Page last updated: 2024-10-21

1-anilino-8-naphthalenesulfonate and Chronic Hepatitis B

1-anilino-8-naphthalenesulfonate has been researched along with Chronic Hepatitis B in 17 studies

1-anilino-8-naphthalenesulfonate: RN given refers to parent cpd
8-anilinonaphthalene-1-sulfonic acid : A naphthalenesulfonic acid that is naphthalene-1-sulfonic acid substituted by a phenylamino group at position 8.

Research Excerpts

ExcerptRelevanceReference
" Overall, 32 (26%) patients reported an adverse event."6.90Safety and efficacy of stopping tenofovir disoproxil fumarate in patients with chronic hepatitis B following at least 8 years of therapy: a prespecified follow-up analysis of two randomised trials. ( Buti, M; Crans, G; Flaherty, J; Flisiak, R; Gaggar, A; Gane, E; Janssen, HLA; Jump, B; Kaita, K; Kitrinos, K; Manns, M; Marcellin, P; Op den Brouw, M; Wong, DK, 2019)
" Overall, 32 (26%) patients reported an adverse event."2.90Safety and efficacy of stopping tenofovir disoproxil fumarate in patients with chronic hepatitis B following at least 8 years of therapy: a prespecified follow-up analysis of two randomised trials. ( Buti, M; Crans, G; Flaherty, J; Flisiak, R; Gaggar, A; Gane, E; Janssen, HLA; Jump, B; Kaita, K; Kitrinos, K; Manns, M; Marcellin, P; Op den Brouw, M; Wong, DK, 2019)
"Currently, the population prevalence of NAFLD in Asia is around 25%, like many Western countries."2.55New trends on obesity and NAFLD in Asia. ( Fan, JG; Kim, SU; Wong, VW, 2017)
"The prevalence of steatohepatitis increased with PNPLA3 CC (14%), CG (20%) and GG (43%) (P < 0."1.42The impact of PNPLA3 (rs738409 C>G) polymorphisms on liver histology and long-term clinical outcome in chronic hepatitis B patients. ( Boonstra, A; Brouwer, WP; de Knegt, RJ; de Man, RA; Hansen, BE; Janssen, HL; Pas, SD; ten Kate, FJ; van der Meer, AJ, 2015)
"In patients with both CHB and NAFLD, these genotypes of PNPLA3 polymorphisms were associated with increased susceptibility to nonalcoholic steatohepatitis (NASH) (NAFLD activity score ≥ 3; P = 0."1.42Linked PNPLA3 polymorphisms confer susceptibility to nonalcoholic steatohepatitis and decreased viral load in chronic hepatitis B. ( Chen, GY; Chen, YM; Fan, JG; Liu, WB; Lu, JF; Mi, YQ; Pan, Q; Shen, F; Sun, WL; Wang, YQ; Zhang, RN; Zhang, SY; Zheng, RD; Zhu, CY, 2015)
"Patients with liver cirrhosis had serum levels of amylase and lipase significantly higher than both the healthy subjects and the patients with CAH, while no significant differences were found in serum levels of these enzymes in patients with CAH as compared to the healthy subjects."1.30Serum pancreatic enzyme concentrations in chronic viral liver diseases. ( Andreone, P; Barakat, B; Bernardi, M; Billi, P; Cursaro, C; Fiocchi, M; Gramenzi, A; Miglio, F; Morselli-Labate, AM; Pezzilli, R; Sama, C, 1999)

Research

Studies (17)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's1 (5.88)18.2507
2000's2 (11.76)29.6817
2010's13 (76.47)24.3611
2020's1 (5.88)2.80

