<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT02982837</url>
  </required_header>
  <id_info>
    <org_study_id>PDU15001</org_study_id>
    <nct_id>NCT02982837</nct_id>
  </id_info>
  <brief_title>To Study the Effect of Adding on Pegylated Interferon (PEG-INF) Therapy for Patients Diagnosed With Chronic Hepatitis B</brief_title>
  <acronym>RC14/055</acronym>
  <official_title>Randomized, Multicenter, Open -Label Clinical Trial to Study the Effect of Adding on Pegylated Interferon Therapy for Patients Diagnosed With Chronic Hepatitis B Showing Maintained Response While Receiving Ongoing Nucleotide Analogues</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>King Abdullah International Medical Research Center</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
    <collaborator>
      <agency>Hoffmann-La Roche</agency>
      <agency_class>Industry</agency_class>
    </collaborator>
  </sponsors>
  <source>King Abdullah International Medical Research Center</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      To assess whether PEG-INF (Peglyated - interferon) Add-on therapy in patients of CHB who have&#xD;
      achieved a maintained viral suppression (HBV DNA PCR( polymerase chain reaction) &lt;200 for&#xD;
      last 3-6 month) with NA's can result in increased rate of HBV infection eradication (HbsAg is&#xD;
      undetectable by serological blood testing with or without seroconversion to HBs antibody).&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Hepatitis B virus (HBV) infection remains a global health care problem with more than one&#xD;
      third of world's population having serological evidence of been exposed to the virus and&#xD;
      about 5% of global population ( 350-400 million) being chronically infected. About 15-40% of&#xD;
      Patients with chronic hepatitis B (CHB) infection develop complications of liver cirrhosis,&#xD;
      liver failure and hepatocellular carcinoma(HCC) in their life time , resulting in an&#xD;
      estimated of 500,000 to 1.2 million deaths each year. In Saudi Arabia, chronic hepatitis B&#xD;
      remains a serious medical problem, despite the implementation of mandatory HBV vaccination of&#xD;
      children since 1989. According to a recent study conducted in Saudi hospital, HBV accounts&#xD;
      for 49% of the hepatitis cases . Persistent viral replication is associated with disease&#xD;
      progression to liver fibrosis, cirrhosis and development of HCC. Currently two classes of&#xD;
      drugs are available for treatment of CHB namely immunomodulatory therapy (conventional &amp;&#xD;
      pegylated interferon (Pegasys) PEG-IFN) and nucleoside/nucleotide analogues(NA).&#xD;
      Interferon(IFN)-α with its dual immunomodulatory and antiviral effects was the first drug&#xD;
      (recombinant standard IFN- α) licensed for Chronic hepatitis B treatment in the 1990's&#xD;
      followed by introduction of nucleos(t)ide analogues(NA) in 1998 that directly inhibit HBV&#xD;
      polymerase and provide an effective on treatment maintained viral suppression . With the&#xD;
      introduction of pegylated interferon- α (PEG-IFN) in 2005 that allows a convenient once a&#xD;
      week dosing interval and of equal or superior treatment efficacy than conventional (IFN), the&#xD;
      interferon based therapy has markedly improved its utility. Due to its predominant&#xD;
      immunomodulatory effect peginterferon (PEG-IFN) offers the advantage of higher sustained off&#xD;
      treatment response rate compared to NA thus allowing a finite duration of treatment. The NA&#xD;
      act by directly inhibiting HBV polymerase resulting in effective on treatment maintained&#xD;
      viral suppression (HBV DNA PCR &lt;200 for last 3-6 month)). However, long term NA therapy has&#xD;
