Concurrent Obesity, Diabetes, and Steatosis Increase Risk of Advanced Fibrosis Among HCV Patients: A Systematic Review

Dyal, Harleen K.; Aguilar, María; Bhuket, Taft; Liu, Benny; Holt, Edward W.; Torres, Sharon; Cheung, Ramsey; Wong, Robert J.

doi:10.1007/s10620-015-3760-3

Cited by 57 publications

(46 citation statements)

References 38 publications

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“…Consistent with the literature 8,21,26,45,46 , diabetes was a major predictor of progression to advanced fibrosis in our cohort. Notably diabetes remained a risk factor even after adjusting for HCV coinfection and BMI.…”

Section: Discussionsupporting

confidence: 92%

Poorly Controlled HIV Infection: An Independent Risk Factor for Liver Fibrosis

Kim¹,

Nance²,

Rompaey³

et al. 2016

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Background Liver disease is a major cause of mortality among HIV-infected persons. There is limited information about the extent to which HIV disease severity impacts liver disease progression. Methods We determined the incidence and predictors of advanced hepatic fibrosis measured by the FIB-4 index (≥3.25) in a large diverse population of HIV-infected patients without significant liver disease at baseline (FIB-4<1.45) in care between January 2000 and March 2014. We used Cox proportional hazards analysis to examine factors associated with progression to FIB-4 ≥3.25. Results Among 14,198 HIV-infected patients, HCV coinfection (adjusted hazard ratio [aHR] 1.9, 95% CI 1.6–2.1), HBV coinfection (aHR 1.5, 95% CI 1.2–1.8), alcohol use disorder (aHR 1.4, 95% CI 1.2–1.6) and diabetes (aHR 1.9, 95% CI 1.6–2.3) were associated with progression to advanced fibrosis in multivariable analysis. In addition, patients at each lower level of time-varying CD4 count had a significantly greater risk of progression, with a nearly 7-fold higher risk in those with CD4 <100 cells/mm3 (aHR 6.9, 95% CI 5.8–8.3) compared with CD4 ≥500 cells/mm3. An increasing gradient of risk was also observed among patients with higher time-varying HIV viral load (VL), with the greatest risk noted with VL ≥100,000 copies/ml (aHR 2.6, 95% CI 2.2–3.1) compared with VL <500 copies/ml. Conclusion Lower CD4 count and higher HIV VL were significantly associated with progression to advanced hepatic fibrosis in a dose-dependent manner, independent of the risk associated with traditional factors: HCV or HBV coinfection, alcohol, and diabetes. Our findings suggest that early treatment of HIV infection could mitigate liver disease.

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Section: Discussionsupporting

confidence: 92%

Poorly Controlled HIV Infection: An Independent Risk Factor for Liver Fibrosis

Kim¹,

Nance²,

Rompaey³

et al. 2016

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…In chronic hepatitis B, presence of DM could prevent fibrosis regression after antiviral therapy for chronic hepatitis B and also associated with progression of liver fibrosis and complications of liver cirrhosis. 34–36 DM appears to be a significant factor of advanced liver fibrosis in NAFLD and chronic hepatitis C. 37,38 Taking together of lines of evidence indicated that DM seems to play an universal role in liver fibrosis progression either in general population or in coexisting chronic liver diseases.…”

Section: Discussionmentioning

confidence: 99%

The Application of Liver Stiffness Measurement in Residents Without Overt Liver Diseases Through a Community-Based Screening Program