Authors

AuthorsStudies
Wang, P1
Wu, C1
Li, Y1
Gong, Y1
Shen, N1
Gao, X1
Liu, W1
Yang, L1
Zhang, X1
Ma, N1
Wang, L1
Yan, L1
Tang, L1
Yang, H1
Liu, D1
Fan, JG2
Kim, SU1
Wong, VW1
Ghalamkari, S1
Sharafi, H1
Alavian, SM1
Raksayot, M1
Chuaypen, N1
Khlaiphuengsin, A1
Pinjaroen, N1
Treeprasertsuk, S1
Poovorawan, Y1
Tanaka, Y1
Tangkijvanich, P1
Wang, LQ1
Guo, WH1
Guo, ZW1
Qin, P1
Zhang, R1
Zhu, XM1
Liu, DW1
Buti, M1
Wong, DK1
Gane, E1
Flisiak, R1
Manns, M1
Kaita, K1
Janssen, HLA1
Op den Brouw, M1
Jump, B1
Kitrinos, K1
Crans, G1
Flaherty, J1
Gaggar, A1
Marcellin, P1
Viganò, M1
Valenti, L2
Lampertico, P1
Facchetti, F1
Motta, BM1
D'Ambrosio, R1
Romagnoli, S1
Dongiovanni, P2
Donati, B2
Fargion, S1
Colombo, M1
Fares, R1
Lombardi, R1
Mancina, RM1
Romeo, S1
Jiang, M1
Xin, Y1
Wang, W1
Lin, Z1
Zhang, D1
Li, C1
Jiang, X1
Xuan, S1
Brouwer, WP1
van der Meer, AJ1
Boonstra, A1
Pas, SD1
de Knegt, RJ1
de Man, RA1
Hansen, BE1
ten Kate, FJ1
Janssen, HL1
Zampino, R1
Coppola, N1
Cirillo, G1
Boemio, A1
Grandone, A1
Stanzione, M1
Capoluongo, N1
Marrone, A1
Macera, M1
Sagnelli, E1
Adinolfi, LE1
del Giudice, EM1
Pan, Q1
Zhang, RN1
Wang, YQ1
Zheng, RD1
Mi, YQ1
Liu, WB1
Shen, F1
Chen, GY1
Lu, JF1
Zhu, CY1
Zhang, SY1
Chen, YM1
Sun, WL1
Takeuchi, Y1
Ikeda, F1
Moritou, Y1
Hagihara, H1
Yasunaka, T1
Kuwaki, K1
Miyake, Y1
Ohnishi, H1
Nakamura, S1
Shiraha, H1
Takaki, A1
Iwasaki, Y1
Nouso, K1
Yamamoto, K1
Katakura, Y1
Yotsuyanagi, H1
Hashizume, K1
Okuse, C1
Okuse, N1
Nishikawa, K1
Suzuki, M1
Iino, S1
Itoh, F1
Chen, CL1
Yang, HI1
Yang, WS1
Liu, CJ1
Chen, PJ1
You, SL1
Wang, LY1
Sun, CA1
Lu, SN1
Chen, DS1
Chen, CJ1
Pezzilli, R1
Andreone, P1
Morselli-Labate, AM1
Sama, C1
Billi, P1
Cursaro, C1
Barakat, B1
Gramenzi, A1
Fiocchi, M1
Miglio, F1
Bernardi, M1

Clinical Trials (5)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Non Invasive Evaluation of Liver Fibrosis and Steatosis in Type 2 Diabetic Patient in Assiut University Hospitals[NCT05605717]60 participants (Anticipated)Observational2022-11-01Not yet recruiting
Clinical Study on the Value of Quantitative MRI Imaging in Diffuse Liver Diseases[NCT04626492]150 participants (Anticipated)Observational [Patient Registry]2020-08-01Recruiting
Effect of Intermittent Calorie Restriction on Metabolic Dysfunction-Associated Steatotic Liver Disease Patients With Abnormal Glucose Metabolism[NCT04283942]60 participants (Actual)Interventional2020-07-30Completed
A Randomized, Double-Blind, Controlled Evaluation of Tenofovir DF Versus Adefovir Dipivoxil for the Treatment of Presumed Pre-Core Mutant Chronic Hepatitis B[NCT00117676]Phase 3382 participants (Actual)Interventional2005-02-28Completed
A Randomized, Double-Blind, Controlled Evaluation of Tenofovir DF Versus Adefovir Dipivoxil for the Treatment of HBeAg Positive Chronic Hepatitis B[NCT00116805]Phase 3266 participants (Actual)Interventional2005-06-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Percentage of Participants With ALT Normalization at Week 48

ALT normalization was defined as ALT > upper limit of normal (ULN) at baseline and within the normal range at the end of blinded treatment. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Week 48

Interventionpercentage of participants (Number)
TDF-TDF76.3
ADV-TDF77.1

Percentage of Participants With ALT Normalization at Weeks 96

ALT normalization was defined as ALT > ULN at baseline and within the normal range at Week 96. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Week 96

Interventionpercentage of participants (Number)
TDF-TDF72.4
ADV-TDF68.5

Percentage of Participants With HBV DNA < 400 Copies/mL at Week 48

(NCT00117676)
Timeframe: Week 48

Interventionpercentage of participants (Number)
TDF-TDF93.2
ADV-TDF63.2

Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 96

(NCT00117676)
Timeframe: Week 96

Interventionpercentage of participants (Number)
TDF-TDF90.6
ADV-TDF89.3

Change From Baseline in ALT at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00117676)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionunits per liter (Mean)
Week 48Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-124.4-138.5-140.0-140.3-139.5-134.7-143.1-132.6-131.9-129.2
TDF-TDF-95.0-93.7-99.1-99.6-97.7-98.9-98.9-96.1-97.0-94.9

