High-sensitivity C-reactive protein is an independent clinical feature of nonalcoholic steatohepatitis (NASH) and also of the severity of fibrosis in NASH

Yoneda, Masato; Mawatari, Hironori; Fujita, Koji; Iida, Hiroshi; Yonemitsu, Kenji; Kato, Shingo; Takahashi, Hirokazu; Kohno, Hiroyuki; Inamori, Masahiko; Nozaki, Yuichi; Abe, Yasunobu; Kubota, Kensuke; Saito, Satoru; Iwasaki, Tomoyuki; Terauchi, Yasuo; Togo, Shinji; Maeyama, Shiro; Nakajima, Atsushi

doi:10.1007/s00535-007-2060-x

Cited by 260 publications

(209 citation statements)

References 46 publications

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“…CRP originates in the liver and is increased in people with liver steatosis [32], suggesting a link between chronic inflammation and non-alcoholic fattyliver disease. The association of GGT with insulin resistance, fasting blood glucose and triacylglycerols [33][34][35] and type 2 diabetes [22][23][24] is well described.…”

Section: Discussionmentioning

confidence: 99%

Association of C-reactive protein with type 2 diabetes: prospective analysis and meta-analysis

et al. 2009

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Aims/hypothesis We examined the association between serum C-reactive protein (CRP) and incident diabetes in a prospective study, and added these data to a literature-based meta-analysis to explore potential sources of heterogeneity between studies. Methods We analysed a case-control study nested within the European Prospective Investigation of Cancer (EPIC)-Norfolk cohort, including 293 incident diabetes cases and 708 controls. We combined 16 published studies on CRP and incident diabetes in a random-effect meta-analysis. Results In the EPIC-Norfolk cohort, serum CRP was associated with a higher risk of diabetes after adjusting for age, sex, BMI, family history of diabetes, smoking and physical activity (OR 1.49, comparing the extreme thirds of CRP distribution [95% CI 1.03-2.15], p=0.03). However, the association was completely attenuated after further adjustment for WHR, serum γ-glutamyltransferase and serum adiponectin (OR 1.00; 95% CI 0.66-1.51, p=1.0). In a meta-analysis of 16 published studies with 3,920 incident diabetes cases and 24,914 controls, the RR was 1.72 (95% CI 1.54-1.92), comparing the extreme thirds of CRP distribution, with substantial heterogeneity between studies (I 2 =52.8%, p=0.007). Conclusions/interpretation Initial evidence of association between CRP and incident diabetes was confounded by central adiposity, markers of liver dysfunction and adiponectin in the primary analysis. Despite an overall positive association in the meta-analysis, considerable heterogeneity existed between studies. The degree of adjustment for central adiposity and baseline glycaemia explained some of this heterogeneity and suggests that CRP may not be an independent risk factor for type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Association of C-reactive protein with type 2 diabetes: prospective analysis and meta-analysis

et al. 2009

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“…IL-6 and TNF-α are the major stimuli responsible for increased hepatic production of C-reactive protein (CRP), fibrinogen and other acute-phase proteins [44,52]. It has been shown that fibrinogen and CRP levels, which are known CVD risk factors, are increased in NAFLD patients, particularly in those with NASH [61,62]. The liver is also an important site of production of plasminogen activator inhibitor-1 (PAI-1), another known risk factor for CVD [44].…”

Section: Biological Mechanisms Potentially Responsible For Acceleratementioning

confidence: 99%

Increased risk of cardiovascular disease in non-alcoholic fatty liver disease: causal effect or epiphenomenon?