      the problems of emergence of viral resistance, long -term safety, cost and patient&#xD;
      compliance.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Recruiting</last_known_status>
  <start_date type="Actual">March 2015</start_date>
  <completion_date type="Anticipated">May 2019</completion_date>
  <primary_completion_date type="Anticipated">March 2019</primary_completion_date>
  <phase>Phase 4</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>Randomized</allocation>
    <intervention_model>Parallel Assignment</intervention_model>
    <primary_purpose>Treatment</primary_purpose>
    <masking>None (Open Label)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>The loss of HbsAg between groups (NA) group and NA +Peg_INF group assessed by HbsAg test</measure>
    <time_frame>48 weeks</time_frame>
    <description>The loss of HbsAg between groups (NA) group and NA +Peg_INF group assessed by HbsAg test</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>The seroconversion to HBs antibody between groups (NA) group and NA +Peg_INF group assessed by Hbe Ab test</measure>
    <time_frame>6 ,12 months &amp; 48 weeks</time_frame>
    <description>The seroconversion to HBs antibody between groups (NA) group and NA +Peg_INF group assessed by Hbe Ab test</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>The HBeAg (Hepatitis B e-Antigen) loss in CHRONIC HBV eAg positive patient between groups (NA) group and NA +Peg_INF group assessed by HbeAg test</measure>
    <time_frame>6,12 months &amp; 48 weeks</time_frame>
    <description>HBeAg loss in CHRONIC HBV eAg positive patient between groups (NA) group and NA +Peg_INF group assessed by HbeAg test</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>The conversion of HBeAg to HBe-antibody in CHRONIC HBV eAg (eAntigen) positive patient between groups (NA) group and NA +Peg_INF group assessed by HBe-antibody test</measure>
    <time_frame>6,12 months &amp; 48 weeks</time_frame>
    <description>The conversion of HBeAg to HBe-antibody in CHRONIC HBV eAg positive patient between groups (NA) group and NA +Peg_INF group assessed by HBe-antibody test</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>The correlation between HBsAg ( Hepatitis B Surface Antigen) levels while on therapy at the a defined interval ie 8,12.24,36,48 weeks and rate of HBsAg loss at end of therapy assessed by measuring HBV s Ag during the period 8,12.24,36 and 48 weeks</measure>
    <time_frame>8,12,24 and 48 weeks</time_frame>
    <description>The correlation between HBsAg levels while on therapy at the a defined interval ie 8,12.24,36,48 weeks and rate of HBsAg loss at end of therapy assessed by measuring HBV s Ag during that period 8,12.24,36 and 48 weeks</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>The relationship between HBV genotype and HBsAg loss at the end of the study assessed by measuring HBV genotype only at base line and see if any particular genotype have more HBV sAg loss at the end of the study</measure>
    <time_frame>At base line &amp; 48 weeks</time_frame>
    <description>The relationship between HBV genotype and HBsAg loss at the end of the study assessed by measuring HBV genotype only at base line and see if any particular genotype have more HBV sAg loss at the end of the study</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>The relationship between IL28B (Interleukin 28B) genotypes ( polymorphism) and HBsAg loss with or without seroconversion to HBs antibody</measure>
    <time_frame>At base line &amp; 48 weeks</time_frame>
