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ABSTRACT: Portal hypertension (PHT) is defined as a pathological increase in portal venous pressure and frequently accompanies cirrhosis. Portal pressure can be increased by a rise in portal blood flow, an increase in vascular resistance, or the combination. In cirrhosis, the primary factor leading to PHT is an increase in intra-hepatic resistance to blood flow. Although much of this increase is a mechanical consequence of architectural disturbances, there is a dynamic and reversible component that represents up to a third of the increased vascular resistance in cirrhosis. Many vasoactive substances contribute to the development of PHT. Among these, nitric oxide (NO) is the key mediator that paradoxically regulates the sinusoidal (intra-hepatic) and systemic/splanchnic circulations. NO deficiency in the liver leads to increased intra-hepatic resistance while increased NO in the circulation contributes to the hyperdynamic systemic/splanchnic circulation. NO mediated-angiogenesis also plays a role in splanchnic vasodilation and collateral circulation formation. NO donors reduce PHT in animals models but the key clinical challenge is the development of an NO donor or drug delivery system that selectively targets the liver.
World Journal of Gastroenterology 03/2013; 19(11):1707-17. · 2.47 Impact Factor
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ABSTRACT: Single nucleotide polymorphisms (SNPs) in the proximity of the interleukin-28B (IL28B) gene can predict spontaneous resolution of hepatitis C virus (HCV) infection and response to interferon therapy. Screening for this polymorphism has become part of the standard criteria for the management of HCV-infected patients, hence the need for a rapid, cost-effective screening method. Here, we describe a rapid PCR-based test to screen for two IL28B SNPs (rs12979860 and rs8099917). We used this test to investigate IL28B polymorphism and prevalence in a cohort of French Canadian injection drug users who are part of a unique population known to have a strong genetic founder effect. This population had lower linkage disequilibrium between the two tested SNPs as compared to other cohorts (|d'| = 0.68, r = 0.59). The special genetic makeup should be considered in the management of HCV-infected patients within that population.
Immunogenetics 03/2013; · 2.93 Impact Factor
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ABSTRACT: BACKGROUND: To increase cure rates for Hepatitis C, barriers to treatment adherence and completion must be identified and overcome. AIMS: This study systematically reviewed evidence on the psychological, lifestyle and social determinants of achieving viral eradication with antiviral therapy. METHODS: An electronic search strategy was used to identify relevant studies that examined psychological, lifestyle and social factors related to achieving a sustained virological response (SVR). RESULTS: Thirty-four studies that matched our criteria were identified. Of the factors that predict response to treatment, Asian ethnicity was an independent predictor of SVR. We found an indirect relationship between diet and SVR, with non-responders to treatment consuming more polyunsaturated fatty acids, fats and carbohydrates than those who attained SVR. The effect of alcohol consumption relied on the amount consumed; fewer than 30 grams daily had no effect on SVR, whereas >70 grams daily had an adverse impact on a patient's ability to achieve SVR, with termination rates up to 44% in those who drank >2 drinks a day. Patients with psychiatric illnesses had comparable SVR rates to controls if they continued psychological therapy (average 42%), although discontinuation rates were high with 11 studies reporting rates from 14 to 48%. CONCLUSIONS: There are major gaps in current knowledge of the impact of variables such as diet, exercise, attitudes and coping skills on cure rates in chronic Hepatitis C. Those who drink limited amounts of alcohol or have psychiatric disorders should be offered treatment for their disease, with adjunctive education and support to improve treatment completion.
Liver international: official journal of the International Association for the Study of the Liver 02/2013; · 3.82 Impact Factor
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ABSTRACT: To evaluate the long-term treatment outcomes of entecavir monotherapy in treatment naive patients in an Australian tertiary care setting.
A retrospective analysis of treatment naive patients receiving entecavir monotherapy through Westmead Hospital was performed. Patients were excluded if they had received previous treatment with another nucleoside or nucleotide analogue, were pregnant or less than 18 years old.
Out of 336 patients, 163 patients fulfilled the selection criteria. Range of follow up was 3-46 mo (mean 26 mo). 134 patients (82.2%) had pre-treatment biopsies, with 26 patients (16.0 %) demonstrating F3-4 fibrosis. In total, 153 patients (93.9%) achieved at least Partial Virological Suppression (PVS), with 134 patients (82.2%) achieving complete virological suppression. The cumulative CVS and PVS rates at 36 mo were 82.1% and 96.4%, respectively. 3 patients (1.8%) failed to achieve PVS, while 5 patients (3.0%) developed virological rebound. 128 patients (78.5%) maintained CVS throughout follow up. Predictors of CVS included lower baseline DNA level (P = 0.001), hepatitis B virus e antigen negative status (P = 0.001) and increasing age at treatment (log rank 0.001). No significant adverse effects were reported necessitating cessation of entecavir.
