Enhanced serum concentrations of transforming growth factor-beta1 in simple fatty liver: is it really benign?

Tarantino, Giovanni; Conca, Paolo; Riccio, Antonio; Tarantino, Marianna; Minno, Matteo Nicola Dario Di; Chianese, Donato; Pasanisi, Fabrizio; Contaldo, Franco; Scopacasa, Francesco; Capone, Domênico

doi:10.1186/1479-5876-6-72

Cited by 76 publications

(48 citation statements)

References 23 publications

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“…In fact, up to 5% of patients may progress from steatosis to NASH and even cirrhosis [34]. In further support of the notion that steatosis by itself has profound clinical ramifications is the finding, reported by Tarantino et al [35], of similar levels of transforming growth factor-beta 1 in serum of patients with steatosis as well as NASH. This data suggests that these two seemingly disparate conditions share common pathophysiology and that ''simple steatosis'' might not be benign.…”

Section: Natural History and Prognosismentioning

confidence: 84%

Nonalcoholic Fatty Liver Disease: A Review and Update

2010

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The spectrum of nonalcoholic fatty liver disease (NAFLD) ranges from asymptomatic steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. Hepatic steatosis occurs when free fatty acids, released in the setting of insulin resistance and the metabolic syndrome, are taken up by the liver. Additional biochemical insults, including oxidative stress, upregulation of inflammatory mediators, and dysregulated apoptosis, can result in inflammation (producing NASH) and fibrosis. Noninvasive methods (e.g., abdominal ultrasonography) are safe ways to support a diagnosis of hepatic steatosis, but advanced liver histopathologic findings including NASH and fibrosis cannot be identified without pursuing liver biopsy. Recent advances in serologic and imaging methods aim to determine severity of inflammation and fibrosis noninvasively. Currently, therapeutic options for NAFLD are limited to medications that reduce risk factors, but the future holds promise for therapies that might slow the progression of this increasingly prevalent disorder.

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Section: Natural History and Prognosismentioning

confidence: 84%

Nonalcoholic Fatty Liver Disease: A Review and Update

2010

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“…In a study by Cayón et al revealed that non-obese and non-fibrotic NASH patients had significant increase in hepatic gene expression of CTGF compared to non-NASH cases [24]. In the study of Tarantino et al TGFβ-1 levels were found to be higher in simple steatosis cases compared to patients with chronic hepatitis C [25]. Even though it is not statistically significant, serum CTGF levels were slightly elevated in simple steatosis cases compared to healthy controls in our study.…”

Section: Discussionmentioning

confidence: 99%

Concentrations of Connective Tissue Growth Factor in Patients with Nonalcoholic Fatty Liver Disease: Association with Liver Fibrosis

et al. 2012

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Aim:In this study, we aimed to investigate the relationship between the histological fibrosis stage of nonalcoholic fatty liver disease (NAFLD) and serum connective tissue growth factor (CTGF) to determine the usefulness of this relationship in clinical practice.Methods:Serum samples were collected from 51 patients with biopsy-proven NAFLD and 28 healthy controls, and serum levels of CTGF were assayed by ELISA.Results:Levels of CTGF were significantly higher in patients with NAFLD compared with controls (P= 0.001). The serum CTGF levels were significantly increased, that correlated with histological fibrosis stage, in patients with NAFLD [in patients with no fibrosis (stage 0) 308.2 ± 142.9, with mild fibrosis (stage 1–2) 519.9±375.2 and with advanced fibrosis (stage 3–4) 1353.2 ± 610 ng/l,P< 0.001]. Also serum level of CTGF was found as an independent predictor of histological fibrosis stage in patients with NAFLD (β= 0.662,t= 5.6,P< 0.001). The area under the ROC curve was estimated 0.931 to separate patients with severe fibrosis from patients with other fibrotic stages.Conclusion:Serum levels of CTGF may be a clinical utility for distinguishing NAFLD patients with and without advanced fibrosis.

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“…The limitations and strengths of our study deserve [43] , is correlated with HS grade. A further drawback may have been the lack of liver biopsies to assess the severity of NAFLD, even though the canonical difference between FL and NASH has been challenged recently [44] . Finally, we did not determine serum levels of folate which are related to elevated homocysteine or blood pressure.…”

Section: Discussionmentioning

confidence: 99%

Hepatic steatosis in overweight/obese females: Newscreening method for those at risk

Tarantino¹,

Pizza²,

Colao³

et al. 2009

WJG

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AIM:To identify which parameters could help to distinguish the "metabolically benign obesity", which is not accompanied by insulin resistance (IR) and early atherosclerosis. METHODS:Eighty two of 124 overweight/obese females formed the study population, which was divided into two groups (52 and 30 subjects, respectively) with and without IR according to a HO meostatic Metabolic Assessment (HOMA) cut-off of 2, and were studied in a cross-sectional manner. The main outcome measures were waist circumference, serum uric acid, high-density lipoprotein-cholesterol and triglycerides, alanine aminotransferase, blood pressure and the two imaging parameters, hepatic steatosis and longitudinal diameter of the spleen, which were measured in relation to the presence/absence of IR. RESULTS:A variable grade of visceral obesity was observed in all subjects with the exception of three.Obesity of a severe grade was represented more in the group of IR individuals (P = 0.01). Hepatic steatosis, revealed at ultrasound, was more pronounced in IR than in non-IR subjects (P = 0.005). The two groups also demonstrated a clear difference in longitudinal spleen diameter and blood pressure, with raised and significant values in the IR group. Metabolic syndrome was frequent in the IR group, and was not modified when adjusted for menopause (P = 0.001). At linear regression, the β values of waist circumference and body mass index predicting HOMA were 0.295, P = 0.007 and 0.41, P = 0.0001, respectively. Measures of spleen longitudinal diameter were well predicted by body mass index (BMI) values, β = 0.35, P = 0.01, and by HOMA, β = 0.41, P = 0.0001. Blood pressure was predicted by HOMA values, β = 0.39, P = 0.0001). HOMA and hepatic steatosis were highly associated (rho = 0.34, P = 0.002). Interestingly, IR patients were almost twice as likely to have hepatic steatosis as non-IR patients. Among the MS criteria, blood pressure was very accurate in identifying the presence of IR (AUROC for systolic blood pressure 0.66, cut-off 125 mm of Hg, sensibility 64%, specificity 75%; AUROC for diastolic blood pressure 0.70, cut-off 85 mm of Hg, sensibility 54.5%, specificity 75%). CONCLUSION:As health care costs are skyrocketing, reliable and mainly inexpensive tools are advisable to better define subjects who really need to lose weight.

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Enhanced serum concentrations of transforming growth factor-beta1 in simple fatty liver: is it really benign?

Cited by 76 publications

References 23 publications

Nonalcoholic Fatty Liver Disease: A Review and Update

Nonalcoholic Fatty Liver Disease: A Review and Update

Concentrations of Connective Tissue Growth Factor in Patients with Nonalcoholic Fatty Liver Disease: Association with Liver Fibrosis

Hepatic steatosis in overweight/obese females: Newscreening method for those at risk

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