Post recovery manifestations have become another concern in patients who have recovered from coronavirus disease 2019 (COVID‐19). Numerous reports have shown that COVID‐19 has a variety of long‐term effects on almost all systems including respiratory, cardiovascular, gastrointestinal, neurological, psychiatric, and dermatological systems. We aimed to investigate the prevalence and characteristics of the post‐COVID syndrome among COVID‐19 survivors and to determine the factors associated with persistent symptoms. This prospective study enrolled in patients with COVID‐19 followed in hospital or outpatient clinics in Ankara City Hospital. We performed a special questionnaire to inquire about the presence of persistent symptoms beyond 12 weeks from the first diagnosis. Demographic data, comorbid diseases, characteristics of acute COVID‐19, presence of persistent symptoms by systems, and knowledge about outpatient clinic visits after recovery were assessed. Of a total of 1007 participants, 39.0% had at least one comorbidity, and 47.5% had persistent symptoms. Fatigue/easy fatigability, myalgia, and loss of weight were the most frequent persistent symptoms (overall 29.3%) followed by respiratory symptoms (25.4%). A total of 235 participants had visited outpatient clinics due to several reasons during the post‐COVID‐19 period, and 17 of them were hospitalized. Severe acute COVID‐19, hospitalization, and presence of comorbidity were independent factors for the development of persistent symptoms. Fully understanding the spectrum of the post‐COVID syndrome is essential for appropriate management of all its long‐term effects. Our study once again underlined the fact that the prevalence of post‐COVID syndrome is higher than expected and concerns many systems, and a multidisciplinary follow‐up should be provided to COVID‐19 survivors in the post recovery period.

Severe COVID‐19 patients in ICU are at high risk for candidemia due to exposure to multiple risk factors for candidemia. We aimed to compare the incidence of candidemia in ICU patients with and without COVID‐19, and to investigate epidemiologic and clinical characteristics of candidemia patients and risk factors for mortality in candidemia patients. This retrospective study was conducted in patients followed in the ICUs of Ankara City Hospital for 2 years, divided into pre‐pandemic and pandemic periods. The incidence (event per 1000 patient‐days) and epidemiology of candidemia, clinical and laboratory characteristics of patients were compared in COVID‐19 and non‐COVID‐19 groups. Candidemia incidence was higher in the COVID‐19 group (2.16, 95% CI 1.77–2.60) than the non‐COVID‐19 group (1.06, 95% CI 0.89–0.125) (p < .001). A total of 236 candidemia episodes (105 in COVID‐19 patients and 131 in non‐COVID‐19 patients) were detected during the study periods. COVID‐19 cases had a higher rate of corticosteroid use (63.8% vs. 9.9%, p < .001). Epidemiology of candidemia and antifungal susceptibility were similar. Candidemia developed 2 weeks earlier in COVID‐19 groups and resulted in higher mortality (92.5% vs. 79.4%, p .005). One‐third of candidemia patients died before receiving any antifungal treatment, and this rate was higher in the COVID‐19 group. In multivariate logistic regression analysis, corticosteroid use, presence of sepsis and age older than 65 years were independent risk factors for mortality in candidemia patients. Candidemia with high mortality is a more serious problem for COVID‐19 patients due to its increased incidence, earlier occurrence and a higher rate of mortality.

