The syndrome of decreased immunity caused by cirrhosis is a combination of different immunological mechanisms and reactions which result from an advanced stage of the liver disease. The synthesis of proteins of the acute phase becomes impaired, there develop different deficiencies of the complement system, and there ensues a decrease of receptors that are meant to recognize antigens. The negative changes become apparent in the field of cell responses, e.g. there are changes in the amounts of generated monocytes and macrophages, and their phagocytic capabilities and chemotaxic reactions are impacted as well. The humoral response results in distorted synthesis of particular antigen categories. The risk of detrimental immunoresponses with the end result of endotoxemia is not rarely coupled with both local and global infections. The combination of the aforesaid immunodeficiencies worsens the healing chances of cirrhosis sufferers and more often than not it increases the mortality of the affected patients.

The aim of the studyWas to assess current prevalence of hepatitis C virus (HCV) genotypes in Poland, including their geographic distribution and changes in a given period of time.Material and methodsData were collected with questionnaires from 29 Polish centers and included data of patients diagnosed with HCV infection between 1 January 2013 and 31 March 2016.ResultsIn total, data of 9800 patients were reported. The highest prevalence was estimated for genotype 1b (81.7%), followed by 3 (11.3%), 4 (3.5%), 1a (3.2%) and 2 (0.2%). Genotype 5 or 6 was reported in 6 patients only (0.1%). The highest prevalence of genotype 1 was observed in central (łódzkie, mazowieckie, świętokrzyskie), eastern (lubelskie) and southern (małopolskie, śląskie) Poland. The highest rate for genotype 3 was observed in south-western (dolnośląskie, lubuskie) and eastern (podlaskie, warmińsko-mazurskie and podkarpackie) Poland. Compared to historical data, we observed an increasing tendency of G1 prevalence from 72.0% in 2003 to 87.5% in 2016, which was accompanied by a decrease of G3 (17.9% vs. 9.1%) and G4 (9.0% vs. 3.1%).ConclusionsAlmost 85% of patients with HCV in Poland are infected with genotype 1 (almost exclusively subgenotype 1b), and its prevalence shows an increasing tendency, accompanied by a decrease of genotypes 3 and 4.

We followed for 2 years patients treated with direct-acting agents (DAA) to assess long-term durability of virologic response, improvement of liver function, reduction in liver stiffness (LS) and risk of hepatocellular carcinoma (HCC). The study included patients from 16 hepatologic centres involved in the AMBER, investigator-initiated study on treatment of chronic hepatitis C patients within a programme preceding EU registration of ombitasvir/paritaprevir/ritonavir±dasabuvir±ribavirin. A total of 204 patients among 209 from the primary study were enrolled, 200 with available testing at 2-year follow-up (2yFU) with undetectable HCV RNA (198 responders and 2 nonresponders retreated). During 2yFU, 4 patients died, 17 had hepatic decompensation and 3 needed liver transplantation. De novo hepatocellular carcinoma was diagnosed in 4 and its recurrence in 3 patients. Significant decreases in bilirubin, MELD, Child-Pugh scores and liver stiffness, and increases in albumin level were observed during 2yFU. Strengths of the study were a fixed period of post-treatment follow-up, prospective character of the study and high proportion of available patients from the primary study. The major weaknesses were lack of a comparative arm and relatively insufficient number of patients for subsets analysis. In conclusion, 2-year follow-up confirmed durability of virologic response after treatment of HCV infection with ombitasvir/paritaprevir/ritonavir±dasabuvir±ribavirin. It was accompanied by significant improvement of major measures of hepatic function and reduction of hepatic stiffness. Successful therapy did not prevent hepatic decompensation, HCC or death in cirrhotics that support the need for longer than 2-year monitoring for possible disease progression.

The aim of the studyWas to analyze the efficacy achieved with regimens available for chronic hepatitis C (CHC) in Poland between 2013 and 2016.Material and methodsData were collected from 29 centers and included 6786 patients with available sustained virologic response (SVR) data between 1 January 2013 and 31 March 2016.ResultsThe sustained virologic response rate for genotypes (G) 1a, 1b, 2, 3 and 4 was 62%, 56%, 92%, 67% and 56% respectively; 71% patients (n = 4832) were treated with pegylated interferon α (Peg-IFNα) and ribavirin (RBV), with SVR rates of 58%, 49%, 92%, 67% and 55% respectively. The sustained virologic response among 5646 G1 infected patients was the lowest with natural interferon α (7%, n = 70) or PegIFN (50%, n = 3779) with RBV, and improved in those receiving triple regimens of Peg-IFN + RBV combined with boceprevir (47%, n = 485), telaprevir (64%, n = 805), simeprevir (73%, n = 132) or sofosbuvir (70%, n = 23). The sustained virologic response with interferon-free regimens of sofosbuvir and RBV (n = 7), sofosbuvir and simeprevir (n = 53), and ledipasvir and sofosbuvir (n = 64) achieved 86%, 89% and 94% respectively. The highest SVR of 98% was observed with ombitasvir/paritaprevir combined with dasabuvir (n = 227). Patients infected with G3 (n = 896) and G4 (n = 220) received mostly Peg-IFN + RBV with SVR of 67% and 56% respectively. Interferon-free regimens were administered in 18 G3/G4 patients and all achieved an SVR. Sofosbuvir combined with Peg-IFN and RBV was administered to 33 patients with an SVR rate of 94%, and a similar rate was achieved among 13 G2 patients treated with interferon and RBV.ConclusionsWe observed significant differences in efficacy of HCV regimens available in Poland at the turn of the interferon era. The data will be useful as a comparison for therapeutic options expected in the next few years.

Coronaviruses are RNA viruses causing infectious diseases. They had been responsible for 15% cases of a common cold before December 2019. With the new strain of coronavirus SARS CoV2 which causes COVID-19 disease, the ongoing pandemic surprised with the severity of symptoms and its course compared to the previously known mild respiratory tract infections. In the end of December 2021, over 274 million people were diagnosed with COVID-19 disease, and the total mortality amounted to nearly 5.4 million deaths in more than 200 countries. One of the potentially fatal complications of COVID-19 is pulmonary embolism (PE). It appears that PE has been associated with several coagulation abnormalities as well as with frequent significantly elevated concentration of D‑dimer's. A higher D‑dimer concentration in blood serum, in turn, has been associated with an increased risk of premature death. Moreover, inflammation, typical in the course of COVID-19, is considered a prothrombotic condition; higher interleukin 6 (Il-6) and C‑reactive protein concentrations have been found in patients with more severe forms of COVID-19. So far, none specific for COVID-19 studies have been available with regard to the diagnosis and treatment of PE. Therefore, the practical approach is based on the experience of other groups of patients. Prevention of thrombotic events seems reasonable, at least in COVID-19 patients with the risk factors of developing venous thromboembolism. Low‑molecular‑weight heparins are most commonly prescribed (e.g. enoxaparin, dalteparin). Following the confirmed definite PE diagnosis, proper anticoagulation or, if necessary, thrombolytic treatment must be introduced.