    <description>The relationship between IL28B genotypes ( polymorphism) and HBsAg loss with or without seroconversion to HBs antibody assess by doing IL28B genotypes ( polymorphism) once during the study and see if any specific IL28B genotypes ( polymorphism) associated more with HBV sAg loss at the end of the study with or without seroconversion to HBs antibody).</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>The relationship between vitamin D deficiency and (HbsAg loss with or without seroconversion to HBs antibody) assess by measuring Vitamin D level at base line And correlate the baseline level of Vitamin with HBV sAg loss at the end of the study</measure>
    <time_frame>At base line &amp; 48 weeks</time_frame>
    <description>The relationship between vitamin D deficiency and (HbsAg loss with or without seroconversion to HBs antibody) assess by measuring vitamin D level at base line And correlate the base line level of vitamin D with HBV sAg loss at the end of the study</description>
  </secondary_outcome>
  <number_of_arms>2</number_of_arms>
  <enrollment type="Anticipated">214</enrollment>
  <condition>Hepatitis B</condition>
  <arm_group>
    <arm_group_label>PEG-IFN &amp; NUCLEOTIDE ANALOGUES</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>Peginterferon alfa-2a 180 Mcg infusion per week with ongoing NUCLEOTIDE ANALOGUES for 48 weeks.</description>
  </arm_group>
  <arm_group>
    <arm_group_label>NUCLEOTIDE ANALOGUES</arm_group_label>
    <arm_group_type>Active Comparator</arm_group_type>
    <description>Nucleoside same dose as they started the study.</description>
  </arm_group>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>PEG-IFN &amp; Nucleos(t)tide analogues</intervention_name>
    <description>Subjects who will be randomized to receive 180 Mcg/ week as an add-on Pegylated Interferon therapy α-2 A with their ongoing NUCLEOTIDE analogues for 48 weeks.</description>
    <arm_group_label>PEG-IFN &amp; NUCLEOTIDE ANALOGUES</arm_group_label>
    <other_name>Immunomodulatory therapy</other_name>
  </intervention>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Nucleos(t)tide analogues</intervention_name>
    <description>Subjects will continue on the same dose of Nucleoside/nucleotide analogues as they started the study.</description>
    <arm_group_label>NUCLEOTIDE ANALOGUES</arm_group_label>
    <arm_group_label>PEG-IFN &amp; NUCLEOTIDE ANALOGUES</arm_group_label>
    <other_name>Nucleoside/nucleotide analogues</other_name>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Adults ≥18 &amp; &lt; 70 years of both genders.&#xD;
&#xD;
          -  CHB on NA's in maintained viral suppression (HBV DNA PCR &lt;200 for last 3-6 month)&#xD;
&#xD;
          -  Patients with measurable HBsAg quantitative levels&#xD;
&#xD;
          -  Patients with any HBV genotypes.&#xD;
&#xD;
          -  Patients with either CHB e Ag positive or eAg negative&#xD;
&#xD;
          -  Patients who sign an informed consent for inclusion into the study.&#xD;
&#xD;
          -  Patients with hepatitis Delta co-infection.&#xD;
&#xD;
          -  only patients with a negative pregnancy test who are of child bearing potential and&#xD;
             agree to utilize a strict birth control method will be enrolled&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Patients with following characteristics will not be considered for the trial:&#xD;
&#xD;
          -  Decompensated liver Cirrhosis&#xD;
&#xD;
          -  HCV (hepatitis C virus) or HIV co infection.&#xD;
&#xD;
          -  Autoimmune disorders like SLE (Systemic lupus erythematosus), RA (Rheumatoid Arthritis&#xD;
             ), AIH (Autoimmune Hemolytic Anemia), ITP (Immune thrombocytopenic purpura), psoriasis&#xD;
             etc.&#xD;
&#xD;
          -  Untreated psychiatric conditions like depression and alcohol or drug abuse.&#xD;
&#xD;
          -  Comorbid conditions like chronic renal failure or post renal/liver transplantation on&#xD;
