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Brivudin
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
BVDU and its closely related congener IVDU [(E)-5-(2-iodovinyl)-2’-deoxyuridine] proved more potent against HSV-1 than all other antiherpes compounds, including aciclovir (De Clercq et al., 1979b). Brivudine is a uridine analog with the chemical name (E)-5-(2-bromovinyl)-2’-deoxyuridine, formula C11H13BrN2O5 and molecular weight 333 (Figure 217.1). As a nucleoside analog, it inhibits synthesis of DNA, inhibiting replication of the DNA genomes of DNA viruses (e.g. herpesviruses) at much lower concentrations than the concentrations affecting human DNA polymerases.
Postherpetic Neuralgia
Published in Gary W. Jay, Practical Guide to Chronic Pain Syndromes, 2016
Rajbala Thakur, Annie G. Philip, Jonathan C. Weeks
Three oral antiviral medications, including acyclovir, famciclovir, and valacyclovir, have been assessed in patients with herpes zoster for their role in the prevention of PHN or lessening its severity. Results of clinical trials indicate that all three agents mentioned decrease both zoster pain and the risk of developing PHN to some degree. The results of the individual trials could be questioned for consistency of evidence, but taken together, a strong case can be made for the use of antiviral therapy in treatment for herpes zoster–associated pain and in decreasing the incidence and chronicity of PHN pain (4,9,48-55). Early antiviral therapy is recommended to reduce viral replication and resultant neural damage and, thus, decrease the incidence and severity of PHN. A meta-analysis of the trials involving the use of acyclovir showed that in patients who were at least 50 years of age, the proportion with persistent pain at six months was 15%, as compared with 35% in the placebo group (4). In comparing famciclovir (500 mg every eight hours) to placebo in a subgroup of subjects who were at least 50 years of age and who had persistent pain after skin healing, the median duration of PHN was 163 days in the placebo group and 63 days in the famciclovir group (P = 0.004) (53). In a randomized trial of patients who were at least 50 years of age, comparison of valacyclovir (1000 mg every eight hours) and acyclovir resulted in equivalent rates of cutaneous healing (54). Valacyclovir significantly shortened the median time to resolution of zoster-associated pain (38 days vs. 51 days, P = 0.001). The proportion of patients experiencing pain at six months was 25.7% in the acyclovir group and 19.3% in the valacyclovir group (P = 0.02). Famciclovir and valacyclovir were compared (55) and showed similar effect on rash healing, acute pain resolution, and the percentage of patients with persistent pain at six months. All three drugs are comparable in their efficacy and safety profile. Valacyclovir and famciclovir enjoy a more favorable dosing regimen (three times per day) compared to acyclovir (five times per day) and are thus easier to use. On the other hand, acyclovir is the least expensive of the three. Other antiviral agents include brivudine and foscarnet. Brivudine with once-a-day dosing is not available in the United States. Foscarnet is only available in intravenous formulation and has not been studied in PHN prevention.
Capecitabine for the treatment of pancreatic cancer
Published in Expert Opinion on Pharmacotherapy, 2019
Nauman S. Siddiqui, Amandeep Godara, Margaret M. Byrne, Muhammad Wasif Saif
In addition to warfarin, few other agents warrant revision here. Allopurinol metabolites can lead to the decreased conversion of capecitabine to 5-FU and hence potentially can decrease 5-FU antitumor activity [63]. Consideration should be given to use of alternate agent rather than the continuation of allopurinol while on capecitabine [64]. Cimetidine, an over the counter H2 blocker can decrease the clearance of 5-FU. Therefore, cimetidine should be discontinued or replaced with other anti-acid medications such as ranitidine if necessary [65]. 5-bromovinyluracil, a metabolite of two antivirals agents, named sorivudine and brivudine is known to be a potent inhibitor of DPD. Patients should not receive concurrent therapy with either of these antiviral agents while receiving capecitabine. If a patient has received prior sorivudine or brivudine, then at least four weeks must elapse before the patient receives capecitabine therapy [66]. Finally, capecitabine can lead to higher phenytoin levels in the plasma. Patients on active treatment should b routinely monitored for phenytoin toxicity and drug levels [66].
A life-threatening drug-drug interaction between capecitabine and brivudine in a patient with metastatic breast cancer
Published in Journal of Chemotherapy, 2019
Angeliki Tsifi, George Papaxoinis, Panagiotis Diamantopoulos, Marina Mantzourani, Vasiliki Antoniadou, Asimina Halioti, Helen Gogas
Brivudine [(E)-5-(2-bromovinyl)-2΄-deoxyuridine] is a thimydine nucleoside analogue with activity against Varicella-Zoster virus.9,10 After its phosphorylation it interacts with the viral DNA polymerase and inhibits the replication of the virus.10 Similarly to its predecessor, brivudine is also implicated in DDI’s with 5-FU, an interaction that is explicitly mentioned in the drug’s label.7,11 Nevertheless, it was given to our patient and as a consequence, the toxic effects of orally administered capecitabine were intensified by the simultaneous administration of a drug that inhibits DPD.
Insights from pharmacokinetic models of host-microbiome drug metabolism
Published in Gut Microbes, 2020
Maria Zimmermann-Kogadeeva, Michael Zimmermann, Andrew L. Goodman
Although the initial model parameter values were employed from the study of brivudine, the reported analysis is in principle generally applicable. Our model can also be further extended to incorporate processes relevant for particular drugs and physiological conditions. For example, the model could be expanded to include drug metabolism in the intestinal epithelium,20,21 or microbiota drug metabolism in the small intestine.5 The effect of meal intake on gallbladder flow22 or on intestinal transporter activity23 could be represented as time-dependent coefficients of enterohepatic circulation and intestinal absorption, respectively. Pharmacokinetic models can be combined with host genome-scale models to simulate drug and nutrient effects on host physiology, which can lead to dietary recommendations for enhanced drug effect,24 predicted drug–drug interactions25 or adverse drug reactions.26–28 Since intestinal motility, nutrient intake,29,30 and drugs affect bacterial growth,31 physiology and microbiome composition,32,33 incorporation of genome-scale metabolic models of the microbiota into the pharmacokinetic modeling framework might further enhance the ability of these integrative models to predict in vivo metabolism of specific drugs. Improved in silico estimation of drug absorption,34,35 and putative host36–39 and bacterial40–42 xenobiotic biotransformation in combination with systematic experimental studies of microbial drug metabolism,6 will facilitate accurate prediction of in vivo drug metabolism with integrative pharmacokinetic models in the near future.43,44