Entecavir monotherapy is efficacious and safe in an Australian tertiary care setting. Resistance and rebound rates are very low. This is similar to data from controlled and uncontrolled trials around the world.
World Journal of Gastroenterology 02/2013; 19(5):721-6. · 2.47 Impact Factor
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ABSTRACT: Attempts to elucidate the mechanism underpinning the genetic association between IFNL3, previously called IL28B, and clearance of hepatitis C virus have, by and large, been unsuccessful. A study in this issue suggests that a new gene, IFNL4, may be responsible.
Nature Genetics 02/2013; 45(2):119-20. · 35.53 Impact Factor
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Jason Grebely,
Jordan J Feld,
Tanya Applegate,
Gail V Matthews,
Margaret Hellard,
Alana Sherker,
Kathy Petoumenos,
Geng Zang,
Ineke Shaw,
Barbara Yeung, Jacob George,
Suzy Teutsch,
John M Kaldor,
Vera Cherepanov,
Julie Bruneau,
Naglaa H Shoukry,
Andrew R Lloyd,
Gregory J Dore
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ABSTRACT: Systemic levels of interferon-gamma-inducible protein-10 (IP-10) are predictive of treatment-induced clearance in chronic HCV. In the present study, factors associated with plasma IP-10 levels at the time of acute HCV detection and the association between IP-10 levels and spontaneous clearance were assessed in three cohorts of acute HCV infection. Among 300 individuals, 245 (181 male, 47 HIV+) were HCV RNA+ at acute HCV detection. In adjusted analysis, factors independently associated with IP-10 levels ≥150 pg/mL (median level) included HCV RNA levels >6 log IU/mL, HIV co-infection and non-Aboriginal ethnicity. Among 245 HCV RNA+ at acute HCV detection, 214 were untreated (n=137) or had persistent infection (infection duration ≥26 weeks) at treatment initiation (n=77). Spontaneous clearance occurred in 14% (29 of 214). Individuals without spontaneous clearance had significantly higher mean plasma IP-10 levels at the time of acute HCV detection than those with clearance (248±32 vs. 142±22 pg/mL, P=0.008). The proportion of individuals with spontaneous clearance was 0% (0 of 22, P=0.048) and 16% (27 of 165) and in those in those with and without plasma IP-10 levels ≥380 pg/mL. In adjusted analyses, favourable IL28B genotype was associated with spontaneous clearance, while higher HCV RNA level was independently associated with lower odds of spontaneous clearance. Conclusion: High IP-10 levels at acute HCV detection were associated with failure to spontaneously clear HCV. Patients with acute HCV and high baseline IP-10 levels, particularly >380 pg/mL, should be considered for early therapeutic intervention, and those with low levels should defer therapy for potential spontaneous clearance. (HEPATOLOGY 2013.).
Hepatology 01/2013; · 11.66 Impact Factor
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ABSTRACT: In Australia, chronic hepatitis B (CHB) disproportionately affects migrants born in hepatitis B endemic countries, but its detection and management in high risk populations remains suboptimal. We piloted a primary care based program for CHB detection and management in an area of high disease prevalence in Sydney, Australia. Prior to its launch, all local general practitioners were invited to take part in a continuing medical education (CME) program on hepatitis B diagnosis and management.
Preceding each CME activity, participants completed an anonymous survey recording demographic data and hepatitis B knowledge, confidence in CHB management, and preferred CME modalities. We compared knowledge scores of first-time and repeat attendees.
Most participants (75%) were males, spoke more than one language with their patients (91%), self-identified as Asian-Australians (91%), and had graduated over 20 years previously (69%). The majority (97%) knew what patient groups require CHB and hepatocellular cancer screening, but fewer (42%-75%) answered hepatitis B management and vaccination questions correctly. Knowledge scores were not significantly improved by seminar attendance and the provision of hepatitis B resources. At baseline, participants were fairly confident about their ability to screen for CHB, provide vaccinations, and manage CHB. This did not change with repeat attendances, and did not correlate with survey outcomes. Large group CMEs were the preferred learning modality.