             immunosuppressive therapy.&#xD;
&#xD;
          -  Complicated diabetes mellitus and advanced heart failure.&#xD;
&#xD;
          -  Pregnancy or not willing to practice contraception.&#xD;
&#xD;
          -  Known allergy to Interferons.&#xD;
&#xD;
          -  Concomitant treatment with Telbivudine&#xD;
&#xD;
          -  Evidence of portal hypertension by Biochemical (Low Platelets less than 100), imaging&#xD;
             or UGI (upper gastrointestinal)endoscopy&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>70 Years</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Abduljaleel Alalwan, MD</last_name>
    <role>Principal Investigator</role>
    <affiliation>National Guards Health Affairs-Riyadh</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Abduljaleel Alalwan, MD</last_name>
    <phone>801 111</phone>
    <phone_ext>11622</phone_ext>
    <email>alwana@ngha.med.sa</email>
  </overall_contact>
  <overall_contact_backup>
    <last_name>Ansif Majeed, MBA</last_name>
    <phone>(011)429-9999</phone>
    <phone_ext>94436</phone_ext>
    <email>pallathmajeedan@ngha.med.sa</email>
  </overall_contact_backup>
  <location>
    <facility>
      <name>King Abdulaziz Medical City</name>
      <address>
        <city>Jeddah</city>
        <zip>22384</zip>
        <country>Saudi Arabia</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Faisal Sanai, MD</last_name>
      <phone>+966 12 2266666</phone>
      <phone_ext>24828</phone_ext>
      <email>sanaifa@ngha.med.sa</email>
    </contact>
  </location>
  <location>
    <facility>
      <name>King Abdulaziz Hospital</name>
      <address>
        <city>Jeddah</city>
        <zip>31982</zip>
        <country>Saudi Arabia</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Elsadig Ahmed Nour Mohamed, MD</last_name>
      <email>mohamedel1@ngha.med.sa</email>
    </contact>
  </location>
  <location>
    <facility>
      <name>King Abdulaziz Medical City</name>
      <address>
        <city>Riyadh</city>
        <zip>11426</zip>
        <country>Saudi Arabia</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Abduljaleel Alwan, MD</last_name>
      <phone>801 111</phone>
      <phone_ext>11622</phone_ext>
      <email>alwana@ngha.med.sa</email>
    </contact>
    <contact_backup>
      <last_name>Ansif Majeed, MBA</last_name>
      <phone>(011)429-9999</phone>
      <phone_ext>94436</phone_ext>
      <email>pallathmajeedan@ngha.med.sa</email>
    </contact_backup>
  </location>
  <location_countries>
    <country>Saudi Arabia</country>
  </location_countries>
  <reference>
    <citation>Goldstein ST, Zhou F, Hadler SC, Bell BP, Mast EE, Margolis HS. A mathematical model to estimate global hepatitis B disease burden and vaccination impact. Int J Epidemiol. 2005 Dec;34(6):1329-39. doi: 10.1093/ije/dyi206. Epub 2005 Oct 25.</citation>
    <PMID>16249217</PMID>
  </reference>
  <reference>
    <citation>Beasley RP. Hepatitis B virus. The major etiology of hepatocellular carcinoma. Cancer. 1988 May 15;61(10):1942-56. doi: 10.1002/1097-0142(19880515)61:103.0.co;2-j. No abstract available.</citation>
    <PMID>2834034</PMID>
  </reference>
  <reference>
    <citation>Bosch FX, Ribes J, Cleries R, Diaz M. Epidemiology of hepatocellular carcinoma. Clin Liver Dis. 2005 May;9(2):191-211, v. doi: 10.1016/j.cld.2004.12.009.</citation>
    <PMID>15831268</PMID>
  </reference>
  <reference>
    <citation>Liaw YF, Chu CM. Hepatitis B virus infection. Lancet. 2009 Feb 14;373(9663):582-92. doi: 10.1016/S0140-6736(09)60207-5.</citation>
    <PMID>19217993</PMID>
  </reference>
  <reference>
    <citation>Al-Tawfiq JA, Anani A. Profile of viral hepatitis A, B, and C in a Saudi Arabian hospital. Med Sci Monit. 2008 Jan;14(1):CR52-56.</citation>