Change From Baseline in HBV DNA at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00117676)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionlog10 copies/mL (Mean)
Week 48Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-4.07-4.74-4.77-4.75-4.77-4.81-4.81-4.79-4.69-4.75
TDF-TDF-4.57-4.54-4.61-4.56-4.59-4.61-4.61-4.56-4.60-4.57

Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 240

The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00117676)
Timeframe: Baseline; Week 240

,
Interventionunits on a scale (Mean)
Knodell ScoreIshak Score
ADV-TDF-4.9-4.2
TDF-TDF-4.6-4.0

Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 48

The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00117676)
Timeframe: Baseline; Week 48

,
Interventionunits on a scale (Mean)
Knodell Necroinflammatory ScoreIshak Necroinflammatory Score
ADV-TDF-3.4-2.6
TDF-TDF-3.5-2.6

Change From Week 48 in ALT at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00117676)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionunits per liter (Mean)
Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-0.6-0.3-3.6-3.9-4.1-2.0-3.9-8.9-5.9
TDF-TDF2.4-0.60.7-2.5-3.9-2.6-2.9-4.6-2.8

Change From Week 48 in HBV DNA at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00117676)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionlog10 copies/mL (Mean)
Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-0.60-0.63-0.61-0.61-0.64-0.65-0.66-0.67-0.72
TDF-TDF0.02-0.030.01-0.04-0.04-0.05-0.02-0.04-0.05

Number of Participants With HBV Genotypic Changes From Baseline at Week 144 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 144 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 96 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 96 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 97 to 144

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF00000
TDF-TDF40121
TDF-TDF With Addition of FTC00000

Number of Participants With HBV Genotypic Changes From Baseline at Week 192 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 192 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 144 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 144 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 145 to 192

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF00000
TDF-TDF30111
TDF-TDF With Addition of FTC10010

Number of Participants With HBV Genotypic Changes From Baseline at Week 240 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 240 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 192 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 192 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 193 to 240

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF20002
TDF-TDF11000
TDF-TDF With Addition of FTC20200

Number of Participants With HBV Genotypic Changes From Baseline at Week 288 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 288 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 240 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 240 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 241 to 288

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF10100
TDF-TDF30210
TDF-TDF With Addition of FTC10100

Number of Participants With HBV Genotypic Changes From Baseline at Week 336 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 336 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 288 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 288 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 289 to 336

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF10001
TDF-TDF00000
TDF-TDF With Addition of FTC10010

Number of Participants With HBV Genotypic Changes From Baseline at Week 384 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 384 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 336 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 336 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 337 to 384

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF00000
TDF-TDF10001
TDF-TDF With Addition of FTC00000

Number of Participants With HBV Genotypic Changes From Baseline at Week 432 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 432 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 384 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 384 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 385 to 432

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF10100
TDF-TDF20020
TDF-TDF With Addition of FTC00000

Number of Participants With HBV Genotypic Changes From Baseline at Week 48 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 48, those with viral breakthrough, and those who discontinued after Week 24 with HBV DNA ≥ 400 copies/mL. (NCT00117676)
Timeframe: Baseline; Week 48

,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF42714201
TDF-TDF80341

Number of Participants With HBV Genotypic Changes From Baseline at Week 480 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 480 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 432 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 432 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 433 to 480

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to genotype
ADV-TDF00000
TDF-TDF00000
TDF-TDF With Addition of FTC00000

Number of Participants With HBV Genotypic Changes From Baseline at Week 96 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 96 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 48 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 49 to 96

,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites within HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF00000
TDF-TDF60240
TDF-TDF With Addition of FTC10100

Percentage of Participants With ALT Normalization at Weeks 144, 192, 240, 288, 336, and 384

ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, and 384

,
Interventionpercentage of participants (Number)
Week 144Week 192Week 240Week 288Week 336Week 384
ADV-TDF70.076.475.772.965.469.2
TDF-TDF74.368.270.369.965.965.3

Percentage of Participants With ALT Normalization at Weeks 432 and 480

ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Weeks 432 and 480

,
Interventionpercentage of participants (Number)
Week 432Week 480
ADV-TDF87.288.9
TDF-TDF86.580.0

Percentage of Participants With HBsAg Loss and/or Seroconversion to Anti-HBs at Week 96

HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at Week 96. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at Week 96. (NCT00117676)
Timeframe: Baseline; Week 96

,
Interventionpercentage of participants (Number)
HBsAg LossAnti-HBs Seroconversion
ADV-TDF00
TDF-TDF00

