Autochthonous acute hepatitis E: treatment with sofosbuvir and ribavirin

Introduction: Hepatitis E virus (HEV) is an emerging cause of autochthonous-acute-hepatitis and acute-on-chronic-liver-failure in western countries. Treatment is not routinely used, despite ribavirin has a good antiviral effect. In vitro sofosbuvir inhibits HEV replication, but clinical data are lacking. Case report: We report a case of acute-on-chronic-liver-failure due to HEV treated with sofosbuvir and ribavirin. The treatment was capable of rapidly inducing both HCV and HEV viral suppression. Conclusion: In conclusion, although more data are required before firm conclusions could be drawn, the combination of sofosbuvir and ribavirin in not immunosuppressed patients with acute hepatitis E may be able to clear HEV infection

HCV cirrhotic patients treated with direct acting antivirals: detection of tubular dysfunction and resolution after viral clearance

Background/aims: Hepatitis C virus (HCV) has been identified in tubular epithelial cells of infected patients, however the presence of tubular dysfunction, which is a risk factor for chronic kidney disease, has never been examined in vivo. The present prospective longitudinal study aimed to estimate the prevalence of tubular dysfunction alone or with glomerular damage and its evolution after HCV clearance in cirrhotic patients. Methods: One-hundred-thirty-five consecutive Child-Pugh-A cirrhotic patients were evaluated before antiviral treatment and six months after the end of therapy. Tubular dysfunction was evaluated by urinary-alpha1-microglobulin-to-creatinine-ratio (α1-MCR), glomerular damage was assessed by urinary-albumin-to-creatinine-ratio (ACR). Results: Almost all the patients (93.3%) showed a normal or mildly decreased e-GFR (KDIGO-G1/G2-categories). Tubular dysfunction was found in 23.7% (32/135) of patients, co-occurring with glomerular damage in 37.5% (12/32) of cases, while glomerular damage was found in 16.3% (22/135) of patients. In multiple logistic regression, glomerular damage and the concomitant presence of diabetes and hypertension were the only predictors significantly associated with tubular dysfunction. After HCV-clearance, patients experienced a significant reduction of α1-MCR levels (21.0 vs 10.5 μg/mg, p=0.009) and tubular dysfunction resolved in 57.1% of subjects. Conclusions: Tubular dysfunction is an unrecognized feature of HCV-related kidney disease in cirrhotic patients and its presence should be primarily investigated in subjects with glomerular damage, diabetes and hypertension, despite normal e-GFR. Tubular dysfunction resolves in the majority of cases after HCV clearance, however, it may persist after antiviral treatment and further studies should evaluate its long term impact on kidney function

Brief report: Atrial fibrillation with aberrant ventricular conduction after receiving Bamlanivimab/Etesevimab: a case report

Coronavirus Disease 2019 (COVID-19) is affecting millions of people globally. Several neutralizing monoclonal antibodies have been developed to limit the progression and complications of the disease. These treatments provide immediate and passive immunity. The combination therapy with Bamlanivimab plus Etesevimab led to a lower incidence of COVID-19-related hospitalization and death and a faster reduction in the SARS-CoV-2 viral load. No or rare cases of cardiovascular side effects are reported. We present the case of a high-risk 79-years-old woman who developed atrial fibrillation with aberrant ventricular conduction after administration of neutralizing monoclonal-antibodies Bamlanivimab plus Etesevimab. The woman with a history of insulin-dependent diabetes and Grade II follicular Non-Hodgkin Lymphoma previously vaccinated with two doses of Pfizer COVID-19 vaccine, presented with malaise, headache, and SARS-CoV-2 nasal swab reverse transcription-polymerase chain reaction tested positive for the infection. She received a single dose of Bamlanivimab (70 mg) + Etesevimab (1400 mg). After about a week, she developed atrial fibrillation with uncontrolled response to frequent premature ventricular complexes and aberrant ventricular conduction. This case presents a high-risk woman with SARS-CoV-2 infection who developed a serious adverse cardiovascular event some days after receiving neutralizing monoclonal antibodies. Risk factors including sex, age, anxiety related to isolation and infection, and COVID-19 itself may have all contributed to atrial fibrillation. Arrhythmia may rarely occur after monoclonal-antibodies treatment, although recommended timing to monitor patients is from 1 to 24 h after the administration of these antibodies. Appreciation of this potential association is important for evaluating monoclonal-antibody treatments’ safety and optimizing patient monitoring and follow-up

Fatal Listeria monocytogenes septicemia and meningitis complicated by Candida glabrata fungemia: a case report

Listeria monocytogenes is a Gram-positive bacteria and etiological agent of listeriosis. It has the ability to colonize the intestinal lumen and cross the intestinal, blood–brain, and placental barriers, leading to invasive listeriosis responsible for septicemia and meningitis in subjects at risk such as patients with diabetes mellitus, the elderly, and immunocompromised individuals and, for maternal-neonatal infection in pregnant women. We report a rare case of L. monocytogenes septicemia and meningitis complicated by Candida glabrata fungemia on a patient with a history of type 2 diabetes mellitus, hypothyroidism, hypertension, chronic kidney failure, chronic ischemic vascular encephalopathy, and atrial fibrillation. Although adequate therapy was rapidly started with an initial partial clinical improvement, the patient suddenly experienced clinical worsening concomitantly with Candida septicemia resulting in a fatal outcome. To our knowledge, this is the first described case of an invasive L. monocytogenes infection complicated by Candida sepsis. We hypothesize that concomitant Candida infection may play a significant role in the pathogenesis and virulence of L. monocytogenes