    <PMID>18160946</PMID>
  </reference>
  <reference>
    <citation>Memish ZA, Knawy BA, El-Saed A. Incidence trends of viral hepatitis A, B, and C seropositivity over eight years of surveillance in Saudi Arabia. Int J Infect Dis. 2010 Feb;14(2):e115-20. doi: 10.1016/j.ijid.2009.03.027. Epub 2009 Jun 21.</citation>
    <PMID>19540786</PMID>
  </reference>
  <reference>
    <citation>Chen CJ, Yang HI, Su J, Jen CL, You SL, Lu SN, Huang GT, Iloeje UH; REVEAL-HBV Study Group. Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level. JAMA. 2006 Jan 4;295(1):65-73. doi: 10.1001/jama.295.1.65.</citation>
    <PMID>16391218</PMID>
  </reference>
  <reference>
    <citation>Chan HL, Tse CH, Mo F, Koh J, Wong VW, Wong GL, Lam Chan S, Yeo W, Sung JJ, Mok TS. High viral load and hepatitis B virus subgenotype ce are associated with increased risk of hepatocellular carcinoma. J Clin Oncol. 2008 Jan 10;26(2):177-82. doi: 10.1200/JCO.2007.13.2043.</citation>
    <PMID>18182659</PMID>
  </reference>
  <reference>
    <citation>Zoulim F, Locarnini S. Hepatitis B virus resistance to nucleos(t)ide analogues. Gastroenterology. 2009 Nov;137(5):1593-608.e1-2. doi: 10.1053/j.gastro.2009.08.063. Epub 2009 Sep 6.</citation>
    <PMID>19737565</PMID>
  </reference>
  <reference>
    <citation>Cooksley WG, Piratvisuth T, Lee SD, Mahachai V, Chao YC, Tanwandee T, Chutaputti A, Chang WY, Zahm FE, Pluck N. Peginterferon alpha-2a (40 kDa): an advance in the treatment of hepatitis B e antigen-positive chronic hepatitis B. J Viral Hepat. 2003 Jul;10(4):298-305. doi: 10.1046/j.1365-2893.2003.00450.x.</citation>
    <PMID>12823597</PMID>
  </reference>
  <reference>
    <citation>Lok AS, McMahon BJ. Chronic hepatitis B. Hepatology. 2007 Feb;45(2):507-39. doi: 10.1002/hep.21513. No abstract available. Erratum In: Hepatology. 2007 Jun;45(6):1347.</citation>
    <PMID>17256718</PMID>
  </reference>
  <reference>
    <citation>Liaw YF, Leung N, Kao JH, Piratvisuth T, Gane E, Han KH, Guan R, Lau GK, Locarnini S; Chronic Hepatitis B Guideline Working Party of the Asian-Pacific Association for the Study of the Liver. Asian-Pacific consensus statement on the management of chronic hepatitis B: a 2008 update. Hepatol Int. 2008 Sep;2(3):263-83. doi: 10.1007/s12072-008-9080-3. Epub 2008 May 10. Erratum In: Hepatol Int. 2008 Sep;2(3):395-6.</citation>
    <PMID>19669255</PMID>
  </reference>
  <reference>
    <citation>Lee A. Prevention of Helicobacter pylori infection. Scand J Gastroenterol Suppl. 1996;215:11-5.</citation>
    <PMID>8722377</PMID>
  </reference>
  <verification_date>January 2018</verification_date>
  <study_first_submitted>August 7, 2016</study_first_submitted>
  <study_first_submitted_qc>December 1, 2016</study_first_submitted_qc>
  <study_first_posted type="Estimate">December 6, 2016</study_first_posted>
  <last_update_submitted>March 8, 2018</last_update_submitted>
  <last_update_submitted_qc>March 8, 2018</last_update_submitted_qc>
  <last_update_posted type="Actual">March 9, 2018</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Hepatitis A</mesh_term>
    <mesh_term>Hepatitis B</mesh_term>
    <mesh_term>Hepatitis B, Chronic</mesh_term>
    <mesh_term>Hepatitis</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT02982837
org study id: PDU15001
nct id: NCT02982837
lead sponsor: 
collaborator: 
has dmc: No
To assess whether PEG-INF (Peglyated - interferon) Add-on therapy in patients of CHB who have
      achieved a maintained viral suppression (HBV DNA PCR( polymerase chain reaction) <200 for
      last 3-6 month) with NA's can result in increased rate of HBV infection eradication (HbsAg is
      undetectable by serological blood testing with or without seroconversion to HBs antibody).
