Browsing by Author "Simonović, Jasmina (6507086058)"

Introduction: Chronic hepatitis C virus (HCV) infection can progress to liver cirrhosis that causes bleeding from the gastrointestinal tract, liver failure and primary hepatocellular carcinoma. Use of standard therapeutic option consists of recombinant pegylated interferon alpha 2a/b with ribavirin in order to eradicate virus and prevent complications. Objective: The aim of investigation was to evaluate efficiency of combination therapy (pegylated interferon alpha 2a/b plus ribavirin) in patients with chronic HCV infection and to estimate predictive factors for successful treatment. Methods: A total of 387 patients with confirmed diagnosis of hepatitis C were evaluated (aged 18-65 years of both genders). Patients were treated with pegylated interferon alpha 2a/b and ribavirin according to a standard regimen lasting 24 or 48 weeks, dependent on virus genotype. Results: Negative HCV RNA (PCR assay) was recorded in 79.7% of patients at the end of treatment. Six months after completed therapy, negative HCV RNA, i.e. stained virologic response (SVR) was assessed in 70.5% of patients. Statistical summary of our results concerning SVR confirmed better efficiency of combination therapy for the following parameters compared to other investigated variables: age ≤40 (843% vs. 59.1%; p<0.0005), absence of cirrhosis (75.6% vs. 58.3%; p=0.003), lack of genotype 1 (86.6% vs. 61.8%; p<0.0005), and in patients who received full doses of pegylated interferon alpha 2a (78.3% vs. 633%; p=0.002). Conclusion: Combination therapy of recombinant pegylated interferon alpha 2a with ribavirin leads to SVR in the majority of treated patients (70.5%). Successful treatment depends on a variety of host and virus factors.

Introduction Toxic liver injury is becoming greater problem in today´s hepatology. Until today more than 900 drugs, toxins and herbs have been identified that can cause different liver injury. There was no significant research of this problem in Serbia so far. The aim of this study is to present the patient with severe form of acute hepatitis, whose etiology is exclusively toxic. Case outline A 23-year-old male, from Belgrade, previously healthy, got sick with signs and symptoms that correlated with acute hepatitis. Biochemical analyses pointed to severe form of acute hepatitis with impending hepatocellular failure. The diagnosis of toxic liver injury was set. It was caused by the use of number substances and supplements: Ecstasy, whey protein, branched-chain amino acid (BCAA), creatine, high doses of vitamin D, glutamine, and multivitamin complex. He was treated with infusion, gastroprotective, and substitution therapy. During hospitalization, the patient’s symptoms disappeared with gradual normalization of biochemical analyses of the liver. When the patient’s condition was satisfying, blind percutaneous liver biopsy was performed, with the following pathohistological findings: Lobular hepatitis, with no fibrosis, etiology correlates to toxic. After a month and a half since the disease had begun, the patient fully recovered. Conclusion Increased number of persons with toxic liver injury is being registered in developed countries worldwide. Similar trend can be noted in Serbia as well. By presenting young previously healthy man with the severe form of toxic acute hepatitis and impending liver failure, we are pointing out the significance of this problem. Multidisciplinary approach is needed to reach the most effective solutions. © 2019, Serbia Medical Society. All rights reserved.

Introduction Acute liver failure is a rare and very complex clinical syndrome, a consequence of sudden and severe liver dysfunction. There are several causes of this condition (viruses, medications, toxins, metabolic, autoimmune and malignant diseases), but etiological agent often remains undiscovered. Case outline A 40-year-old male patient had suddenly taken ill with signs and symptoms of acute hepatitis, which was confirmed through biochemical analyses. The cause of acute liver failure was not determined. Despite all therapeutic measures, the clinical course of the disease was unfavorable: severe icterus, decreased synthetic function of the liver and hepatic encephalopathy developed. In the later, subacute course of the disease, ascites and episodes of hepatic encephalopathy developed, and biochemical findings indicated chronic hepatocellular failure. After three months of treatment in hepatic coma there was lethal outcome. Histopathological findings confirmed the diagnosis of decompensated liver cirrhosis of unknown origin. Conclusion The cause of acute liver failure often remains unclear; potential causes should be looked for in infections by unknown viruses or in exposures to toxins. The disease is most commonly presented as a subacute failure with the development of liver cirrhosis. Survival rate is low. © 2018, Serbia Medical Society. All rights reserved.