Budd Chiari syndrome defines an obstruction of the hepatic venous outflow. Primary causes include pro-coagulant states resulting in venous thrombosis, while secondary Budd Chiari syndrome appears in conditions associated with extrinsic compression of the hepatic veins or tumor invasion. Clinical presentation is greatly varied, from incidentally discovered asymptomatic thrombosis to fulminant liver failure due to hepatic congestion. Abdominal ultrasonography is the key diagnostic tool of Budd Chiari syndrome. This pictorial essay aims to show the ultrasonographic aspect of Budd-Chiari syndrome associated with other medical conditions (abdominal malignancy, hematologic disorders and abdominal surgery).
Background: This is a real-world evidence study that aims to analyze the efficacy, tolerability and safety profile of paritaprevir/ombitasvir/ritonavir and dasabuvir, in patients with renal impairment. Methods: We conducted an observational prospective study, on 232 patients with chronic kidney disease, undergoing treatment with paritaprevir/ombitasvir/ritonavir and dasabuvir, for chronic hepatitis C infection -genotype 1b. Renal and liver function were assessed at the beginning of therapy, monthly during treatment and three months after therapy completion. Results: All patients achieved sustained virologic response. Common side effects were nausea, fatigue and headache. Close monitoring of tacrolimus blood levels and dose reduction was required in kidney transplant recipients. Conclusions: HCV therapy in the setting of renal dysfunction has always been a challenging topic. Direct-acting antivirals have shown promising effects, demonstrating good tolerance and efficacy in patients with HCV infection and renal impairment. Sustained virologic response within our study population was 100%.
Context. Hepatitis C and diabetes represent important health problems globally. The new-onset diabetes after transplantation is a particular entity that appears due to the use of immunosuppression among transplanted patients.Objective. We aim to describe the clinical and biological aspects of severe hyperglycemia in a kidney transplant recipient undergoing Interferon-free therapy for chronic hepatitis C, discussing the interference of different factors with the glucose metabolism.Design. The occurrence of diabetes in a patient with history of renal transplantation and Interferon-free treated hepatitis C was studied from both clinical and paraclinical points of view.Subjects and methods. When presenting to the hospital, extensive blood tests were performed on the patient, revealing significant hyperglycemia and an elevated level of blood tacrolimus. Creatinine clearance was calculated. ECG presented T-wave alterations. Intensive insulin protocol was applied, the case being managed in a multidisciplinary approach.Results. Blood glucose and tacrolimus were slowly normalized, under therapy. The antiviral treatment was continued, with the achievement of sustained virologic response.Conclusions. Diabetes mellitus can have many causes, hepatitis C and transplantation both having an impact on glucose metabolism. The association of the three entities should be carefully managed, due to its enhancing effect on morbidity and mortality.
This article states the importance of ultrasonographic evaluation regarding the splenic pathology, by revealing clinical and imagistic findings in 3 cases of hepatitis C-associated lymphoma.
Aim:This study aims to analyze the particularities of hepatitis C induced hepatocellular carcinoma (HCC), developed during or after treatment with direct-acting antivirals.
Methods:We conducted an observational prospective study on 278 patients, who underwent treatment for hepatitis C related liver cirrhosis and respectively for F3 chronic hepatitis C. Liver status was assessed using biological parameters and imagistic evaluation (ultrasonography, computed tomography scan, magnetic resonance imaging).
Results:The follow-up time was 14 months. Before therapy, 69.3% of the cirrhotic patients and 26.7% of those with F3 degree of liver fibrosis had high levels of alpha-fetoprotein, with no imagistic evidence of HCC. During treatment, HCC was confirmed in 5 patients, 2 of them presenting portal vein thrombosis (PVT). Antiviral therapy was not interrupted. Two patients developed HCC at the end of treatment, while 4 of them were diagnosed with HCC after three months of ending the treatment. Excepting the ones with PVT, all patients underwent trans-arterial chemoembolization.
Conclusion:All patients acquired sustained virological response. The screening for HCC should not be stopped after achievement of sustained virological response. Patients who develop HCC after antiviral treatment often need to be evaluated by magnetic resonance imaging in order to detect the extension of the disease.
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