Background Much attention has been paid to the study and reporting of gastrointestinal (GI) symptoms in COVID-19 patients. Moreover, an increasing number of COVID-19 patients have been noted to experience hepatic and pancreatic injury. In this study, we retrospectively investigated symptoms and laboratory findings related to the GI system in a single center in Athens, Greece, and assessed the role of these parameters in relation to survival and disease severity. Method We retrospectively studied 61 adult COVID-19 patients admitted to the Army Share Fund Hospital (NIMTS) in Athens, Greece, from April 6th to May 6 th , 2020. Results Sixty-one COVID-19 cases were assessed in the study period. Regarding both survival and disease severity, diarrhea was the most common finding. The multivariate analysis revealed that elevated serum aspartate aminotransferase levels and low serum albumin levels were associated with worse patient survival (odds ratio [OR] 1.029, 95% confidence interval [CI] 1.007-1.05, P=0.0088; and OR 0.219, 95%CI 0.066-0.723, P=0.0127, respectively). As far as disease severity is concerned, only a low serum albumin level (measured at hospital admission) was correlated with more severe disease (OR 0.025, 95%CI 0.004-0.161, P=0.0001). Conclusions Outpatients with new-onset GI symptoms should be considered for COVID-19 testing in a high COVID-19 prevalence setting, as these symptoms are observed more and more in clinical settings. As prospective studies begin to emerge, clinicians will have more robust research data to diagnose COVID-19 patients earlier and identify patients in need of more intensive treatment.
Hepatitis D virus (HDV) globally affects nearly 5% of people with chronic hepatitis B virus (HBV) infection. Bulevirtide (BLV) is an HDV/HBV entry inhibitor recently approved for adult patients with chronic hepatitis delta (CHD). In this real-life case report, we describe the virological efficacy, the safety, and the liver function amelioration of one patient with liver compensated cirrhosis with esophageal varices after one-year combo treatment with BLV (2 mg/day in sub-cutaneous injection) and tenofovir disoproxil fumarate (TDF) (245 mg/day). The patient had HDV RNA levels of 9300 IU/mL, 1100 IU/mL, and undetectable at baseline, after three months, and after six months of treatment, respectively. In addition, the model for end-stage liver disease (MELD) score has declined from 11 at baseline to 8 after twelve months of treatment accompanied by alanine aminotransferase (ALT) normalization. Moreover, the treatment significantly improved the liver stiffness measurement (LSM) since a reduction from 34.3 kPa to 24.5 kPa was observed after twelve months of treatment. Furthermore, the treatment was well tolerated, and no dose reduction was needed.
Hepatitis B virus reactivation (HBVr) is a well described result of immunosuppressive therapy initiation in a variety of diseases with dose and duration of treatment being the main factors determining the probability for reactivation. Such cases have been described also in Covid-19 patients treated with immunosuppressive therapies. Nevertheless, there have also been reported cases of Covid-19 infection that led to HBVr with no concurrent immunosuppressive therapy or any other described cause. In accordance with that observation, we present a patient followed for a period spanning 20 years with HBeAg negative chronic HBV infection and non-detectable HBV DNA who after a mild Covid-19 infection treated only with low dose and short duration inhaled corticosteroids (ICS), developed elevated AST and ALT as well as elevated HBV DNA levels. During the diagnostic workout other etiologies of abnormal liver biochemistries were excluded and thus the diagnosis of HBV reactivation was established and treated with entecavir. Since other causes of reactivation were excluded, and ICS dose and duration was found baring only a very low risk (<1%) for HBVr, Covid-19 infection could be considered the most probable cause of reactivation.
Hepatitis B virus reactivation (HBVr) is a well-described result of immunosuppressive therapy initiation in various diseases, with the dose and duration of treatment being the main factors determining the probability for reactivation. Such cases have also been described in COVID-19 patients treated with immunosuppressive therapies. Nevertheless, cases of COVID-19 infection that led to HBVr with no concurrent immunosuppressive treatment or any other related cause have also been reported. By that observation, we present a patient followed for a period spanning 20 years with HBeAg negative chronic HBV infection and non-detectable HBV DNA who, after a mild COVID-19 infection treated only with low-dose and short-duration-inhaled corticosteroids (ICS), developed elevated AST and ALT as well as elevated HBV DNA levels. Other etiologies of abnormal liver biochemistries during the diagnostic workout were excluded; thus, the diagnosis of HBV reactivation was established. Treatment with entecavir was initiated, leading to the normalization of AST and ALT levels and a decreasing trend of HBV DNA levels. Since other causes of reactivation were excluded, and the ICS dose and duration were found baring only a very low risk (<1%) for HBVr, COVID-19 infection could be considered the most probable cause of reactivation, hence underlining the need for the close monitoring of those patients.
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