2008

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Non-alcoholic fatty liver disease (NAFLD), comprising a spectrum of conditions ranging from pure steatosis to steatohepatitis and cirrhosis, has reached epidemic proportions and represents the most common cause of chronic liver disease in the community. The prevalence of NAFLD has been estimated to be between 20% and 30% in the general population, but this value is much higher (∼70-80%) in type 2 diabetic patients, who are also at higher risk of developing advanced fibrosis and cirrhosis. Increasing recognition of the importance of NAFLD and its strong relationship with the metabolic syndrome has stimulated an interest in the possible role of NAFLD in the development of cardiovascular disease (CVD). Several epidemiological studies indicate that NAFLD, especially in its more severe forms, is linked to an increased risk of CVD, independently of underlying cardiometabolic risk factors. This suggests that NAFLD is not merely a marker of CVD, but may also be actively involved in its pathogenesis. The possible molecular mediators linking NAFLD and CVD include the release of pro-atherogenic factors from the liver (C-reactive protein, fibrinogen, plasminogen activator inhibitor-1 and other inflammatory cytokines) as well as the contribution of NAFLD per se to whole-body insulin resistance and atherogenic dyslipidemia, in turn favouring CVD progression. The clinical impact of NAFLD on CVD risk deserves particular attention in view of the implications for screening and surveillance strategies in the growing number of patients with NAFLD.

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“…This criteria was validated in pediatric NAFLD. 118 Yoneda et al 82 have published the first report to demonstrate consistent and profound elevation of high-sensitivity CRP in cases of NASH compared with simple steatosis. The high-sensitivity CRP is superior to anthropometric parameters as a marker of the metabolic consequences of obesity.…”

Section: Biomarkersmentioning

confidence: 99%

“…27,46,[79][80][81] Research results has shown HOMA-IR has notably higher levels in NASH in comparison with simple steatosis, especially in obese children. 32,36,44,[82][83][84][85] In addition, the degree of liver involvement as diagnosed by ultrasonography and level of insulin secretion (oral glucose tolerance test) and IR (HOMA-IR) have shown compatible results. 22,30 There are also some studies based on comparison between different techniques of insulin sensitivity measurement, cutoff point 26,79 and accompanying biochemical test such as a lipid profile.…”

Section: Insulin Resistance Testsmentioning

confidence: 99%

“…111,122,123 Hypoadiponectinemia in NAFLD is part of a metabolic disturbance characterized by decreased hepatic insulin sensitivity and by increased ectopic fat accumulation in the central compartment, especially in the liver. 82 Recently, a rabbit model producing the key features of pediatric NASH concluded that adiponectin levels partially reflect the severity of liver steatosis, but not the degree of liver inflammation. 122 Systemic inflammatory substances and adipocytokines are of key importance in pathogenesis of NASH.…”

Section: Biomarkersmentioning

confidence: 99%

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Nonalcoholic fatty liver disease: a challenge for pediatricians

Widhalm

Ghods

2010

Int J Obes

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Background: Nonalcoholic fatty liver disease (NAFLD) is the most common cause of pediatric liver disease. Its prevalence is related to the growing epidemic in childhood obesity during the past decades. At present, NAFLD and nonalcoholic steatohepatitis (NASH) are increasingly recognized worldwide. In spite of alarming trend in the epidemiology in pediatric field and growing risk of end stage liver disease, there is no significant advance in its diagnosis and treatment. Aim: To provide a detailed review for diagnosis and management of NAFLD and NASH. Methods: By using Pubmed to find review articles and relevant research. Results: The prevalence ranges from at least 3% in children overall to about 50% in obese children. The noninvasive biomarkers can be used to identify NAFLD/NASH patients. Diagnostic criteria based on biochemical and immunological indicators in the high-risk group of children could prevent about half of cases from receiving an invasive test. The pharmacological and surgical interventions have shown a growing role in pediatric NAFLD. Novel treatment modalities, such as probiotics, have hardly been studied. Conclusion: Early diagnosis by using noninvasive screening methods in high-risk groups is the most effective strategy against the NAFLD. The biology of early growth and development, including hepatic metabolism, may hold the key to pediatric NAFLD. Prevention of overweight children and childhood obesity is undoubtedly the best strategy for treating NAFLD.

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High-sensitivity C-reactive protein is an independent clinical feature of nonalcoholic steatohepatitis (NASH) and also of the severity of fibrosis in NASH

Cited by 260 publications

References 46 publications

Association of C-reactive protein with type 2 diabetes: prospective analysis and meta-analysis

Association of C-reactive protein with type 2 diabetes: prospective analysis and meta-analysis

Increased risk of cardiovascular disease in non-alcoholic fatty liver disease: causal effect or epiphenomenon?

Nonalcoholic fatty liver disease: a challenge for pediatricians

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