Percentage of Participants With HBsAg Loss and/or Seroconversion to Anti-HBs at Weeks 144, 192, 240, 288, 336, 384, 432, and 480

HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at the subsequent time point. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at the subsequent time point. (NCT00117676)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionpercentage of participants (Number)
HBsAg Loss - Week 144Anti-HBs Seroconversion - Week 144HBsAg Loss - Week 192Anti-HBs Seroconversion - Week 192HBsAg Loss - Week 240Anti-HBs Seroconversion - Week 240HBsAg Loss - Week 288Anti-HBs Seroconversion - Week 288HBsAg Loss - Week 336Anti-HBs Seroconversion - Week 336HBsAg Loss - Week 384Anti-HBs Seroconversion - Week 384HBsAg Loss - Week 432Anti-HBs Seroconversion - Week 432HBsAg Loss - Week 480Anti-HBs Seroconversion - Week 480
ADV-TDF00000.800.80.80.80.80.80.81.60.82.40.8
TDF-TDF00000000000.80.41.20.41.20.8

Percentage of Participants With HBV DNA < 400 Copies/mL and Histological Improvement (2-point Reduction in Knodell Necroinflammatory Score Without Worsening in Knodell Fibrosis Score) at Week 48

"Complete response was a composite endpoint defined as histological response and HBV DNA < 400 copies/mL. Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4.~A participant was a nonresponder for the primary endpoint if either biopsy (baseline or end-of-treatment) was missing or if there was not an HBV DNA value available at or beyond Week 40." (NCT00117676)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
YesNo
ADV-TDF48.851.2
TDF-TDF70.829.2

Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 144, 192, 240, 288, 336, and 384

(NCT00117676)
Timeframe: Weeks 144, 192, 240, 288, 336, and 384

,
Interventionpercentage of participants (Number)
Week 144Week 192Week 240Week 288Week 336Week 384
ADV-TDF88.486.883.982.978.076.3
TDF-TDF86.784.082.880.577.074.3

Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 432 and 480

(NCT00117676)
Timeframe: Weeks 432 and 480

,
Interventionpercentage of participants (Number)
Week 432Week 480
ADV-TDF97.7100.0
TDF-TDF97.6100.0

Percentage of Participants With Hepatitis B S-Antigen (HBsAg) Loss or Seroconversion Antibody to HBs (Anti-HBs) at Week 48

HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at Week 48. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at Week 48. (NCT00117676)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
HBsAg LossSeroconversion to anti-HBs
ADV-TDF00
TDF-TDF00

Percentage of Participants With Histological Response at Week 240

Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00117676)
Timeframe: Baseline; Week 240

,
Interventionpercentage of participants (Number)
YesNo
ADV-TDF85.114.9
TDF-TDF87.312.7

Percentage of Participants With Histological Response at Week 48

Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00117676)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
YesNo
ADV-TDF68.831.2
TDF-TDF72.427.6

Ranked Assessment of Necroinflammation and Fibrosis at Week 240

Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00117676)
Timeframe: Baseline; Week 240

,
Interventionpercentage of participants (Number)
Improvement - NecroinflammationNo Change - NecroinflammationWorsening - NecroinflammationImprovement - FibrosisNo Change - FibrosisWorsening - Fibrosis
ADV-TDF94.61.44.159.533.86.8
TDF-TDF96.72.70.762.034.04.0

Ranked Assessment of Necroinflammation and Fibrosis at Week 48

Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00117676)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
Improvement - NecroinflammationNo Change - NecroinflammationWorsening - NecroinflammationMissing Data - NecroinflammationImprovement - FibrosisNo Change - FibrosisWorsening - FibrosisMissing Data - Fibrosis
ADV-TDF81.68.00.89.625.654.410.49.6
TDF-TDF82.06.84.86.422.063.28.46.4

Percentage of Participants With Alanine Aminotransferase (ALT) Normalization at Week 48

ALT normalization was defined as ALT > upper limit of normal (ULN) at baseline and within the normal range at the end of blinded treatment. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Week 48

Interventionpercentage of participants (Number)
TDF-TDF68.0
ADV-TDF54.4

Percentage of Participants With ALT Normalization at Week 96

ALT normalization was defined as ALT > ULN at baseline and within the normal range at Week 96. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Week 96

Interventionpercentage of participants (Number)
TDF-TDF65.2
ADV-TDF74.4

Percentage of Participants With HBV DNA < 400 Copies/mL and Histological Improvement (2-point Reduction in Knodell Necroinflammatory Score Without Worsening in Knodell Fibrosis Score) at Week 48