Hepatitis B virus (HBV) infection remains a global health care problem with more than one
      third of world's population having serological evidence of been exposed to the virus and
      about 5% of global population ( 350-400 million) being chronically infected. About 15-40% of
      Patients with chronic hepatitis B (CHB) infection develop complications of liver cirrhosis,
      liver failure and hepatocellular carcinoma(HCC) in their life time , resulting in an
      estimated of 500,000 to 1.2 million deaths each year. In Saudi Arabia, chronic hepatitis B
      remains a serious medical problem, despite the implementation of mandatory HBV vaccination of
      children since 1989. According to a recent study conducted in Saudi hospital, HBV accounts
      for 49% of the hepatitis cases . Persistent viral replication is associated with disease
      progression to liver fibrosis, cirrhosis and development of HCC. Currently two classes of
      drugs are available for treatment of CHB namely immunomodulatory therapy (conventional &
      pegylated interferon (Pegasys) PEG-IFN) and nucleoside/nucleotide analogues(NA).
      Interferon(IFN)-α with its dual immunomodulatory and antiviral effects was the first drug
      (recombinant standard IFN- α) licensed for Chronic hepatitis B treatment in the 1990's
      followed by introduction of nucleos(t)ide analogues(NA) in 1998 that directly inhibit HBV
      polymerase and provide an effective on treatment maintained viral suppression . With the
      introduction of pegylated interferon- α (PEG-IFN) in 2005 that allows a convenient once a
      week dosing interval and of equal or superior treatment efficacy than conventional (IFN), the
      interferon based therapy has markedly improved its utility. Due to its predominant
      immunomodulatory effect peginterferon (PEG-IFN) offers the advantage of higher sustained off
      treatment response rate compared to NA thus allowing a finite duration of treatment. The NA
      act by directly inhibiting HBV polymerase resulting in effective on treatment maintained
      viral suppression (HBV DNA PCR <200 for last 3-6 month)). However, long term NA therapy has
      the problems of emergence of viral resistance, long -term safety, cost and patient
      compliance.
allocation: Randomized
intervention model: Parallel Assignment
primary purpose: Treatment
masking: None (Open Label)
measure: The loss of HbsAg between groups (NA) group and NA +Peg_INF group assessed by HbsAg test
time frame: 48 weeks
description: The loss of HbsAg between groups (NA) group and NA +Peg_INF group assessed by HbsAg test
measure: The seroconversion to HBs antibody between groups (NA) group and NA +Peg_INF group assessed by Hbe Ab test
time frame: 6 ,12 months & 48 weeks
description: The seroconversion to HBs antibody between groups (NA) group and NA +Peg_INF group assessed by Hbe Ab test
measure: The HBeAg (Hepatitis B e-Antigen) loss in CHRONIC HBV eAg positive patient between groups (NA) group and NA +Peg_INF group assessed by HbeAg test
time frame: 6,12 months & 48 weeks
description: HBeAg loss in CHRONIC HBV eAg positive patient between groups (NA) group and NA +Peg_INF group assessed by HbeAg test
measure: The conversion of HBeAg to HBe-antibody in CHRONIC HBV eAg (eAntigen) positive patient between groups (NA) group and NA +Peg_INF group assessed by HBe-antibody test
time frame: 6,12 months & 48 weeks
description: The conversion of HBeAg to HBe-antibody in CHRONIC HBV eAg positive patient between groups (NA) group and NA +Peg_INF group assessed by HBe-antibody test
measure: The correlation between HBsAg ( Hepatitis B Surface Antigen) levels while on therapy at the a defined interval ie 8,12.24,36,48 weeks and rate of HBsAg loss at end of therapy assessed by measuring HBV s Ag during the period 8,12.24,36 and 48 weeks
time frame: 8,12,24 and 48 weeks
