Delta Hepatitis and Liver Disease in Hemophiliacs
|First Received Date ICMJE||May 25, 2000|
|Last Updated Date||June 23, 2005|
|Start Date ICMJE||September 1986|
|Primary Completion Date||Not Provided|
|Current Primary Outcome Measures ICMJE||Not Provided|
|Original Primary Outcome Measures ICMJE||Not Provided|
|Change History||Complete list of historical versions of study NCT00005304 on ClinicalTrials.gov Archive Site|
|Current Secondary Outcome Measures ICMJE||Not Provided|
|Original Secondary Outcome Measures ICMJE||Not Provided|
|Current Other Outcome Measures ICMJE||Not Provided|
|Original Other Outcome Measures ICMJE||Not Provided|
|Brief Title ICMJE||Delta Hepatitis and Liver Disease in Hemophiliacs|
|Official Title ICMJE||Not Provided|
To determine the prevalence of hepatitis delta virus (HDV) in a large cohort of hemophiliacs and to elucidate the role of HDV in the development and progression of liver disease in this population.
Patients with classical hemophilia (hemophilia A) and Christmas disease (hemophilia B) were exposed to many hepatotropic viruses during the course of their therapy. Severe chronic hepatitis among these patients was most likely related to persistent infection with non-A,non-B hepatitis virus, hepatitis B virus, or delta hepatitis virus, a defective RNA virus which is dependent upon coinfection with HBV for essential helper functions. Carriers of HBV could contract an acute delta hepatitis infection that was invariably more severe than the illness caused by HBV alone. The morbidity and mortality of delta hepatitis infection was remarkably high. Transmission of the delta hepatitis agent appeared to follow the same routes of transmission as HBV. Direct parenteral inoculation was the classic mode of transmission of HBV which suggested a similar mode of transmission for delta hepatitis.
Hemophiliacs treated with commercial concentrates of coagulation factors prepared from pools of plasma were at great risk to contract delta hepatitis infection. About 50 percent of these patients had delta hepatitis virus antibodies. Also, studies of small cohorts indicated that hepatitis delta infection was a major cause of chronic liver disease and cirrhosis. Therefore, there was a critical need to evaluate the frequency and effect of hepatitis delta infection in hemophiliacs in order to obtain data on the natural history of chronic liver disease, comparing those with presumed chronic non-A,non-B hepatitis B alone, and combined chronic delta and HBV infections.
This grant was awarded in response to a Request for Applications issued in 1986 on the Prevalence and Consequences of Hepatitis Delta Infection in Hemophiliacs. The concept for the initiative originated in the Blood Resources Working Group of the Blood Diseases and Resources Advisory Committee and was approved by the National Heart, Lung, and Blood Advisory Council in February 1985.
Both a prevalence study and a longitudinal study were conducted at several centers. In the prevalence study, active hepatitis delta viral infection was established by non-invasive serologic techniques such as hepatitis delta virus RNA/cDNA probes to detect hepatitis delta virus RNA and an immunoblotting method to detect hepatitis delta antigen. These tests avoided the need for liver biopsies to verify infection. In the longitudinal study, patients were assigned to a core or auxiliary groups with those in the core group sampled every six months for biochemical evidence of liver disease and those in the auxiliary group once a year. Serogroups 0,3,5, and 6 and other participants with evidence of delta hepatitis infection were assigned to the core group. Those patients who were immune to hepatitis B virus but were anti-hepatitis delta virus positive were assigned two controls, matched by center, age, sex, and hemophilia diagnosis and severity, from serogroups 5 who were without evidence of hepatitis delta virus infection. Thus, the role of delta virus infection in liver disease in hepatitis delta virus immune patients was evaluated. Follow-up continued for four years.
|Study Type ICMJE||Observational|
|Study Design ICMJE||Observational Model: Natural History|
|Target Follow-Up Duration||Not Provided|
|Sampling Method||Not Provided|
|Study Population||Not Provided|
|Intervention ICMJE||Not Provided|
|Study Group/Cohort (s)||Not Provided|
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
|Recruitment Status ICMJE||Completed|
|Enrollment ICMJE||Not Provided|
|Completion Date||September 1991|
|Primary Completion Date||Not Provided|
|Eligibility Criteria ICMJE||
No eligibility criteria
|Accepts Healthy Volunteers||No|
|Contacts ICMJE||Contact information is only displayed when the study is recruiting subjects|
|Location Countries ICMJE||Not Provided|
|NCT Number ICMJE||NCT00005304|
|Other Study ID Numbers ICMJE||3005|
|Has Data Monitoring Committee||Not Provided|
|Responsible Party||Not Provided|
|Study Sponsor ICMJE||National Heart, Lung, and Blood Institute (NHLBI)|
|Collaborators ICMJE||Not Provided|
|Investigators ICMJE||Not Provided|
|Information Provided By||National Heart, Lung, and Blood Institute (NHLBI)|
|Verification Date||April 2000|
ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP