Background
Hepatocellular carcinoma (HCC) comprises 5.6% of all cancers worldwide representing the sixth most common cancer. It is also the fourth most common cause of cancer-related mortality. Angiogenesis is a main factor in the development of HCC. Vascular endothelial growth factor (VEGF) is considered as the force for physiological and pathological angiogenesis, and overexpression of VEGF is prominent in HCC. We aimed to study the effect of direct-acting antivirals (DAAs) on VEGF considered as the key regulator of angiogenesis in HCC. This cross-sectional study involved fifty patients who were divided into two groups: group I—twenty-five chronic hepatitis C virus (HCV) patients as (cases) subjected to treatment with direct-acting antiviral drugs for 3 months; group II—twenty-five chronic HCV patients developed HCC as (controls). Serum VEGF level was measured in of group I at baseline, at end of treatment, and 3 months after the end of treatment by sofosbuvir 400 mg plus daclatasvir 60 mg for 3 months in the HCV patient group, also VEGF was assessed in group II with HCC.
Results
Serum VEGF was high in both groups, but it was higher in the HCC group with a statistically significant difference (p < 0.001), also serum VEGF in the HCV group decreased after 3 months at the end of DAA treatment from 209.5 ± 137.6 to 44.1 (31.8–55.3) mg/ml, and all patients who received DAAs achieved sustained virologic response (SVR).
Conclusion
We found that change in serum VEGF in HCV patients treated with DAAs in this study cannot explain the risk of HCC after treatment by DAAs.
Background: Patients with end stage renal disease (ESRD) have elevated levels of inflammatory mediators including Creactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Neutrophil to lymphocyte ratio was introduced as a novel inexpensive indicator that reflects the severity and extension of systemic inflammation and atherosclerosis, and predicts adverse clinical outcomes in cardiac and non-cardiac disorders including ESRD.The aim of this study is to evaluate the frequency of subclinical inflammation using neutrophil to lymphocyte ratio (NLR) and its relation to other biochemical parameters in ESRD patients on maintenance haemodialysis (HD) in comparison to high-sensitivity C-reactive protein (hsCRP).
Methods:A cross sectional observational study including 100 clinically stable ESRD patients on regular haemodialysis (mean age 48.25 ± 13.67, 57% were males), NLR was calculated from complete blood count and hsCRP was recorded for all patients where 8.2 mg/L indicated inflammation.Results: NLR was positively correlated to hsCRP, using ROC curve (AUC=0.647) and the best cut off point to detect subclinical inflammation in HD patients was calculated with NLR greater than or equal 1.54, with sensitivity 68.25% and specificity 54%. By using univariate and multiple variate analysis in our work to test for independent predictors of hsCRP levels as an indicator for inflammation, it was found that NLR can be used as an independent predictor of hsCRP as an inflammatory marker, with statistically significant correlation (p=0.015). Spearman coefficient (rs=0.220) shows statistically significant (p=0.028) positive correlation between NLR and hsCRP.
Conclusion:NLR is an easy, simple and non-expensive method that can be used as a marker of inflammation in HD patients when compared to hsCRP.
Background
Cardiovascular disease is the commonest cause of death in patients with end-stage renal disease (ESRD) under maintenance hemodialysis. Dyslipidemia, oxidative stress, and low-grade inflammation with increased circulating cytokines are factors that increase the cardiovascular risk in patients with chronic kidney disease, in addition to traditional risk factors, such as obesity, hypertension, and diabetes. We aimed to investigate the possible anti-inflammatory effects of atorvastatin in prevalent hemodialysis patients. Fifty-three stable adult hemodialysis patients were assigned into two groups (a drug group and a control group). Patients in the drug group received 20 mg of atorvastatin daily for 6 months. Serum levels of highly sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6) were measured in both groups at baseline and at the end of the study period.
Results
Atorvastatin therapy caused a statistically significant decrease in levels of hs-CRP but no change in levels of IL-6 after 6 months of therapy.
Conclusions
In addition to its favorable effect on lipid profile parameters, atorvastatin therapy can be considered as an effective and safe modality to overcome the problem of chronic inflammation encountered in end-stage renal disease patients.
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