description: The correlation between HBsAg levels while on therapy at the a defined interval ie 8,12.24,36,48 weeks and rate of HBsAg loss at end of therapy assessed by measuring HBV s Ag during that period 8,12.24,36 and 48 weeks
measure: The relationship between HBV genotype and HBsAg loss at the end of the study assessed by measuring HBV genotype only at base line and see if any particular genotype have more HBV sAg loss at the end of the study
time frame: At base line & 48 weeks
description: The relationship between HBV genotype and HBsAg loss at the end of the study assessed by measuring HBV genotype only at base line and see if any particular genotype have more HBV sAg loss at the end of the study
measure: The relationship between IL28B (Interleukin 28B) genotypes ( polymorphism) and HBsAg loss with or without seroconversion to HBs antibody
time frame: At base line & 48 weeks
description: The relationship between IL28B genotypes ( polymorphism) and HBsAg loss with or without seroconversion to HBs antibody assess by doing IL28B genotypes ( polymorphism) once during the study and see if any specific IL28B genotypes ( polymorphism) associated more with HBV sAg loss at the end of the study with or without seroconversion to HBs antibody).
measure: The relationship between vitamin D deficiency and (HbsAg loss with or without seroconversion to HBs antibody) assess by measuring Vitamin D level at base line And correlate the baseline level of Vitamin with HBV sAg loss at the end of the study
time frame: At base line & 48 weeks
description: The relationship between vitamin D deficiency and (HbsAg loss with or without seroconversion to HBs antibody) assess by measuring vitamin D level at base line And correlate the base line level of vitamin D with HBV sAg loss at the end of the study
arm group label: PEG-IFN & NUCLEOTIDE ANALOGUES
arm group type: Experimental
description: Peginterferon alfa-2a 180 Mcg infusion per week with ongoing NUCLEOTIDE ANALOGUES for 48 weeks.
arm group label: NUCLEOTIDE ANALOGUES
arm group type: Active Comparator
description: Nucleoside same dose as they started the study.
intervention type: Drug
intervention name: PEG-IFN & Nucleos(t)tide analogues
description: Subjects who will be randomized to receive 180 Mcg/ week as an add-on Pegylated Interferon therapy α-2 A with their ongoing NUCLEOTIDE analogues for 48 weeks.
arm group label: PEG-IFN & NUCLEOTIDE ANALOGUES
other name: Immunomodulatory therapy
intervention type: Drug
intervention name: Nucleos(t)tide analogues
description: Subjects will continue on the same dose of Nucleoside/nucleotide analogues as they started the study.
arm group label: NUCLEOTIDE ANALOGUES
arm group label: PEG-IFN & NUCLEOTIDE ANALOGUES
other name: Nucleoside/nucleotide analogues
criteria: 
gender: All
minimum age: 18 Years
maximum age: 70 Years
healthy volunteers: No
last name: Abduljaleel Alalwan, MD
role: Principal Investigator
affiliation: National Guards Health Affairs-Riyadh
last name: Abduljaleel Alalwan, MD
phone: 801 111
phone ext: 11622
email: alwana@ngha.med.sa
last name: Ansif Majeed, MBA
phone: (011)429-9999
phone ext: 94436
email: pallathmajeedan@ngha.med.sa
facility: 
status: Recruiting
contact: 
facility: 
status: Recruiting
contact: 
facility: 
status: Recruiting
contact: 
contact backup: 
country: Saudi Arabia
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PMID: 18160946
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PMID: 19540786
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PMID: 16391218
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PMID: 18182659
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PMID: 19737565
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PMID: 12823597
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PMID: 17256718
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PMID: 19669255
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PMID: 8722377
responsible party type: Sponsor
mesh term: Hepatitis A
mesh term: Hepatitis B
mesh term: Hepatitis B, Chronic
mesh term: Hepatitis
sharing ipd: No