"Complete response was a composite endpoint defined as histological response and HBV DNA < 400 copies/mL. Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4.~A participant was a nonresponder for the primary endpoint if either biopsy (baseline or end-of-treatment) was missing or if there was not an HBV DNA value available at or beyond Week 40." (NCT00116805)
Timeframe: Baseline; Week 48

Interventionpercentage of participants (Number)
TDF-TDF66.5
ADV 10 mg12.2

Percentage of Participants With HBV DNA < 400 Copies/mL at Week 48

(NCT00116805)
Timeframe: Week 48

Interventionpercentage of participants (Number)
TDF-TDF76.1
ADV-TDF13.3

Percentage of Participants With HBV DNA < 400 Copies/mL at Week 96

(NCT00116805)
Timeframe: Week 96

Interventionpercentage of participants (Number)
TDF-TDF77.6
ADV-TDF77.9

Change From Baseline in ALT at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00116805)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
InterventionU/L (Mean)
Week 48Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-106.1-120.4-126.2-139.6-134.8-130.9-132.3-133.7-162.1-157.5
TDF-TDF-107.2-107.8-100.7-101.4-95.9-102.3-101.9-108.1-105.0-92.3

Change From Baseline in HBV DNA at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00116805)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionlog10 IU/mL (Mean)
Week 48Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-3.93-6.38-6.31-6.49-6.45-6.49-6.46-6.28-6.45-6.37
TDF-TDF-6.17-6.26-6.32-6.30-6.22-6.27-6.35-6.38-6.13-6.18

Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 240

The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00116805)
Timeframe: Baseline; Week 240

,
Interventionunits on a scale (Mean)
Knodell Necroinflammatory ScoreIshak Necroinflammatory Score
ADV-TDF-5.1-4.5
TDF-TDF-4.8-4.1

Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 48

The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00116805)
Timeframe: Baseline; Week 48

,
Interventionunits on a scale (Mean)
Knodell Necroinflammatory ScoreIshak Necroinflammatory Score
ADV-TDF-3.2-2.6
TDF-TDF-3.6-2.7

Change From Week 48 in ALT at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00116805)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
InterventionU/L (Mean)
Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-6.9-0.7-7.8-8.1-10.3-9.3-6.9-11.6-7.1
TDF-TDF-2.0-0.4-1.33.7-1.6-1.2-4.4-4.3-5.5

Change From Week 48 in HBV DNA at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

(NCT00116805)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionlog10 IU/mL (Mean)
Week 96Week 144Week 192Week 240Week 288Week 336Week 384Week 432Week 480
ADV-TDF-2.43-2.27-2.41-2.49-2.62-2.59-2.34-2.32-2.16
TDF-TDF-0.10-0.19-0.20-0.14-0.18-0.25-0.29-0.13-0.24

Number of Participants With HBV Genotypic Changes From Baseline at Week 144 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 144 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 96 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 96 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 97 to 144

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF52300
ADV-TDF With Addition of FTC50031
TDF-TDF21010
TDF-TDF With Addition of FTC72320

Number of Participants With HBV Genotypic Changes From Baseline at Week 192 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 192 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 144 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 144 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 145 to 192

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF10100
ADV-TDF With Addition of FTC10100
TDF-TDF20101
TDF-TDF With Addition of FTC50013

Number of Participants With HBV Genotypic Changes From Baseline at Week 240 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 240 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 192 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 192 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 193 to 240

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF00000
ADV-TDF With Addition of FTC11000
TDF-TDF30210
TDF-TDF With Addition of FTC30021

Number of Participants With HBV Genotypic Changes From Baseline at Week 288 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 288 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 240 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 240 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 241 to 288

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF00000
ADV-TDF With Addition of FTC00000
TDF-TDF30021
TDF-TDF With Addition of FTC00000

Number of Participants With HBV Genotypic Changes From Baseline at Week 336 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 336 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 288 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 288 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 289 to 336

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF10010
ADV-TDF With Addition of FTC00000
TDF-TDF10001
TDF-TDF With Addition of FTC00000

Number of Participants With HBV Genotypic Changes From Baseline at Week 384 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 384 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 336 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 336 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 337 to 384

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF21100
ADV-TDF With Addition of FTC20110
TDF-TDF10001
TDF-TDF With Addition of FTC00000

Number of Participants With HBV Genotypic Changes From Baseline at Week 432 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 432 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 384 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 384 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 385 to 432

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF00000
ADV-TDF With Addition of FTC10010
TDF-TDF10100
TDF-TDF With Addition of FTC30030

