Clinical and laboratory characteristics associated with dyslipidemia and liver steatosis in chronic HBV carriers

Nau, Angélica Luciana; Soares, Júlia Cristina; Shiozawa, Maria Beatriz Cacese; Dantas-Corrêa, Esther Buzaglo; Schiavon, Leonardo de Lucca; Narciso-Schiavon, Janaína Luz

doi:10.1590/0037-8682-0009-2014

Cited by 14 publications

(13 citation statements)

References 39 publications

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“…And some studies have suggested that dyslipidemia and diabetes may increase risk of advanced liver diseases in HBV infected patients [4–6]. Therefore, PPAR agonists are often used in these patients.…”

Section: Introductionmentioning

confidence: 99%

Peroxisome Proliferators Activated Receptor (PPAR) agonists activate hepatitis B virus replication in vivo

Liu

et al. 2017

Virol J

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BackgroundPPAR agonists are often used in HBV infected patients with metabolic disorders. However, as liver-enriched transcriptional factors, PPARs would activate HBV replication. Risks exsit in such patients. This study aimed to assess the influence of commonly used synthetic PPAR agonists on hepatitis B virus (HBV) transcription, replication and expression through HBV replicative mouse models, providing information for physicians to make necessary monitoring and therapeutic adjustment when HBV infected patients receive PPAR agonists treatment.MethodsThe HBV replicative mouse model was established by hydrodynamic injection of HBV replicative plasmid and the mice were divided into four groups and treated daily for 3 days with saline, PPAR pan-agonist (bezafibrate), PPARα agonist (fenofibrate) and PPARγ agonist (rosiglitazone) respectively. Their serum samples were collected for ECLIA analysis of HBsAg and HBeAg and real-time PCR analysis of Serum HBV DNA. The liver samples were collected for DNA (Southern) filter hybridization of HBV replication intermediates, real-time PCR analysis of HBV mRNA and immunohistochemistry (IHC) analysis of hepatic HBcAg. The alternation of viral transcription, replication and expression were compared in these groups.ResultSerum HBsAg, HBeAg and HBV DNA were significantly elevated after PPAR agonist treatment. So did the viral replication intermediates in mouse livers. HBV mRNA was also significantly increased by these PPAR agonists, implying that PPAR agonists activate HBV replication at transcription level. Moreover, hepatic HBcAg expression in mouse livers with PPAR agonist treatment was elevated as well.ConclusionOur in vivo study proved that synthetic PPAR agonists bezafibrate, fenofibrate and rosiglitazone would increase HBV replication. It suggested that when HBV infected patients were treated with PPARs agonists because of metabolic diseases, HBV viral load should be monitored and regimens may need to be adjusted, an antiviral therapy may be added.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-017-0765-x) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Peroxisome Proliferators Activated Receptor (PPAR) agonists activate hepatitis B virus replication in vivo

Liu

et al. 2017

Virol J

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“…In contrast to simple chronic hepatitis B, concurrence of chronic hepatitis B and hepatic steatosis demonstrates a significant impact on both insulin sensitivity and glucose metabolism [5–10]. By multivariate analysis, body mass index (BMI) [5–7, 9], fasting insulin [5], homeostasis model assessment index (HOMA-IR) [8–10], and fasting blood glucose (FBG) [6–8] are positively associated with the hepatic steatosis in different ethnicities independent of HBV infection.…”

Section: Introductionmentioning

confidence: 99%

“…By multivariate analysis, body mass index (BMI) [5–7, 9], fasting insulin [5], homeostasis model assessment index (HOMA-IR) [8–10], and fasting blood glucose (FBG) [6–8] are positively associated with the hepatic steatosis in different ethnicities independent of HBV infection. Glycosylated haemoglobin (HbA1c), another critical biomarker of glucose regulation, is correlated to indexes of hepatic steatosis, including ultrasonography scores (FLUS) and serum cholinesterase (ChE) [11].…”

Section: Introductionmentioning

confidence: 99%

PNPLA3rs1010023 Predisposes Chronic Hepatitis B to Hepatic Steatosis but Improves Insulin Resistance and Glucose Metabolism