The COVID-19 pandemic has created a major alteration in the medical literature including the sepsis discussion. From the outset of the pandemic, various reports have indicated that although there are some unique features pertinent to COVID-19, many of its acute manifestations are similar to sepsis caused by other pathogens. As a consequence, the old definitions now require consideration of this new etiologic agent, namely SARS-CoV-2. Although the pathogenesis of COVID-19 has not been fully explained, the data obtained so far in hospitalized patients has revealed that serum cytokine and chemokine levels are high in severe COVID-19 patients, similar to those found with sepsis. COVID-19 may involve multiple organ systems. In addition to the lungs, the virus has been isolated from blood, urine, faeces, liver, and gallbladder. Results from autopsy series in COVID-19 patients have demonstrated a wide range of findings, including vascular involvement, congestion, consolidation, and hemorrhage as well as diffuse alveolar damage in lung tissue consistent with acute respiratory distress syndrome (ARDS). The presence of viral cytopathic-like changes, infiltration of inflammatory cells (mononuclear cells and macrophages), and viral particles in histopathological samples are considered a consequence of both direct viral infection and immune hyperactivation. Thromboembolism and hyper-coagulopathy are other components in the pathogenesis of severe COVID-19. Although the pathogenesis of hypercoagulability is not fully understood, it has been pointed out that all three components of Virchow’s triad (endothelial injury, stasis, and hypercoagulable state) play a major role in contributing to clot formation in severe COVID-19 infection. In severe COVID-19 cases, laboratory parameters such as hematological findings, coagulation tests, liver function tests, D-dimer, ferritin, and acute phase reactants such as CRP show marked alterations, which are suggestive of a cytokine storm. Another key element of COVID-19 pathogenesis in severe cases is its similarity or association with hemophagocytic lymphohistiocytosis (HLH). SARS-CoV-2 induced cytokine storm has significant clinical and laboratory findings overlapping with HLH. Viral sepsis has some similarities but also some differences when compared to bacterial sepsis. In bacterial sepsis, systemic inflammation affecting multiple organs is more dominant than in COVID-19 sepsis. While bacterial sepsis causes an early and sudden onset clinical deterioration, viral diseases may exhibit a relatively late onset and chronic course. Consideration of severe COVID-19 disease as a sepsis syndrome has relevance and may assist in terms of determining treatments that will modulate the immune response, limit intrinsic damage to tissue and organs, and potentially improve outcome.

Introduction: The presence of new coronavirus (SARS-CoV-2) in semen and the possibility of sexual transmission have become new subjects of curiosity. There is a discrepancy regarding this issue in the literature. The presence of SARS-CoV-2 in semen has been investigated in a limited number of studies, and mostly in recovering patients. We aimed to investigate the presence of SARS-CoV-2 RNA in semen of patients with a positive nasopharyngeal swab test for SARS-CoV-2 in the acute stage. Methods: We enrolled adult male patients who were hospitalized with confirmed SARS-COV-2 infection in the study. In addition to routine laboratory and radiological tests, semen sample was obtained from volunteers and transferred to the Turkish Public Health Institution, National Virology Laboratory. The samples were processed for the detection of SARS-CoV-2 RNA on the day of collection. Results: Sixteen patients were included in the study. The median age was 33.5 years (18–54). All but one had respiratory symptoms. None of the patients had a history or symptoms of urogenital disease. All semen samples were obtained during hospitalization and in the acute stage of the infection. The median time to obtain a semen sample after positive nasopharyngeal test was 1 day (0–7). All semen samples were detected as negative for SARS-CoV-2 PCR. Discussion/Conclusion: Although all semen samples were obtained in acute stage of the infection when the nasopharyngeal swab test was positive, we did not detect SARS-CoV-2 in semen. The results of our study support the thought that sexual transmission via semen does not have an important role in the person-to-person transmission of SARS-CoV-2. We think that our study will provide new information to fill the gap in the literature.

Oral nucleoside/nucleotide analogues (NAs) are currently the backbone of chronic hepatitis B (CHB) infection treatment. They are generally well-tolerated by patients and safe to use. To date, a significant number of patients have been treated with NAs. Safety data has accumulated over the years. The aim of this article is to review and update the adverse effects of oral NAs. NAs can cause class adverse effects (i.e., myopathy, neuropathy, lactic acidosis) and dissimilar adverse effects. All NAs carry a “Black Box” warning because of the potential risk for mitochondrial dysfunction. However, these adverse effects are rarely reported. The majority of cases are associated with lamivudine and telbivudine. Adefovir can lead to dose- and time-dependent nephrotoxicity, even at low doses. Tenofovir has significant renal and bone toxicity in patients with human immunodeficiency virus (HIV) infection. However, bone and renal toxicity in patients with CHB are not as prominent as in HIV infection. Entecavir and lamivudine are not generally associated with renal adverse events. Entecavir has been claimed to increase the risk of lactic acidosis in decompensated liver disease and high Model for End-Stage Liver Disease scores. However, current studies reported that entecavir could be safely used in decompensated cirrhosis. An increase in fetal adverse events has not been reported with lamivudine, telbivudine and tenofovir use in pregnant women, while there is no adequate data regarding entecavir and adefovir. Further long-term experience is required to highlight the adverse effects of NAs, especially in special patient populations, including pregnant women, elderly and patients with renal impairment.