Knowledge gaps in hepatitis B diagnosis and management translate into missed opportunities to screen for CHB, to vaccinate those susceptible, and to prevent disease complications. The results suggest that a range of innovative CME programs are required to update general practitioners on the modern management of CHB infection.
International Journal of General Medicine 01/2013; 6:115-22.
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ABSTRACT: It is a widely held view that drug response genes have not proved as useful in clinical practice as anticipated at the start of the genomic era. An exception is in the treatment for chronic hepatitis C virus (HCV) genotype 1 infection with pegylated interferon α and ribavirin. In 2009, four independent genome-wide analyses identified IL28B polymorphisms that predict drug response in chronic hepatitis C (CHC). This discovery had immediate clinical impact. First, the IL28B genotype could be used to personalize therapy. In the 2 years since discovery, most of the more than 100,000 CHC patients commencing therapy for CHC in the West will have considered IL28B genotype testing. Second, the discovery has supported clinical trials for the use of the protein encoded by the gene known as interferon lambda. Third, it is expected that new insights into HCV pathogenesis will follow from studies of how IL28B affects HCV viral clearance and, ultimately, this will lead to new therapeutic strategies for CHC. This review discusses how IL28B genotyping is now used in personalizing therapy and, with the dramatically changing clinical landscape in CHC, with the advent of direct-acting antivirals, the prospects ahead.
Genome Medicine 12/2012; 4(12):99.
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Salvatore Petta,
Chiara Rosso,
Reynold Leung,
Maria Lorena Abate,
David Booth,
Federico Salamone,
Roberto Gambino,
Mario Rizzetto,
Paolo Caviglia,
Antonina Smedile,
Stefania Grimaudo,
Calogero Cammà,
Antonio Craxì, Jacob George,
Elisabetta Bugianesi
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ABSTRACT: BACKGROUND & AIMS: Patients with genotype 1 chronic hepatitis C (G1-CHC) frequently develop steatosis and insulin resistance (IR), caused by metabolic and viral factors. These accelerate progression of liver disease progression and reduce the response to therapy. A sustained virologic response (SVR) to therapy in patients with G1-CHC is strongly associated with polymorphisms near the IL28B gene, but the interaction between IL28B genotype and IR, and their combined effects on SVR, have not been defined. We tested the association between the IL28B rs12979860 single nucleotide polymorphism (SNP) and metabolic features, including IR, and evaluated their effects on SVR. METHODS: We performed genotype analysis of IL28B rs12979860 for 434 Caucasian G1-CHC patients who underwent consecutive biopsy analysis at 3 tertiary centers. Metabolic profile analyses included assessments of lipid levels and IR by the homeostasis model assessment (HOMA-IR). RESULTS: Patients with the CC polymorphism in IL28B had higher levels of total and low-density lipoprotein cholesterol, lower levels of triglycerides, and lower prevalences of IR and moderate-severe steatosis (P<.05) than patients without this genotype. By multiple logistic regression analysis, body mass index (odds ratio [OR], 1.223; P<.001), level of triglyceride (OR, 1.007; P=.006), the CC polymorphism in IL28B (OR, 0.378; P=.001) and levels of HCV RNA>850,000 IU/ml (OR, 1.803; P=.01) were associated with IR. The CC polymorphism in IL28B (OR, 8.350; P<.001) and IR (OR, 0.432; P=.005), but not steatosis (OR, 0.582; P=0.25), were associated with an SVR. CONCLUSIONS: In Caucasian patients with G1-CHC, the IL28B rs12979860 CC genotype is associated with reduced IR. IL28B rs12979860 genotype and HOMA-IR strongly affect the outcome of antiviral therapy.
Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 12/2012; · 5.64 Impact Factor
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ABSTRACT: There is emerging evidence that the association between obesity and cancer is mediated by visceral rather than generalised body fat. Visceral fat has been directly implicated in the risk and progression of several gastrointestinal cancers including colorectal, oesophageal, pancreatic and hepatocellular carcinomas. Excess visceral adipose tissue induces a state of chronic systemic inflammation and altered metabolic activity that promotes a pro-oncogenic environment. This review examines the evidence linking visceral fat in gastrointestinal and hepatic carcinogenesis and explores our current understanding of the mechanisms underlying this relationship.