Pan

Chen

Zhang

et al. 2017

Journal of Diabetes Research

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PNPLA3 polymorphisms serve as the genetic basis of hepatic steatosis in normal population and lead to dysregulated glucose metabolism. Whether it underlies the hepatic steatosis and glucose homeostasis in chronic hepatitis B patients remains uncertain. Here, we investigated the PNPLA3 polymorphisms in biopsy-proven chronic hepatitis B patients with (CHB+HS group, n = 52) or without hepatic steatosis (CHB group, n = 47) and non-CHB subjects with (HS group, n = 37) or without hepatic steatosis (normal group, n = 45). When compared to the TT genotype, C-allele at PNPLA3 rs1010023 (CC and TC genotypes) conferred higher risk to hepatic steatosis in chronic hepatitis B patients (odds ratio (OR) = 1.768, 95% confidence interval (CI): 1.027–3.105; P = 0.045) independent of age, gender, and body mass index. In contrast to their role in hepatic steatosis, CC and TC genotypes of PNPLA3 rs1010023 were correlated to significant improvement of homeostasis model assessment index (HOMA-IR) as compared to TT genotype in the CHB+HS group. Downregulated fasting blood glucose also characterized the CHB+HS patients with C-allele at PNPLA3 rs1010023 (CC/TC versus TT: 4.81 ± 0.92 mmol/L versus 5.86 ± 2.11 mmol/L, P = 0.02). These findings suggest that PNPLA3 rs1010023 may predispose chronic hepatitis B patients to hepatic steatosis but protects them from glucose dysregulation by attenuating insulin resistance.

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“…It is known that the prevalence of NASH which is the advanced stage of NAFLD, is six times higher in obese patients compared to persons within a normal weight range (19). Numerous studies have shown that BMI is an important factor associated with NAFLD in patients with hepatitis B and in other segments of society without HBV infection (4,7,8,9,10,13,17,20). Likewise, in our study, we found that weight gain, and thus BMI, is crucial in terms of the presence of NAFLD and makes a significant difference in NAFLD development.…”

Section: Discussionmentioning

confidence: 99%

“…The importance of GGT levels in patients with hepatitis B differs among the studies. Korkmaz et al (16) mentioned that GGT is important for NAFLD, while Altıparmak et al (7) and Nau et al (20) found no significant difference in terms of GGT levels.…”

Section: Discussionmentioning

confidence: 99%

Can Detection of Non-alcoholic Fatty Liver Disease be Coincidental in Young Patients with Chronic Hepatitis B?

Karacaer¹,

Okur²,

Çermik³

et al. 2016

vhd

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ÖZAmaç: Bu araştırmanın amacı hepatit B yüzey antijeni (HBsAg) pozitif ve negatif genç hastalarda alkolik olmayan yağlı karaciğer hastalığının (AOYKH) sıklığını, AOYKH oluşumu ile ilişkili faktörleri ve hepatit B virüsü (HBV) ile AOYKH'nin birlikte saptanmasının rastlantısal olup olmadığını ortaya koymaktı. Objective: The objective of this study was to determine the factors associated with the presence of non-alcoholic fatty liver disease (NAFLD) in young persons who are hepatitis B surface antigene (HBsAg)-positive and negative, and to investigate if NAFLD coexisting hepatitis B virus (HBV) is coincidental. Materials and Methods:This retrospective study, conducted in a military hospital in Turkey, included a total of 384 subjects. The subjects were divided into two groups according to the presence of NAFLD detected by ultrasonography (US). Sociodemographic characteristics, biochemical, histopathological, virological and US results were recorded . Statistical analysis was performed using SPSS 22.0. Results: The median age of the patients, all of whom were male, was 26 years (20-40). NAFLD was identified in 16.9% of patients. HBsAg positivity was found in 36.9% of patients with NAFLD. It was remarkable that no statistically significant difference was found in HBsAg positivity between the patients with and without NAFLD (p=0.661). NAFLD was found in 13.2% of HBsAg-positive patients. NAFLD was determined in 20.3% of HBsAg-negative patients. No significant difference was found in NAFLD grades between HBsAg-positive and negative patients (p=0.158). In the present study, only γ-glutamyl transferase in HBsAg positive patients, and age, alanine transaminase and aspartate transaminase in HBsAg negative patients were determined as the most important factors associated with the presence of NAFLD. Conclusion:We found that HBsAg positivity is not correlated with the development of NAFLD in young patients, and coexistence of NAFLD and HBV might be coincidental.

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Clinical and laboratory characteristics associated with dyslipidemia and liver steatosis in chronic HBV carriers

Cited by 14 publications

References 39 publications

Peroxisome Proliferators Activated Receptor (PPAR) agonists activate hepatitis B virus replication in vivo

Peroxisome Proliferators Activated Receptor (PPAR) agonists activate hepatitis B virus replication in vivo

PNPLA3rs1010023 Predisposes Chronic Hepatitis B to Hepatic Steatosis but Improves Insulin Resistance and Glucose Metabolism

Can Detection of Non-alcoholic Fatty Liver Disease be Coincidental in Young Patients with Chronic Hepatitis B?

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