Number of Participants With HBV Genotypic Changes From Baseline at Week 48 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL, those with viral breakthrough, and those who discontinued after Week 24 with HBV DNA ≥ 400 copies/mL. (NCT00116805)
Timeframe: Baseline; Week 48

,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF75817437
TDF-TDF3121379

Number of Participants With HBV Genotypic Changes From Baseline at Week 480 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 480 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 432 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 432 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 433 to 480

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF10010
ADV-TDF With Addition of FTC00000
TDF-TDF00000
TDF-TDF With Addition of FTC30120

Number of Participants With HBV Genotypic Changes From Baseline at Week 96 (Resistance Surveillance)

Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 96 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 48 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 49 to 96

,,,
Interventionparticipants (Number)
Participants evaluatedChanges at conserved sites in HBV polymeraseChanges at polymorphic sites in HBV polymeraseNo genotypic changes (wild-type virus)Unable to be genotyped
ADV-TDF1621121
ADV-TDF With Addition of FTC103232
TDF-TDF1823103
TDF-TDF With Addition of FTC130157

Percentage of Participants With ALT Normalization at Weeks 144, 192, 240, 288, 336, and 384

ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, and 384

,
Interventionpercentage of participants (Number)
Week 144Week 192Week 240Week 288Week 336Week 384
ADV-TDF67.869.465.970.167.967.1
TDF-TDF60.259.650.051.346.252.6

Percentage of Participants With ALT Normalization at Weeks 432 and 480

ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Weeks 432 and 480

,
Interventionpercentage of participants (Number)
Week 432Week 480
ADV-TDF78.682.8
TDF-TDF79.675.0

Percentage of Participants With HBeAg Loss or Seroconversion to Anti-HBe at Week 96

HBeAg loss was defined as HBeAg positive at baseline and HBeAg negative at Week 96. Seroconversion to anti-HBe was defined as change of detectable antibody to HBeAg from negative at baseline to positive at Week 96. (NCT00116805)
Timeframe: Baseline; Week 96

,
Interventionpercentage of participants (Number)
HBeAg LossSeroconversion to Anti-HBe
ADV-TDF25.622.0
TDF-TDF25.922.8

Percentage of Participants With HBsAg Loss or Seroconversion to Anti-HBs at Week 96

HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at the subsequent time point. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at the subsequent time point. (NCT00116805)
Timeframe: Baseline; Week 96

,
Interventionpercentage of participants (Number)
HBsAg LossAnti-HBs Seroconversion
ADV-TDF5.84.7
TDF-TDF5.34.1

Percentage of Participants With HBsAg Loss or Seroconversion to Anti-HBs at Weeks 144, 192, 240, 288, 336, 384, 432, and 480

HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at the subsequent time point. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at the subsequent time point. (NCT00116805)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, 384, 432, and 480

,
Interventionpercentage of participants (Number)
HBsAg Loss - Week 144Anti-HBs Seroconversion - Week 144HBsAg Loss - Week 192Anti-HBs Seroconversion - Week 192HBsAg Loss - Week 240Anti-HBs Seroconversion - Week 240HBsAg Loss - Week 288Anti-HBs Seroconversion - Week 288HBsAg Loss - Week 336Anti-HBs Seroconversion - Week 336HBsAg Loss - Week 384Anti-HBs Seroconversion - Week 384HBsAg Loss - Week 432Anti-HBs Seroconversion - Week 432HBsAg Loss - Week 480Anti-HBs Seroconversion - Week 480
ADV-TDF8.06.87.96.78.08.08.08.07.97.99.07.910.28.010.17.9
TDF-TDF7.55.29.46.49.26.39.26.410.37.511.08.110.97.610.98.0

Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 144, 192, 240, 288, 336, and 384

(NCT00116805)
Timeframe: Weeks 144, 192, 240, 288, 336, and 384

,
Interventionpercentage of participants (Number)
Week 144Week 192Week 240Week 288Week 336Week 384
ADV-TDF70.571.666.364.862.160.5
TDF-TDF71.767.963.461.359.456.1

Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 432 and 480

(NCT00116805)
Timeframe: Weeks 432 and 480

,
Interventionpercentage of participants (Number)
Week 432Week 480
ADV-TDF100.096.6
TDF-TDF93.098.0

Percentage of Participants With Hepatitis B e Antigen (HBeAg) Loss/Seroconversion at Week 48

HBeAg loss was defined as HBeAg positive at baseline and HBeAg negative at Week 48. Seroconversion to anti-HBe was defined as change of detectable antibody to HBeAg from negative at baseline to positive at Week 48. (NCT00116805)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
HBeAg LossHBeAg Seroconversion
ADV-TDF17.517.5
TDF-TDF22.220.9