Cancer letters 11/2012; · 4.86 Impact Factor
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ABSTRACT: BACKGROUND & AIMS: The relationship between vitamin D status and response to antiviral therapy and liver histology in hepatitis C virus genotype 1 (HCV-1) infection remains unclear with studies to date yielding inconsistent results and failing to use reference assay methodology. We therefore analyzed pre-treatment 25-hydroxyvitamin D [25(OH)D] level using reference liquid chromatography-tandem mass spectrometry methodology in a cohort of treatment-naïve patients with HCV-1 to evaluate the association between vitamin D status, virologic response, and liver histology. METHODS: 274 patients with pre-treatment liver biopsy and up to 48 weeks of pegylated interferon alfa-2a plus ribavirin therapy were tested for serum 25(OH)D level. Predictors of sustained virologic response (SVR), and variables associated with fibrosis stage, activity grade and 25(OH)D status were identified using multivariate analysis. RESULTS: Mean 25(OH)D level was 79.6 nmol/L, with a prevalence of 25(OH)D <75 nmol/L and <50 nmol/L of 48% and 16% respectively. Season, race and geographic latitude were independent predictors of 25(OH)D status, while vitamin D deficiency was more prevalent in those with high activity grade (21% vs 11%; P=0.03). Mean 25(OH)D level was lower (76.6 vs 84.7 nmol/L; P=0.03) and 25(OH)D <75 nmol/L more prevalent (53% vs 40%; P=0.03) in patients with an SVR, but no association between 25(OH)D status and SVR was found on multivariate analysis. Mean 25(OH)D level did not vary between fibrosis stage or activity grade. CONCLUSIONS: Baseline 25(OH)D level is not independently associated with SVR or fibrosis stage in HCV-1, but vitamin D deficiency is associated with high activity grade.
Journal of Hepatology 11/2012; · 9.26 Impact Factor
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ABSTRACT: To compare program costs of chronic hepatitis B (CHB) screening and treatment using Australian and other published CHB treatment guidelines.
Economic modeling demonstrated that in Australia a strategy of hepatocellular cancer (HCC) prevention in patients with CHB is more cost-effective than current standard care, or HCC screening. Based upon this model, we developed the B positive program to optimize CHB management of Australians born in countries of high CHB prevalence. We estimated CHB program costs using the B positive program algorithm and compared them to estimated costs of using the CHB treatment guidelines published by the Asian-Pacific, American and European Associations for the Study of Liver Disease (APASL, AASLD, EASL) and those suggested by an independent United States hepatology panel. We used a Markov model that factored in the costs of CHB screening and treatment, individualized by viral load and alanine aminotransferase levels, and calculated the relative costs of program components. Costs were discounted by 5% and calculated in Australian dollars (AUD).
Using the B positive algorithm, total program costs amount to 13 979 224 AUD, or 9634 AUD per patient. The least costly strategy is based upon using the AASLD guidelines, which would cost 34% less than our B positive algorithm. Using the EASL and the United States Expert Group guidelines would increase program costs by 46%. The largest expenditure relates to the cost of drug treatment (66.9% of total program costs). The contribution of CHB surveillance (20.2%) and HCC screening and surveillance (6.6%) is small - and together they represent only approximately a quarter of the total program costs.
The significant cost variations in CHB screening and treatment using different guidelines are relevant for clinicians and policy makers involved in designing population-based disease control programs.
World Journal of Gastroenterology 11/2012; 18(42):6106-13. · 2.47 Impact Factor
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ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) and its progressive form, nonalcoholic steatohepatitis (NASH), are an increasingly common cause of chronic liver disease in the developed world, with NASH projected to be the leading cause of liver transplantation in the United States by 2020. This review of NASH management addresses current data from the perspective of levels of evidence for therapeutic options in NASH, including lifestyle modification, drug therapies, and bariatric surgery. In particular, behavioral therapies to assist patients in adopting lifestyle changes are highlighted and a research agenda for future NASH management is presented.
Clinics in liver disease 08/2012; 16(3):631-45.
