente. A presença de mutações e/ou deleções no genoma HBV de certos pacientes poderá explicar a ausência de marcadores deste vírus, notadamente o AgHBs circulante. Estas constatações feitas na população de doentes podem, entretanto, ser relacionadas à problemática de falsos negativos observados em certos testes de detecção de AgHBs (ausência de AgHBs circulante, não-produção de AgHBs, AgHBs mutante não detectado...) em doadores de sangue.
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Arq Bras Endocrinol Metab  vol.55 número9

Arq Bras Endocrinol Metab vol.55 número9

T he recent publication on Insulin resistance and chronic hepatitis C in non-dia- betic patients was very interesting (1). Souza and cols. concluded that “Insulin resistance is often present in patients with chronic hepatitis C, and this parameter is associated with more advanced HCV-related hepatic ibrosis (1).” The inding in this study is concordant with the recent report by Itoh and cols. (2). It is believed that direct damage caused by the virus with proinlammatory cytokines will interfere with normal insulin signaling, and this further disturbs glucose metabolism (3). However, some issues on the present study (1) should be mentioned. First, the protocol in the present study cannot exclude the interference of other possible confounding diseases in the patients (such as HIV and other uncommon hepatitis virus infection). Second, this is only an observational study, hence, it is not reasonable to draw conclusions on any association (which would require an analytical study).
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Rev. Soc. Bras. Med. Trop.  vol.47 número2

Rev. Soc. Bras. Med. Trop. vol.47 número2

confi rmed in a larger set of patients. Additionally, the study design was cross-sectional and did not include a longitudinal follow-up. The ultrasounds may not have been uniform in terms of operator and evaluation method, as this was not a prospective study. Indeed, the ultrasound results refl ect a day-to-day medical practice in which one relies on ultrasound to initially defi ne whether the patient presents with LS. As we have demonstrated, ultrasonography does not always match biopsy results perfectly. Data on alcohol ingestion, diet quality, and routine exercise were also lacking; therefore, an analysis of the effect of these variables on metabolic disease in this population was not possible. Another limitation of our study was the absence of a control group; nevertheless, our findings are comparable to previously published data.
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Association of T174M polymorphism of angiotensinogen gene with essential hypertension: A meta-analysis

Association of T174M polymorphism of angiotensinogen gene with essential hypertension: A meta-analysis

for the discrepancies among these studies. The first possi- ble cause may be genetic differences in the population sam- ples and phenotypic differences in the hypertensive populations analyzed (Marco et al., 2005). Second, the ef- fect of the T174M variant on plasma AGT levels may vary among different ethnic groups so that the association be- tween T174M polymorphism and risk of essential hyper- tension may not be detected in every ethnic group, just as shown in the study of Pereira et al. (2008). Most studies in- cluded in current meta-analysis were conducted in Asian populations and only one in a European population, this meaning that the final result may not be generalizable. Therefore, more studies need to be performed in various ethnic groups and subgroup analysis stratified by ethnicity should be conducted in future research. Second, the reli- ability of the findings of a study may be questionable if it lacks an appropriate control group. In some studies, the age and percentage of subjects with alcohol consumption or smoking were significantly different between the hyperten- sive and control groups (Hingorani et al., 1996; Kiema et al., 1996). A third possible cause of discrepancy may be a multiple interaction of polymorphisms or genes. These gene-to-gene interactions make the association of hyper- tension with any single candidate gene more complex (Wang et al., 2002). In addition, the numbers of cases were different in various studies, this leading to variation in pre- cision. Finally, hypertension is an acknowledged multi- factorial disease. Genetic factors may interact with several other factors, such as salt intake, body mass index, and smoking in the development of hypertension.
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Rev. Soc. Bras. Med. Trop.  vol.46 número4

Rev. Soc. Bras. Med. Trop. vol.46 número4

The limitations of this study included the cross-sectional format, which prevented the assessment of risk factors since exposure and outcome are measured at the same time. In addition, data collection through interviews does not guarantee the reliability of all responses, particularly those related to behavioral aspects of drug abuse and condom use. The small number of male SWs who participated prevented a more complex comparative analysis between men and women. Because the participants were selected on a convenience sample basis, and the representativeness of the sample size could not be established, the external validity of this study is impaired. However, it should be highlighted that access to this population for serological testing is very diffi cult, and the fi ndings are relevant to public health.
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Clinical trial of lamivudine in children with chronic hepatitis B.

Clinical trial of lamivudine in children with chronic hepatitis B.

Patients were assessed two, four, and eight weeks after the ini- tiation of therapy, every eight weeks until week 48, and at week 52. Blood samples were drawn at each visit to monitor blood chemical and hematologic values. Female patients with childbear- ing potential were required to have a pregnancy test at every study visit. During the 52-week study, investigators and patients were un- aware of the results of HBV DNA and HBsAg assays. The result of the HBeAg assay was disclosed at week 48 and used for stratifica- tion at week 52 for the follow-up study. Commercially available en- zyme-linked immunoassays were used to measure HBeAg, anti- HBe, HBsAg, and antibody against HBsAg (anti-HBs) (HBe [rDNA] Enzyme Immunoassay, AxSym HBe Microparticle En- zyme Immunoassay, HBs Auszyme Enzyme Immunoassay, and Ausab Enzyme Immunoassay, respectively; all from Abbott Labo- ratories). All samples were analyzed at a central reference laborato- ry (Covance Clinical Laboratory Services); however, prothrombin times were determined at each center, and genotypic analysis for resistance mutations was performed at GlaxoSmithKline Virology Laboratories. Serum samples collected at base line and week 52 were frozen at –80°C for subsequent genotypic analysis for resist- ance mutations. Mutations in the YMDD (tyrosine, methionine, as- partate, and aspartate) motif of the reverse-transcriptase domain in the HBV polymerase gene were assessed by the polymerase chain reaction and restriction-fragment–length polymorphism assay. 6
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Arq Bras Endocrinol Metab  vol.55 número6

Arq Bras Endocrinol Metab vol.55 número6

Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpepti- dase (GGT), albumin and fasting glucose (kinetic me- thod), cholesterol and triglycerides (colorimetric me- thod) were carried out with Abbott reagents. DiaSys and precipitation were employed for HDL cholesterol (HDL-c), and the Friedwald formula was employed for LDL cholesterol (LDL-c). The international normali- zed ratio of prothrombin time (INR) was determined with ISI and PT-Fib recombinant reagent and proces- sed in an ACL 3000 device, with ISI determined by the manufacturer. Ferritin was measured using DiaSys rea- gent and chemiluminescent microparticle immunoassay methodology (CMIA). Ultra-sensitive C-reactive pro- tein (CRP) was determined with immunoturbidimetry. Hepatitis C viral load was determined using real-time polymerase chain reaction (Abbott HCV Real Time) and HCV genotyping (Reverse transcription – polyme- rase chain reaction / nucleic acid sequencing). Serum insulin levels were determined using the microparticle enzyme immunoassay (MEIA), Abbott AxSYMR sys- tem. The level of IR was assessed using HOMA-IR (Homeostasis model assessment of insulin resistance), calculated as fasting blood glucose [mmol/L] X fas- ting blood insulin [mil/L] / 22.5). IR was deined as HOMA-IR > 2.5. Biochemical analyses were performed at the HU-UFJF Central Laboratory; fasting insulin, HOMA-IR and ultra-sensitive CRP were performed at the Cortes Villela Laboratory – Juiz de Fora – MG; molecular biology assays (qualitative HCV-RNA, quan- titative HCV-RNA, HCV genotyping) were performed at the Universidade Federal de Minas Gerais NUPAD Laboratory.
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