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Myocarditis
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Telbivudine is an antiviral synthetic nucleoside analogue that inhibits both DNA and RNA-dependent DNA polymerases, which is especially effective for retroviral and para-retroviral (hepatitis B viruses) infections. In addition, telbivudine exhibits pleiotropic immunomodulatory/anti-inflammatory, endothelial-protective, antiapoptotic and antioxidative properties. The DNA genome of the single-stranded B19V, which has often been linked to the pathogenesis of myocarditis and its progression to DCM, replicates through a specific rolling-hairpin mechanism to generate a double-stranded DNA molecule, mimicking the second strand DNA synthesis during hepatitis B virus replication. Therefore, telbivudine, which preferentially inhibits the DNA-dependent single-stranded DNA synthesis, may interfere with the unique replication mode of B19V. Since data are not available, the use of telbivudine cannot be recommended from studies or registries so far.
Lamivudine
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Jennifer Audsley, Michelle Giles, Sharon R. Lewin
Telbivudine has high-level cross-reactivity with lamivudine-resistant hepatitis B virus strains in vitro (Yang et al., 2005; see Chapter 256, Telbivudine). The signature mutation associated with telbivudine resistance is rtM204I, which is one of the major lamivudine mutations and was detected in 6.8% of participants receiving telbivudine in a phase III trial (Lai et al., 2007). Primary analysis of data has been reported from a clinical trial in patients who had received 3–12 months of lamivudine therapy and were then randomly assigned to a telbivudine switch or to remain on lamivudine. At week 24, those receiving telbivudine had a significantly greater reduction in hepatitis B virus DNA than those who continued on lamivudine (Safadi et al., 2007).
Sexually acquired viral hepatitis B and C
Published in Shiv Shanker Pareek, The Pictorial Atlas of Common Genito-Urinary Medicine, 2018
Acute hepatitis B usually resolves spontaneously, so no treatment is required. If a patient has chronic, active hepatitis B with replicating virus, the following treatments should be administered: interferon alpha-2b (an immune modulator which helps the patients immune system fight the infection) 3 million units (MU) – administered intramuscular three times per weekalternatively: pegylated interferon alpha-2b (a long-acting version) 180 pg – administered intramuscular once weeklyantiviral drugs (these stop the virus replicating):– entecavir 0.5 mg orally once daily, available as a tablet or liquid suspension (if previously resistant to lamivudine, the dose should be 1 g once daily).– adefovir dipivoxil 10 mg orally once daily (not recommended for children under 12 years of age).– telbivudine 600 mg orally once daily, available as a tablet or liquid suspension (not recommended for children under 16 years of age).– tenofovir disoproxil fumarate 300 mg orally once daily (not recommended for children or adolescents with hepatitis B).– lamivudine 100 mg orally once daily in adults. For children two years of age and above, dose at 3 mg/kg bodyweight orally once daily, to a maximum of 100 mg per day.
SOD1-targeting therapies for neurodegenerative diseases: a review of current findings and future potential
Published in Expert Opinion on Orphan Drugs, 2020
John P. Franklin, Mimoun Azzouz, Pamela J. Shaw
Several recent studies have used rational in silico design with the intention of creating small molecules to directly inhibit toxic mutant SOD1 aggregation or mediate its interaction with other proteins. Tryptophan 32 (W32), a solvent-exposed residue which is found in human and primate SOD1 but is not evolutionarily conserved across other species, has recently been hypothesized to play a key role in SOD1 misfolding. Substitution of this residue for a conserved serine residue has been shown to ameliorate motor neuron toxicity in zebrafish relative to human WT and mutant SOD1 [121]. In the same study, in silico screening of previously approved drugs for interaction with this residue identified Telbivudine, a drug used in the treatment of chronic hepatitis B, which rescued SOD1 toxicity in a dose-dependent manner. A second study using a different in silico screening method and crystallographic validation identified a phenanthridinone-based compound as inhibiting oxidation of W32 [122]. In a separate study, five compounds were discovered to inhibit SOD1G85R interaction with tubulin in vitro possibly also through action on W32 [123]. In a similar manner, focus on the important C111 residue has led to the discovery of Ebselen as a promoter of SOD1-maturation through interaction with C111, facilitating dimer formation [32].
Hepatitis B virus reactivation associated with Janus kinase (JAK) inhibitors: a retrospective study of pharmacovigilance databases and review of the literature
Published in Expert Opinion on Drug Safety, 2023
Chen Pan, Mingnan Cao, Cilin Yan, Xiaojuan Ou, Xia Zhang, Wanyi Xu, Ye Xu, Xiangli Cui
Literature review yielded 276 studies. A total of 23 cases in 11 independent studies were identified and included [17,20,21,24–31]. Overall, there were 9 (39.13%) males and 8 (34.78%) females. The median age of 17 patients reported was 60.50 (IQR 58.75–62.25) years. There were six patients did not report gender and age information. The median onset time of HBVr was 6.90 (IQR 2.00–12.00) months. Twelve (52.17%) were treated with Ruxolitinib for MPNs [17,20,24–28], and their median time of HBVr after initiating Ruxolitinib was 5.95 (IQR 1.75, 9.90) months. Ten patients received Entecavir, one received Tenofovir and one not received antiviral drugs for therapy. Ruxolitinib was discontinued in three patients. Time to reach undetectable HBV viral load was reported in eight patients [17,20,24,28], and mean (minimum, maximum) time was 3.38 (1.00,12.00) months. Seven (30.43%) patients reported in the literature received Tofacitinib, 6 for RA and 1 for UC [29–31]. Their median time to HBVr after initiating Tofacitinib was 12 (IQR 4.50–34.00) months. Two patients received Entecavir, one received Tenofovir and four not received antiviral drugs for therapy. No patient discontinued Tofacitinib. Time to reach undetectable HBV was reported in one patient which was 0.5 month [30]. Four (17.39%) patients reported in the literature received Baricitinib for RA [21]. One patient received Telbivudine for HBVr therapy. Baricitinib was discontinued in three patients. Detailed information such as HBV serology, antiviral prophylaxis and treatment about patients who developed HBVr during treatment with JAK inhibitors from literature review are listed in Table S1.
Hepatitis B virus infection as a risk factor for chronic kidney disease
Published in Expert Review of Clinical Pharmacology, 2019
Fabrizio Fabrizi, Roberta Cerutti, Ezequiel Ridruejo
A total of 32 patients with HBV-associated GN and chronic hepatitis B received telbivudine monotherapy for 104 weeks; the percentages of complete+ partial remission were 90.7% and 95.3%, respectively, at 52 and 104 weeks [44]. Compared to baseline, eGFR were significantly increased from 69.2 ± 23.11 mL/min/1.73m2 to 116.2 ± 26.3 mL/min/1.73m2 at 104 weeks of treatment. Multivariate analysis suggested that baseline HBV DNA viral load (OR, 1.19, 95% CI, 1.11 to 2.19, P = 0.02) and baseline urinary protein (OR = 1.08, 95% CI, 1.04 to 2.44, P = 0.03) were independent risk factors associated with CR after telbivudine [44].