Development of tenofovir disoproxil fumarate resistance after complete viral suppression in a patient with treatment-naïve chronic hepatitis B: A case report and review of the literature.

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hepatitis B 14 infectiousdiseases
lamivudine 1 infectiousdiseasesdrugs
tenofovir 8 infectiousdiseasesdrugs

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lamivudine 4387 rtS106C, rtH126Y and rtD134E. These patients had previously been treated with various therapies, including lamivudine (LAM), adefovir (ADV) and ETC. We observed the development of TDF resistance in a patient who had no
tenofovir 55 Title: World Journal of GastroenterologyDevelopment of tenofovir disoproxil fumarate resistance after complete viral suppression in a patient with treatment-naïve chronic
tenofovir 1767 mutation sites, most of which had not been well-known as mutation sites. We changed the therapy from tenofovir to entecavir with a regimen of 0.5 mg once daily. After 4 mo, the HBV DNA titer decreased to 267 copies/mL,
tenofovir 3291 therapeutic benefits are diminished because of the emergence of drug-resistant viruses.Entecavir (ETC) and tenofovir disoproxil fumarate (TDF) are the two first-line therapies recommended for the treatment of CHB because
tenofovir 6901 rtS106, rtH126, rtD134, and rtL269 sites, which have been revealed as mutation sites associated with tenofovir resistance, and only the rtS106C mutation was detected. We performed full genome sequencing to find
tenofovir 7134 associated with virologic breakthrough because the rtS106C mutation alone was not sufficient to cause tenofovir resistance (Figure 1). The results showed mutations at 9 sites, namely, rtY9H, rtL91I, rtS106C, rtS106G,
tenofovir 7608 the AST and ALT levels increased to 202 IU/L and 539 IU/L, respectively. We changed the therapy from tenofovir to entecavir with a regimen of 0.5 mg once daily. After 4 mo, the HBV DNA titer decreased to 267 copies/mL.
tenofovir 14283 diagnosisWe performed full genome sequencing to find other mutation sites to know it is associated with tenofovir disoproxil fumarate (TDF) resistance.Laboratory diagnosisWe performed full genome sequencing to find
tenofovir 14602 rtT118C, rtT118G, rtQ267L, rtI269L, rtA317S, rtK333Q, and rtN337H.TreatmentWe changed the therapy from tenofovir to entecavir with a regimen of 0.5 mg once daily.Experiences and lessonsWe have to consider possibility
Select Disease Character Offset Disease Term Instance
hepatitis B 172 disoproxil fumarate resistance after complete viral suppression in a patient with treatment-naïve chronic hepatitis B : A case report and review of the literatureWoo Hee ChoDepartment of Internal Medicine, Dankook University
hepatitis B 1009 is a potent nucleotide analogue that is recommended as first-line therapy for patients with chronic hepatitis B . The results of a longitudinal study of TDF treatment demonstrated no development of resistance. We
hepatitis B 1159 of TDF treatment demonstrated no development of resistance. We observed one treatment-naïve chronic hepatitis B (CHB) patient who developed TDF resistance after complete viral suppression during long-term TDF treatment.
hepatitis B 1349 during long-term TDF treatment. A 37-year-old HBeAg-positive man received TDF 300 mg/d for 43 mo. The hepatitis B virus (HBV) DNA titer was 8 log10 copies/mL at baseline and became undetectable at 16 mo after treatment.
hepatitis B 2608 is helpful in revealing the exact mutation sites associated with TDF resistance.INTRODUCTIONChronic hepatitis B (CHB) affects approximately 250 million people worldwide and can lead to liver cirrhosis, liver failure,
hepatitis B 2901 30% of cirrhosis cases and 53% of HCC cases have been attributed to CHB[[2]]. Antiviral therapy for hepatitis B virus (HBV) infection can suppress viral replication and halt disease progression[[4],[5]]. The reduction
hepatitis B 4903 who visited the clinic because of elevated liver enzymes. He was first diagnosed as having chronic hepatitis B at the age of 20 and was followed up regularly in the family medicine department of Dankook University
hepatitis B 5147 the clinic, he had no history of liver enzyme elevation. His mother was also diagnosed with chronic hepatitis B but did not receive antiviral treatment. The patient’s laboratory examination showed that he was positive
hepatitis B 7891 respectively (Figure 3). HBeAg seroconversion had not yet occurred.Figure 1Full sequencing analysis of the hepatitis B virus reverse transcriptase gene from the patient (Korean sample). The sequence analysis shows that
hepatitis B 8263 “?” because the sites contained a substitution by 2 different nucleotides.Figure 2Chromatogram of the hepatitis B virus reverse transcriptase gene from the patient. The rt101 (red arrow) and rt118 (arrow) sites are
hepatitis B 8738 biochemical breakthroughs occurred at 43 mo after treatment initiation.DISCUSSIONThe treatment of chronic hepatitis B has improved in the last decade primarily because of the availability of oral nucleos(t)ide analogue
hepatitis B 9142 best of our knowledge and experience. The major limitation of long-term antiviral therapy for chronic hepatitis B is the emergence of drug resistance followed initially by an increase in HBV DNA level (virologic breakthrough)
hepatitis B 12103 because TDF resistance is rare. A few years ago, a case of TDF resistance was reported in a chronic hepatitis B (CHB) patient who received sequential nucleos(t)ide therapy[[24]]. TDF resistance with virologic and
hepatitis B 14047 HIGHLIGHTSCase characteristicsThe patient had not complained of any specific symptoms.Clinical diagnosisThe hepatitis B virus DNA titer rebounded to 7.5 log10 copies/mL at 43 mo after TDF treatment in a treatment-naive patient.Differential

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