Cheng

Chiu²,

Chiu³

et al. 2016

Medicine

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The application of liver stiffness measurement (LSM) by transient elastography (TE) in general population remains to clarify. This cohort study aimed to examine the usefulness of TE and to identify factors associated with significant liver fibrosis in community-based population.We conducted a hepatitis screening program in 2 remote villages of Southern Taiwan. All residents participated voluntarily and received questionnaire evaluation, blood tests, abdominal sonography, and LSM by TE. Residents with any one of following criteria including hepatitis B virus infection, hepatitis C virus infection, more than moderate alcohol drinking, and failure to obtain valid or reliable LSM were excluded.There were 831 residents participated in program. The valid and reliable LSM were obtained in 98.3% and 96.3% of residents, respectively. Finally, a total of 559 residents including 283 residents with nonalcoholic steatotic fatty liver disease (NAFLD) were enrolled for analysis. The mean liver stiffness was 4.9 ± 1.9 kPa. The liver stiffness increased in residents with diabetes mellitus (DM), higher body mass index (BMI), hypertension, abnormal waist–hip circumference ration (WHR), higher waist circumference (WC), and presence of fatty liver. Higher body weight, higher BMI, higher WC, abnormal WHR, abnormal aspartate aminotransferase (AST), abnormal alanine aminotransferase (ALT), and DM were the factors associated with significant fibrosis (liver stiffness ≥7 kPa) in either all participants or NAFLD residents. As determined by multivariate analysis, abnormal AST values and DM were the 2 independent factors in all participants (abnormal AST: OR 3.648, 95% CI 1.134–11.740, P = .03; DM: OR 2.882, 95% CI 1.282–6.478, P = .01) and in residents with NAFLD (abnormal AST: OR 4.197, 95% CI 1.154–15.262, P = .03; DM: OR 3.254, 95% CI 1.258–8.413, P = .02).LSM by TE is a useful screening tool in community. In residents, who were absence of chronic hepatitis virus infection or consumed less than moderate alcohol drinking, exhibited DM or abnormal AST values may consider a substantial group with significant fibrosis in community.

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“…We hypothesized that AGS inhibits PAR2 signal expression and thereby improves hepatic function during development of hepatic fibrosis. It should be noted that chronic liver diseases and diabetes are often present in the same patient [16, 17]. Clinical studies have shown that diabetic patients have a higher risk to have hepatic fibrosis [16].…”

Section: Introductionmentioning

confidence: 99%

“…It should be noted that chronic liver diseases and diabetes are often present in the same patient [16, 17]. Clinical studies have shown that diabetic patients have a higher risk to have hepatic fibrosis [16]. Notably, numerous cellular and molecular mechanisms are involved in hepatic fibrosis as well as in diabetes [17, 18].…”

Section: Introductionmentioning

confidence: 99%

Astragaloside Alleviates Hepatic Fibrosis Function via PAR2 Signaling Pathway in Diabetic Rats

Wang

Xiang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Astragaloside (AGS) extracted from radix astragalin (Huangqi) has been considered to be beneficial to liver diseases. In this study, we examined the role played by AGS in alleviating hepatic fibrosis function via protease-activated receptor-2 (PAR2) mechanisms. We hypothesized that AGS affects PAR2 signaling pathway thereby improving hepatic function in rats with hepatic fibrosis induced by carbon tetrachloride (CCl₄). We further hypothesized that AGS attenuates impaired hepatic function evoked by CCl₄ to a greater degree in diabetic animals. Methods: ELISA and Western Blot analysis were used to examine PAR2 signaling pathway in diabetic CCl₄-rats and non-diabetic CCl₄-rats. Results: AGS inhibited the protein expression of PAR2 and its downstream pathway PKA and PKCɛ in CCl₄-rats. Notably, the effects of AGS were greater in CCl₄-rats with diabetes. AGS also significantly attenuated the CCl₄-induced upregulations of pro-inflammatory cytokines, namely interleukin-1β, interleukin-6 and tumor necrosis factor-α accompanied with decreases of collagenic parameters such as hexadecenoic acid, laminin and hydroxyproline. Additionally, AGS improved the CCl₄-induced exaggerations of liver index and functions including alanine aminotransferase, aspartate aminotransferase. Moreover, TGF-β1, a marker of hepatic fibrosis, was increased in CCl₄-rats and AGS inhibited increases in TGF-β1 induced by CCl₄. Conclusions: AGS alleviates hepatic fibrosis by inhibiting PAR2 signaling expression and its effects are largely enhanced in diabetic animals. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of hepatic fibrosis; and results of our study are likely to shed light on strategies for application of AGS because it has potentially greater therapeutic effectiveness for hepatic fibrosis in diabetes.

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Concurrent Obesity, Diabetes, and Steatosis Increase Risk of Advanced Fibrosis Among HCV Patients: A Systematic Review

Cited by 57 publications

References 38 publications

Poorly Controlled HIV Infection: An Independent Risk Factor for Liver Fibrosis

Poorly Controlled HIV Infection: An Independent Risk Factor for Liver Fibrosis

The Application of Liver Stiffness Measurement in Residents Without Overt Liver Diseases Through a Community-Based Screening Program

Astragaloside Alleviates Hepatic Fibrosis Function via PAR2 Signaling Pathway in Diabetic Rats

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