Background: Chronic hepatitis C is a major public health problem around the world. In monitoring treatment efficacy, although costly and labour-intensive methods of molecular biology are often used, much cheaper and technically easier serological methods evaluating the concentration of HCV core antigen in serum are available. We evaluated HCVcAg quantification as a possible assessment of the treatment efficacy instead of HCV RNA quantification. Methods: We collected 514 serum samples from treated HCV infected patients. Quantitative evaluation of HCV RNA and HCVcAg was carried out before treatment, at the end of treatment, and at least 12 weeks following treatment termination. HCV RNA was determined by automated assay (Roche COBAS) and HCVcAg quantitation with ARCHITECT ci8200 analyser. Results: There was a significant correlation between HCVcAg and HCV RNA concentrations at baseline and follow-up visits, but not at the end of treatment. Among samples collected before the treatment, at the end of treatment and follow-up visit, concordance of HCV RNA and HCVcAg reached level of 98.1%, 98.9% and 98.7%, respectively. Diagnostic sensitivity, specificity, positive and negative predictive values of HCVcAg detection were >97%. Conclusions: HCVcAg measurement could be an alternative for determining HCV treatment efficacy after chemotherapy and could be an option in the diagnosis of HCV infection.

Background: According to current recommendations diagnosis and management of HCV infection need detection and quantification of nucleic acids. In the era of direct-acting antivirals (DAA) it is essential to develop an inexpensive and simple method replacing polymerase chain reaction. Since there is no available data on HCV core antigen (HCVcAg) versus HCV RNA kinetics in the early phase of treatment with DAA, we carried out this study to evaluate the possible application of HCVcAg quantitative measurement for management of HCV infection. Methods: 33 patients with HCV infection were enrolled and treated with either ombitasvir/paritaprevir/ritonavir ± dasabuvir ± ribavirin (OBV/PRV/r±DSV±RBV) or ledipasvir/ sofosbuvir (LDV/SOF). Samples for quantitative HCV RNA and HCVcAg measurement were collected at the baseline, after 1, 7, 28 days and at the end of treatment, and then after 12 and 24 weeks of post-treatment follow-up. Results: There was positive correlation between HCVcAg and HCV RNA levels at the baseline and after 1 day of treatment. Mean HCVcAg concentration declined faster than HCV RNA levels during the treatment phase. At week 4 HCV RNA was undetectable in 24, whereas HCVcAg in 28 patients. At the end of treatment and after 12 weeks of follow-up all patients were undetectable for both HCV RNA and HCVcAg. Conclusions: HCVcAg concentration and its early on-treatment testing can predict virological response. Simple testing procedures and significantly lower cost compared to HCV RNA testing support possible replacement of the viral load measurement in management of the majority of HCV-infected patients.

To assess a combination of novel measures of therapeutic success in the treatment of chronic hepatitis C (CHC) infection, we evaluated liver stiffness (LS) with shear wave elastography and hepatitis C virus core antigen (HCVcAg) concentrations. We followed 34 patients during and after treatment with direct acting antivirals. All patients achieved a sustained virologic and serologic response and a significant increase of albumin levels. Decreases of alanine aminotransferase (ALT) activity and alpha-fetoprotein (AFP) level were observed during the treatment and follow-up period. A significant decrease in LS was observed between baseline, end of treatment (EOT), and at 24- and 96-week post-treatment follow-up. LS decline between EOT and 96-week follow-up (FU96) was observed in 79% of patients. Significant LS changes were seen in patients with advanced fibrosis, particularly in cirrhotics and in patients with ALT exceeding 100 IU/mL. There was a positive correlation between ALT activity and LS changes at the baseline versus FU96. A negative correlation was demonstrated between individual HCVcAg baseline concentrations and reduction of LS at the baseline versus FU96. In conclusion, we observed that LS significantly declined during and after antiviral treatment. It was accompanied by improvement in some liver function measures, and disappearance of both HCVcAg and HCV ribonucleic acid (HCV RNA).

Introduction: According to WHO data, among patients infected with HIV, tuberculosis occurs in about 30% of patients and causes approximately 25% of deaths due to AIDS worldwide. The incidence rate of tuberculosis in the Polish population was 22.2/100,000 in 2011, while the average in European Union countries in 2011 was 14/100,000. Since 1985 to 30 April 2013 HIV infection in Poland was confirmed in 16,588 patients, while the number of reported tuberculosis cases in HIV-infected individuals in 2011 was 26. The aim of this study was to assess the prevalence and clinical course of tuberculosis and mycobacterial disease in HIV-infected patients treated in the Department of Infectious Diseases and Hepatology in Białystok. Materials and methods: We analysed documentation of 577 HIV-infected patients, their demographic data, epidemiological status, degree of immunosuppression (T CD4 and CD8 numbers) and stage of HIV infection. Results: Complete follow-up was possible in 389 patients, of whom 265 (68%) were male. Tuberculosis (TB) was diagnosed in 41 patients (10.5%) and mycobacteriosis in 4 patients (1.03%). In 19 patients (42%) HIV and TB or mycobacteriosis were diagnosed simultaneously. The median CD4 T lymphocyte count was lower in patients with a simultaneous diagnosis of HIV and tuberculosis or mycobacteriosis compared to the group in whom TB/mycobacteriosis was diagnosed later. The number of CD4 T-cells less than 50 cells/μL was found in 63.2% (12/19) of patients when HIV and TB or mycobacteriosis were diagnosed simultaneously and in 38.5% (10/26) of patients who were diagnosed with TB or mycobacteriosis later than the HIV infection (p = 0.14). The median HIV viral load in patients in whom HIV infection and tuberculosis or mycobacteriosis were diagnosed at the same time was higher than in other patients and this difference was statistically significant. Pulmonary tuberculosis was the most common form of clinical disease and accounted for 60% of all cases. Among the analysed cases with HIV and tuberculosis or mycobacteriosis coinfection, tuberculosis or mycobacteriosis was the cause of death in 8 patients, and 9 died of other causes. Conclusions: In our material of 389 HIV-infected patients, tuberculosis was diagnosed in 41 (10.5%) and mycobacterial diseases in 4 (1.03%). In 42% of co-infected patients (HIV + TB or mycobacteriosis) the diagnosis of both diseases was made at the same time. In these patients, a deep deficit of cellular immunity (CD4 < 50 cells/μL) was observed more frequently than in patients diagnosed with TB or mycobacteriosis in the later course of HIV. HIV RNA viral load was significantly higher in the group diagnosed simultaneously than in the remaining patients with HIV and TB or mycobacteriosis coinfection.