Hepatocellular carcinoma (HCC) is one of the most common aggressive tumors, with a rising prevalence in Egypt. Clusterin is a secretory heterodimeric glycoprotein linked to cancer development and progression. This study was conducted to evaluate the diagnostic and prognostic role of serum clusterin as a possible biomarker of HCC and correlate its level with the mRECIST scoring system. This study included 45 patients with liver cirrhosis and HCC eligible for locoregional treatment and 20 patients with liver cirrhosis without HCC as controls. All patients underwent standard laboratory tests and abdominal ultrasound. For HCC patients, a triphasic CT scan, alpha-fetoprotein (AFP), and clusterin levels were measured at baseline and one month after intervention. HCC patients had a substantially higher baseline clusterin level than cirrhotic patients (122.291 ± 61.898 vs. 74.015 ± 41.571, P = 0.002). Five patients in the HCC group were not eligible for intervention because they had evidence of portal vein invasion. At one month follow-up after HCC treatment, serum clusterin levels declined significantly from baseline (from 122.291 ± 61.898 to 81.125 ± 62.321, P = <0.001). According to the mRECIST scoring, baseline clusterin levels were significantly higher among patients with progressive disease than those with partial response than those with complete response (180.722 ± 55.908, 161.310 ± 56.339, 84.810± 41.389, respectively, overall P = <0.001). Clusterin was a useful marker in detecting HCC with 73.33% sensitivity and 75% specificity at a cutoff of ≥ 86.6 mg/L, and it also had 95.24% sensitivity and 77.78% specificity in detecting tumor progression at a cutoff of ≥ 146.6 mg/L, according to the mRECIST scoring system. In conclusion, clusterin may be a helpful diagnostic and prognostic marker for HCC after locoregional treatment, as its baseline level is useful in predicting response and progression of HCC in correlation with the mRECIST scoring system.
Background Chronic hepatitis C (CHC) virus is associated with insulin resistance and diabetes which have been linked to progressive liver fibrosis and sustained virologic response (SVR) to antiviral treatment. Resistin is a polypeptide hormone belonging to adipokines that may contribute to the development of obesity, insulin resistance, and metabolic syndrome. Also, the link between resistin and insulin resistance in patients with chronic hepatitis C and the effect of new direct acting antivirals on them seems unclear at present. The aim of this study is to evaluate the role of Resistin in detecting Insulin Resistance and their impact on response to direct acting antiviral in chronic hepatitis C patients. Results The Study was prospective Cohort clinical study, in Hepatology outpatient clinic at Ain Shams University Hospitals .This study was performed on 40 Egyptian patients who have Chronic viral hepatitis C, divided into 3 groups: GROUP I includes: 20 patients with Chronic viral hepatitis C on Sofosbovir- Daclatasvir before start of treatment and Sustained viral response after 12 weeks [SVR 12]. GROUP II includes: 20 patients with Chronic viral hepatitis C and non-responders before start of 2nd line of treatment and SVR 12. GROUP III includes: 10 subjects not infected with HCV as control group. The following investigations were done: body mass index calculation, Laboratory investigations including CBC, complete hepatic function tests, FIB-4 calculation, fasting serum insulin, HOMA-IR and serum Resistin level at baseline and re-assessed 12 weeks post end of treatment. Fasting serum Insulin, HOMA-IR and Resistin level were statistically significant higher in both naïve & relapser chronic HCV infected patients than in control group (p value <0.001). SVR 12 weeks post treatment was achieved in all 40 patients received new direct acting antivirals with a Significant reduction in Fasting serum Insulin, HOMA-IR and Resistin level at SVR 12 week (p value 0,001, <0.001, <0.001) respectively. Significant positive correlation was found between Resistin level and HOMA-IR in both naïve and relapse chronic HCV patients. Calculation of FIB-4 among patients showed significant higher FIB-4 in naïve patients than relapser (p value 0,002). Serum Resistin at a cut off value >1800 ng/ml had 38.89 % sensitivity, 86.36 % specificity, 70 % PPV, 63.3 % NPV (with an overall accuracy of 57.1 %) in predicting absence of liver cirrhosis based on FIB-4. And at a cutoff value ≥2400 ng/ml had 93.55% sensitivity, 33.3% specificity, 82.9% positive predictive value, and 60% negative predictive value with an overall accuracy of 62.4% in prediction of significant insulin resistance among chronic HCV patients. Conclusion Serum Resistin level was significantly up regulated in patients with chronic HCV, with significant reduction in its level after achievement of SVR. Resistin has the potential to be a biomarker for screening of insulin resistance among chronic HCV patients.
Background Regional adiposity has a significant impact on the formation of adverse metabolic and cardiovascular risk profiles. While much of the attention was directed to the importance of intra-abdominal adipose tissue, there were several new investigations about mediastinal and epicardial regions’ visceral adiposity. Our study aimed to determine the association between non-alcoholic fatty liver and increased epicardial adipose tissue mass with coronary artery disease severity. Methods This study was conducted on sixty patients who presented with symptoms of coronary artery disease and attended elective coronary angiography to rule out coronary artery disease. All patients have been subjected to full hepatic profile, noninvasive scoring system such as Fibrosis-4 and non-alcoholic fatty liver disease fibrosis score and abdominal ultrasound for diagnosis of non-alcoholic fatty liver disease and trans-thoracic echocardiography for measurement of average epicardial adipose tissue thickness. Student T test, analysis of variance test, chi-square test, and Fisher’s exact test were used for statistical analysis. Results According to the severity of coronary artery disease, patients with significant coronary stenosis had statistically significant higher degree of hepatic steatosis in abdominal ultrasound (P value < 0.001) while regarding the non-alcoholic fatty liver disease fibrosis score and Fibrosis-4 for non-alcoholic fatty liver disease diagnosis, there was no significance between both groups. Also, the epicardial adipose tissue mean thickness was found to be statistically significantly higher among those with significant coronary stenosis than those without [7.859 ± 0.691 mm versus 5.600 ± 0.386 mm]. Moreover, statistically significant higher epicardial adipose tissue thickness values were found among grade 3 hepatic steatosis than in grades 2, 1, or 0 (P value < 0.001). At a cutoff > 6.1 mm, epicardial adipose tissue thickness was a valuable tool in discrimination between significant and non-significant coronary artery disease with specificity and sensitivity of 100%. Conclusion High epicardial adipose tissue thickness may represent a marker of severity of non-alcoholic fatty liver disease as well as an independent predictor of coronary artery disease risk.
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