Percentage of Participants With Hepatitis B S-Antigen (HBsAg) Loss or Seroconversion at Week 48

HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at Week 48. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at Week 48. (NCT00116805)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
HBsAg LossHBsAg Seroconversion
ADV-TDF00
TDF-TDF3.21.3

Percentage of Participants With Histological Response at Week 240

Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00116805)
Timeframe: Baseline; Week 240

,
Interventionpercentage of participants (Number)
YesNo
ADV-TDF89.610.4
TDF-TDF88.211.8

Percentage of Participants With Histological Response at Week 48

Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00116805)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
YesNo
ADV-TDF67.832.2
TDF-TDF74.425.6

Ranked Assessment of Necroinflammation and Fibrosis at Week 240

Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00116805)
Timeframe: Baseline; Week 240

,
Interventionpercentage of participants (Number)
Improvement - NecroinflammationNo Change - NecroinflammationWorsening - NecroinflammationImprovement - FibrosisNo Change - FibrosisWorsening - Fibrosis
ADV-TDF97.92.1058.339.62.1
TDF-TDF96.13.9056.639.53.9

Ranked Assessment of Necroinflammation and Fibrosis at Week 48

Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00116805)
Timeframe: Baseline; Week 48

,
Interventionpercentage of participants (Number)
Improvement - NecroinflammationNo Change - NecroinflammationWorsening - NecroinflammationMissing Data - NecroinflammationImprovement - FibrosisNo Change - FibrosisWorsening - FibrosisMissing Data - Fibrosis
ADV-TDF78.93.35.612.220.061.16.712.2
TDF-TDF81.34.53.410.819.963.65.111.4

Reviews

4 reviews available for 1-anilino-8-naphthalenesulfonate and Chronic Hepatitis B

ArticleYear
PNPLA3 rs738409 is not associated with the risk of hepatocellular carcinoma and persistent infection of hepatitis B virus (HBV) in HBV-related subjects: A case-control study and meta-analysis on Asians.
    Gene, 2020, Jun-05, Volume: 742

    Topics: Adult; Aged; Asian People; Carcinoma, Hepatocellular; Case-Control Studies; Female; Genetic Predispo

2020
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
New trends on obesity and NAFLD in Asia.
    Journal of hepatology, 2017, Volume: 67, Issue:4

    Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide

2017
Association of PNPLA3 rs738409 polymorphism with liver steatosis but not with cirrhosis in patients with HBV infection: Systematic review with meta-analysis.
    The journal of gene medicine, 2018, Volume: 20, Issue:1

    Topics: Fatty Liver; Hepatitis B virus; Hepatitis B, Chronic; Humans; Incidence; Lipase; Liver Cirrhosis; Me

2018
PNPLA3 I148M polymorphism and progressive liver disease.
    World journal of gastroenterology, 2013, Nov-07, Volume: 19, Issue:41

    Topics: Carcinoma, Hepatocellular; Cholangitis, Sclerosing; Disease Progression; Fatty Liver; Fatty Liver, A

2013

Trials

1 trial available for 1-anilino-8-naphthalenesulfonate and Chronic Hepatitis B

ArticleYear
Safety and efficacy of stopping tenofovir disoproxil fumarate in patients with chronic hepatitis B following at least 8 years of therapy: a prespecified follow-up analysis of two randomised trials.
    The lancet. Gastroenterology & hepatology, 2019, Volume: 4, Issue:4

    Topics: Adult; Alanine Transaminase; DNA, Viral; Female; Follow-Up Studies; Hepatitis B e Antigens; Hepatiti

2019
Safety and efficacy of stopping tenofovir disoproxil fumarate in patients with chronic hepatitis B following at least 8 years of therapy: a prespecified follow-up analysis of two randomised trials.
    The lancet. Gastroenterology & hepatology, 2019, Volume: 4, Issue:4

    Topics: Adult; Alanine Transaminase; DNA, Viral; Female; Follow-Up Studies; Hepatitis B e Antigens; Hepatiti

2019
Safety and efficacy of stopping tenofovir disoproxil fumarate in patients with chronic hepatitis B following at least 8 years of therapy: a prespecified follow-up analysis of two randomised trials.
    The lancet. Gastroenterology & hepatology, 2019, Volume: 4, Issue:4

    Topics: Adult; Alanine Transaminase; DNA, Viral; Female; Follow-Up Studies; Hepatitis B e Antigens; Hepatiti

2019
Safety and efficacy of stopping tenofovir disoproxil fumarate in patients with chronic hepatitis B following at least 8 years of therapy: a prespecified follow-up analysis of two randomised trials.
    The lancet. Gastroenterology & hepatology, 2019, Volume: 4, Issue:4

