Over years or decades, people with chronic hepatitis C can develop advanced liver disease including cirrhosis and liver cancer. Cirrhosis is characterized by blockage of the flow of blood through the heavily scarred liver, leading to symptoms such as bleeding varicose veins in the stomach and esophagus, abdominal fluid accumulation, and cognitive impairment due to hepatic encephalopathy.
A new study adds to the evidence showing that sustained response to interferon-based antiviral therapy can improve liver health and prevent development or worsening of cirrhosis and its associated conditions, in this case esophageal varices. None of the 34 participants (out of an initial group of more than 200) who were treated for hepatitis C and achieved SVR developed new varices, compared with 32% of untreated patients and 39% of those who underwent treatment but did not achieve sustained response.
Esophageal varices are enlarged veins in the lower esophagus.
They're often due to obstructed blood flow through the portal vein,
which carries blood from the intestine and spleen to the liver.
The following is the text of a media advisory from Wiley-Blackwell, publisher of Hepatology, describing the study and it's findings.
Antiviral Therapy Impacts Esophageal Varices in HCV-Induced Cirrhosis
Study Shows Sustained Virologic Response Prevents EV
Italian researchers have discovered that antiviral treatment and sustained virologic response (SVR) prevents esophageal varices in patients with compensated hepatitis C (HCV)-induced cirrhosis, indicating that endoscopic surveillance can be safely delayed or avoided in these patients. Full findings are published in the June issue of Hepatology, a journal of the American Association for the Study of Liver Diseases (AASLD).
According to the National Digestive Diseases Information Clearinghouse (NDDIC), an estimated 4.1 million Americans have antibody to HCV (anti-HCV), indicating ongoing or previous infection with the virus. Researchers estimate that at least 20% of patients with chronic HCV develop cirrhosis. Progression of cirrhosis leads to portal hypertension, which can result in esophageal varices (EV) and other complications.
EVs are abnormally enlarged veins in the esophagus that occur when portal hypertension obstructs normal blood flow to the liver, causing blood to back up into the esophageal vessels. Esophageal varices can rupture which can be life-threatening. The onset of EV marks a crucial turning point in the outcome of cirrhosis. The research team led by Savino Burno, MD, set out to determine whether antiviral treatment resulting in SVR could prevent this condition.
The study, spanning from January 1989 to December 1992, evaluated 218 patients less than 70 years of age with compensated Child-Pugh class A cirrhosis who presented at three referral centers in Milan and tested positive for serum anti-HCV. Only subjects who agreed to undergo upper endoscopy at the time of enrolment and who were found to be EV-free were included. All 218 subjects had regular follow up with surveillance ultrasound for hepatocellular carcinoma (HCC) every six months and endoscopy every three years to identify de novo varices.
The standard antiviral regimens of recombinant alpha IFN monotherapy or combination with both IFN and ribavirin were administered, regardless HCV genotype, for at least six months and for an additional six-month period in patients who achieved a complete biochemical response. Combination therapy with IFN or pegylated IFN and ribavirin was administered in agreement with guidelines. SVR was defined as undetectable serum HCV RNA (< 50 IU/mL) six months after stopping therapy.
The primary endpoints were development of de novo varies or HCC. Of the 218 patients, 149 (68%) received HCV therapy and 34 (23%) achieved SVR and no EVs. During the follow-up of median 11.4 years, de novo EVs were detected equally among untreated and treated patients who did not achieve SVR. Sixty-seven patients, 7 of whom achieved SVR, developed HCC.
"Our study provides an accurate estimate of the 10-year cumulative incidence of EV in this population of patients," stated Dr. Bruno. "A major finding of our study, of great importance in clinical practice, is that the achievement of SVR abolishes the development of EV in the long-term. The reliability of our result is guaranteed by the ample length of observation among this group of patients. In routine clinical practice, serial surveillance by EGD can be safely delayed or avoided in SVR patients, sparing a significant amount of useless invasive and costly procedures."
The Milan study is the largest study with the longest follow-up to date that addresses the impact of SVR on the development of esophageal varices. In his editorial also published in Hepatology this month, Dr. Richard Sterling concurs, "If these results are confirmed, it may not be necessary to subject patients with HCV-induced cirrhosis to the expense and risks of repeated endoscopies." He further points out that the current study is the first to demonstrate a pharmacologic treatment to reduce (or in this case, eliminate) the development of varices. However, Dr. Sterling cautions, "Before we get too excited, we must remember that current treatment to achieve SVR in those with cirrhosis is difficult and there are often increased side effects, more cytopenias, and lower response rates than those without cirrhosis. Therefore, given the cost, both in dollars and resources, the increased side effects, and decreased response rates of HCV therapy, it remains to be determined if the "bang is worth the buck" in this select group of patients."
Investigator affiliations: Department of Internal Medicine, A.O. Fatebenefratelli e Oftalmico, Milan, Italy; Department of Internal Medicine, A.O. S. Paolo, Italy; A.O. Sondrio, Italy; Endoscopy Unit, A.O. S. Gerardo, Monza, Italy; Gastroenterology and Gastrointestinal Endoscopy Unit, Ospedale Policlinico, Milan, Italy; Department of Medical Sciences, University of Milan, Milan, Italy; Gastroenterology and Hepatology Unit, University of Palermo, Palermo, Italy; Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy.
7/6/10
References
S Bruno, A Crosignani, C Facciotto, and others. Sustained virologic response prevents the development of esophageal varices in compensated, Child-Pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study. Hepatology 51(6): 2069-2076 (Abstract). June 2010.
RK Sterling. Long-term effects of sustained virologic response on the development of esophageal varices in compensated cirrhosis: "is the bang worth the buck?" Hepatology 51(6): 1891-1893. June 2010.
Other Source
Wiley-Blackwell. Antiviral Therapy Impacts Esophageal Varices in HCV-Induced Cirrhosis. Press release. May 25, 2010.
Source
No comments:
Post a Comment