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Hepatology 06/2012; · 11.66 Impact Factor
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ABSTRACT: OBJECTIVE.: Non alcoholic steatohepatitis is the commonest liver disease in developed countries. However, there is no current data on the cost effectiveness of therapeutic options such as lifestyle modification, pioglitazone or Vitamin E at a population level. We undertook a cost utility analysis to compare these strategies. METHODS.: Using a third party payer perspective, a deterministic Markov model was developed to compare costs and health benefits of lifestyle modification alone or with pioglitazone or Vitamin E in a cohort of patients aged 50 years with biopsy proven NASH and fibrosis level 3 or greater. We assumed an annual cycle length over a lifetime horizon. Probability and utility estimates were derived from a systematic literature review, and uncertainties in parameter estimates were tested using one and two way sensitivity analyses. Our outcome measure was the incremental cost effectiveness ratio (ICER), with $A50,000 or less considered cost effective. RESULTS.: In comparison with lifestyle modification alone, treatment with either pioglitazone or Vitamin E in addition to lifestyle modification was cost effective, with incremental cost effectiveness ratios of $A2058 and $A8083 per quality adjusted life year (QALY) gained, respectively. In a direct comparison, pioglitazone was more cost effective than Vitamin E (ICER $A2056/QALY gained). Sensitivity analyses indicated that pioglitazone was not cost effective if either the total drug cost was greater than $A16,000 per annum, or the annual probability of developing cirrhosis in advanced fibrosis was less than 2%. CONCLUSION.: Our modelled analyses suggest that in patients with advanced fibrosis due to NASH, pharmacological treatment in addition to standard lifestyle modification is likely to be cost effective. (HEPATOLOGY 2012.).
Hepatology 06/2012; · 11.66 Impact Factor
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ABSTRACT: To determine hepatitis C (HCV) treatment effectiveness and predictors of response in the "real-world" Australian clinic setting.
Patients with chronic HCV, who were HCV-treatment-naive at enrolment, and were then treated with standard therapy (pegylated interferon-α plus ribavirin), were recruited prospectively through a national network of 24 HCV clinics between April 2008 and December 2009. Patients were interviewed and a medical record review was conducted at enrolment and at routine follow-up clinic visits.
Proportion of patients achieving a sustained virological response (SVR), predictors of SVR, and impact of treatment on biochemical markers of liver disease (alanine aminotransferase levels and aspartate aminotransferase-to-platelet ratio index scores).
The SVR by intention to treat was 60% (327/550). Infection with HCV genotype 2 or 3 (compared with genotype 1) was an independent predictor of SVR (odds ratio [OR], 2.45; 95% CI, 1.70-3.52), while HIV coinfection (OR, 0.28; 95% CI, 0.10-0.82), cirrhosis (OR, 0.38; 95% CI, 0.18-0.81), and increased body mass index for ≥ 30 kg/m(2) v ≤ 25 kg/m(2) (OR, 0.58; 95% CI, 0.35-0.96) were independently associated with lower SVR. There was a significant improvement in biochemical markers of liver disease following SVR (P< 0.001).
Our findings are similar to those seen in clinical trials, despite the inclusion of patients with a broad range of comorbid conditions such as injecting drug and alcohol use and psychiatric illness. They suggest that, with appropriate patient and infrastructure support, expansion of treatment services to the broader HCV-infected community is warranted.
The Medical journal of Australia 06/2012; 196(10):633-7. · 2.81 Impact Factor
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Jason Grebely,
Margaret Hellard,
Tanya Applegate,
Kathy Petoumenos,
Barbara Yeung,
Jordan J Feld,
William Rawlinson,
Andrew R Lloyd, Jacob George,
John M Kaldor,
Gregory J Dore,
Gail V Matthews
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ABSTRACT: The role of ribavirin (RBV) in the treatment of recent hepatitis C virus (HCV) (acute/early chronic) is unclear, particularly in HIV-infected individuals. This study evaluated early virological decline during recent HCV therapy in HIV-uninfected individuals receiving pegylated interferon (PEG-IFN) monotherapy and HIV-infected individuals receiving PEG-IFN/RBV.
The Australian Trial in Acute Hepatitis C was a nonrandomized prospective study of patients with recent HCV.
All participants received PEG-IFN (24 weeks); HCV/HIV participants also received RBV. Early HCV RNA decline was assessed among adherent participants (≥80% PEG-IFN, ≥80% treatment). Logistic regression identified predictors of rapid virological response (RVR) (<10 IU/ml).
Of 109 treated, 82% were adherent (HCV, n=57; HCV/HIV, n=32). Overall, RVR was 51% (HCV: 55% vs. HCV/HIV: 43%; P=0.323). Factors independently associated with RVR included duration of infection less than 26 weeks, HCV RNA below 5.6 log(10) IU/ml at baseline and HCV genotype 2/3 infection. Between baseline and week 12, mean decline in HCV RNA was greater in HCV/HIV participants (PEG-IFN/RBV) compared to HCV participants (PEG-IFN) (4.19 vs. 3.32 log(10) IU/ml; P=0.029). Greater HCV RNA decline was observed in those treated with RBV, particularly amongst those with an estimated duration of infection at least 26 weeks and those with unfavourable IL28B genotypes. Adherent HIV-uninfected and infected participants had similar early virological response (76 vs. 90%; P=0.102) and sustained virological response (63 vs. 75%; P=0.253), respectively. RVR was highly predictive of sustained virological response (adjusted odds ratio 4.09; 1.49, 11.25).
The results of this study suggest a potential benefit for PEG-IFN and RBV combination therapy in maximizing virological responses in HCV/HIV participants with recent HCV, particularly those with a longer duration of HCV infection and unfavourable IL28B genotypes.
AIDS (London, England) 05/2012; 26(13):1653-61. · 4.91 Impact Factor
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ABSTRACT: Aim: Little is known about the patterns of care and the impact of hepatocellular carcinoma (HCC) treatment on health outcomes at a population level. We conducted a population-based cohort study to examine HCC survival trends among people diagnosed with hepatitis B (HBV) or hepatitis C virus (HCV) infection, to determine predictors of receiving potentially curative therapy for HCC, and to examine the impact of HCC treatment on survival in New South Wales, Australia. Methods: The Kaplan-Meier method was used to estimate survival, logistic regression to determine predictors of potentially curative therapy and Cox proportional hazards models to determine the impact of HCC treatment on survival. Years of potential life lost (YPLL) were calculated. Results: During the period 1993-2007, 1081 cases of HCC were diagnosed. Median survival increased from 10.4 months during 1993-1997 to 18.4 months during 1998-2002, with no further improvement thereafter. Younger age at diagnosis (<65 years), being Asian-born and having multiple comorbid conditions increased the odds of receiving curative therapy. The effect of HCC treatment on the risk of mortality was similar between the HBV- and HCV-related HCC groups. Tumor-specific therapies had adjusted hazard ratios ranging 0.06-0.25 and palliative/supportive therapy alone had adjusted hazard ratios ranging 0.76-1.08. The average YPLL per person was 23.3. Conclusion: The burden of viral hepatitis-related HCC is substantial. Despite treatment advances in recent years, there has been no significant improvement in HCC survival. Efforts to improve HCC screening and early diagnosis are required to deliver curative treatment which clearly has a survival advantage.
Hepatology Research 04/2012; · 2.20 Impact Factor
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ABSTRACT: Visceral adiposity is associated with hepatic steatosis, inflammation, and fibrosis in non-alcoholic fatty liver disease (NAFLD). The visceral adiposity index (VAI), a novel marker of visceral fat distribution and dysfunction, has been correlated with histology in hepatitis C. We assessed the ability of VAI to predict disease severity in NAFLD and hence its role as a non-invasive marker of liver damage.
We examined 190 adults with biopsy-proven NAFLD and 129 controls. All had anthropometric and metabolic profiling. VAI was calculated using waist circumference (WC), body mass index, triglycerides, and HDL-cholesterol. Abdominal fat was quantified by magnetic resonance imaging (MRI) in 38 patients.
On multivariate analysis, NAFLD diagnosis and fasting glucose were independently associated with VAI (p <0.05). VAI increased across control, steatosis, and NASH groups (1.5, 2.3, and 3.2, respectively; p=0.000), however, this association was no stronger than the increase in WC across groups (r=0.452 vs. 0.540 respectively, p <0.001). VAI was not associated with steatosis, lobular inflammation or fibrosis, but WC was associated with fibrosis (p=0.01). VAI and WC correlated with an increasing number of metabolic syndrome components (r=0.623 vs. 0.614, p <0.001) and with metabolic syndrome diagnosis (r=0.559 vs. 0.509, p <0.001). VAI only modestly correlated with visceral fat on MRI (r=0.39, p <0.05) compared to WC (r=0.52, p <0.01).
In NAFLD, VAI is not associated with steatosis, inflammation or fibrosis. VAI is no more powerful than WC in discriminating steatosis from steatohepatitis, reflecting limitations of the formula with what is known about the pathogenesis of NAFLD.
Journal of Hepatology 04/2012; 57(2):392-8. · 9.26 Impact Factor
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Journal of Hepatology 03/2012; 57(2):469-70. · 9.26 Impact Factor