    Topics: Adult; Alanine Transaminase; DNA, Viral; Female; Follow-Up Studies; Hepatitis B e Antigens; Hepatiti

2019

Other Studies

12 other studies available for 1-anilino-8-naphthalenesulfonate and Chronic Hepatitis B

ArticleYear
Association between PNPLA3 gene polymorphisms and risk of hepatitis B virus-related hepatocellular carcinoma in Han population in China:a case-control study.
    Scandinavian journal of gastroenterology, 2017, Volume: 52, Issue:10

    Topics: Adult; Aged; Asian People; Carcinoma, Hepatocellular; Case-Control Studies; China; Female; Genetic P

2017
Independent and additive effects of PNPLA3 and TM6SF2 polymorphisms on the development of non-B, non-C hepatocellular carcinoma.
    Journal of gastroenterology, 2019, Volume: 54, Issue:5

    Topics: Acyltransferases; Aged; Alleles; Carcinoma, Hepatocellular; Case-Control Studies; Chondroitin Sulfat

2019
[Effects of PNPLA3, TM6SF2 gene polymorphisms and its interactions with smoking and alcohol drinking on hepatitis B virus-associated hepatocellular carcinoma].
    Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi, 2018, Dec-10, Volume: 39, Issue:12

    Topics: Alcohol Drinking; Carcinoma, Hepatocellular; Case-Control Studies; Epistasis, Genetic; Gene-Environm

2018
Patatin-like phospholipase domain-containing 3 I148M affects liver steatosis in patients with chronic hepatitis B.
    Hepatology (Baltimore, Md.), 2013, Volume: 58, Issue:4

    Topics: Adult; Alcoholism; Cohort Studies; Disease Progression; Fatty Liver; Female; Genetic Predisposition

2013
[Association between the PNPLA3 I148M polymorphism and chronic hepatitis B in a Qingdao Han Chinese population].
    Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology, 2014, Volume: 22, Issue:5

    Topics: Adult; Aged; Asian People; Case-Control Studies; China; Female; Gene Frequency; Genetic Predispositi

2014
The impact of PNPLA3 (rs738409 C>G) polymorphisms on liver histology and long-term clinical outcome in chronic hepatitis B patients.
    Liver international : official journal of the International Association for the Study of the Liver, 2015, Volume: 35, Issue:2

    Topics: Body Weight; Carcinoma, Hepatocellular; Fatty Liver; Female; Hepatitis B, Chronic; Humans; Iron; Lip

2015
Patatin-Like Phospholipase Domain-Containing 3 I148M Variant Is Associated with Liver Steatosis and Fat Distribution in Chronic Hepatitis B.
    Digestive diseases and sciences, 2015, Volume: 60, Issue:10

    Topics: Abdominal Fat; Adult; Aged; Anthropometry; Body Mass Index; Chi-Square Distribution; Cohort Studies;

2015
Linked PNPLA3 polymorphisms confer susceptibility to nonalcoholic steatohepatitis and decreased viral load in chronic hepatitis B.
    World journal of gastroenterology, 2015, Jul-28, Volume: 21, Issue:28

    Topics: Adult; Asian People; Biomarkers; Biopsy; Case-Control Studies; China; DNA, Viral; Female; Gene Frequ

2015
The impact of patatin-like phospholipase domain-containing protein 3 polymorphism on hepatocellular carcinoma prognosis.
    Journal of gastroenterology, 2013, Volume: 48, Issue:3

    Topics: Adult; Aged; Aged, 80 and over; Body Mass Index; Carcinoma, Hepatocellular; Female; Follow-Up Studie

2013
Pancreatic involvement in chronic viral hepatitis.
    World journal of gastroenterology, 2005, Jun-21, Volume: 11, Issue:23

    Topics: Adult; Aged; Amylases; Female; Hepatitis B, Chronic; Hepatitis C, Chronic; Humans; Lipase; Male; Mid

2005
Metabolic factors and risk of hepatocellular carcinoma by chronic hepatitis B/C infection: a follow-up study in Taiwan.
    Gastroenterology, 2008, Volume: 135, Issue:1

    Topics: Adult; Carbolines; Carcinoma, Hepatocellular; Diabetes Mellitus; Female; Follow-Up Studies; Hepatiti

2008
Serum pancreatic enzyme concentrations in chronic viral liver diseases.
    Digestive diseases and sciences, 1999, Volume: 44, Issue:2

    Topics: Adolescent; Adult; Aged; Amylases; Chronic Disease; Female; Hepatitis B, Chronic; Hepatitis C, Chron

1999