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News Review

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HEPATITIS JOURNAL REVIEW:
A Bi-Monthly Publication of the Hepatitis Support Project

February 28, 2006
Volume 3, Issue 4


Liz Highleyman

To download pdf version click here


In This Issue: Hepatitis C


Spontaneous HCV Clearance

Racial and Ethnic Differences in Hepatitis C

Steatosis and Metabolic Disorders

Retinal Damage as a Side Effect of Interferon


Spontaneous HCV Clearance

In the January 2006 Journal of Viral Hepatitis, Joanne Micallef and colleagues reported results of a systematic review of longitudinal studies looking at spontaneous (without treatment) viral clearance following acute HCV infection. They extracted data on patient populations and factors associated with viral clearance from 31 studies in the medical literature that followed a total of 675 participants for at least six months after acute infection. In the various studies, the spontaneous viral clearance rates ranged from zero to 0.8, with a mean of 0.26. Factors associated with viral clearance were female sex and acute clinical (symptomatic) hepatitis C. This agrees with past research showing that people who experience symptoms at the time of HCV infection are more likely to clear the virus, perhaps due to a more vigorous immune response. The authors concluded that, “[f]urther studies are required to more clearly define predictors of clearance and guide therapeutic intervention strategies.”

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Racial and Ethnic Differences in Hepatitis C

Two recent journal articles explored racial and ethnic differences in the natural history of chronic hepatitis C. In the January 2006 issue of Clinical Infectious Diseases, Brian Pearlman from Emory University discussed HCV infection in African Americans. According to the article, hepatitis C is more prevalent among African Americans than any other racial group in the United States; while they make up 12% of the population, African Americans account for about 22% of U.S. cases of chronic HCV infection. Compared with whites, they have a lower rate of spontaneous viral clearance. For reasons that are not well-understood, African Americans also respond less well to interferon-based therapy than whites – 19% vs 52% sustained virological response (SVR) in one study; 26% vs 39% in another – a fact not fully explained by the higher prevalence of difficult-to-treat genotype 1 HCV. While some data suggest that African Americans have a lower rate of fibrosis progression compared with whites, they are significantly more likely to develop hepatocellular carcinoma once they progress to cirrhosis. Pearlman reviewed some possible mechanisms underlying this disparate natural history, but for now there remain more questions than answers. Results from the VIRAHEP-C study comparing HCV treatment in African Americans and whites, which are expected later this year, will hopefully shed more light in the issue.

In the February 2006 Journal of Viral Hepatitis, Rita Lepe and colleagues looked at ethnic differences in the presentation of chronic hepatitis C in Hispanics/Latinos, who make up 13% of the U.S. population. They conducted a retrospective analysis of data from 1,225 hepatitis C patients – 227 Hispanics, 490 African Americans, and 508 whites – seen at the University of Illinois outpatient hepatology clinic in Chicago. Hispanics had higher liver enzyme (ALT, AST, and alkaline phosphatase) levels and more portal inflammation in liver biopsy specimens than whites or African Americans. Hispanics were also more likely to develop cirrhosis compared with African Americans. Interestingly, given that hepatitis C is usually more aggressive in men, this study found that Hispanic women were more likely to develop cirrhosis than Hispanic men (56% vs 45%); in contrast, cirrhosis rates were higher in white men than white women (47% vs 37%), and similar in African American men and women (25% vs 27%). The authors suggested that the high frequency of cirrhosis in Hispanics “could be related to a cofactor such as nonalcoholic fatty liver disease (NAFLD), particularly in Hispanic women,” given that conditions associated with NAFLD, such as diabetes, are common among U.S. Hispanics.

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Steatosis and Metabolic Disorders

Increased attention has recently focused on steatosis (fatty liver) and associated metabolic disorders – including insulin resistance and diabetes – as contributing factors for liver disease progression in people with and without hepatitis C.

In the February 2006 Journal of Viral Hepatitis, Amedeo Lonardo and colleagues from Italy offered a reappraisal of the link between steatosis and HCV. They noted that steatosis is more often associated with hepatitis C than with other types of chronic liver disease, affecting more than half of HCV patients. Fatty liver is especially prevalent – about 75% — and more severe among people with genotype 3 HCV. Steatosis is associated with fibrosis progression, poorer response to interferon-based therapy, and development of hepatocellular carcinoma. The authors concluded that “metabolic approaches” should be evaluated in addition to antiviral therapy for HCV patients with steatosis. Underlining this theme, Calogero Camma and colleagues reported in the January 2006 issue of Hepatology that insulin resistance is a risk factor for moderate to severe steatosis in individuals with genotype 1 HCV, especially men. However, the overall rate of steatosis was nearly 60%, even among non-diabetic genotype 1 patients at low risk for the metabolic syndrome (a poorly understood collection of metabolic risk factors – including abdominal obesity, blood glucose abnormalities, high blood fat levels, and elevated blood pressure – associated with increased risk of cardiovascular disease). In the December 2005 American Journal of Gastroenterology, Amy Wang and colleagues reported that genotype 1 and genotype 3 HCV appear to be associated with steatosis through different mechanisms; in particular the relationship between insulin resistance and adiponectin (a hormone produced by fat cells that regulates insulin sensitivity) is disturbed in patients with genotype 1 but not genotype 3.

NAFLD and its more severe form, nonalcoholic steatosis (NASH), are common in HCV negative individuals – particularly those with the metabolic syndrome – as well as in people with hepatitis C. In a February special anniversary Hepatology supplement, Geoffrey Farrell and Claire Larter presented a comprehensive overview of NAFLD – which affects an estimated 17%-33% of Americans – including epidemiology, diagnosis, and association with fibrosis and cirrhosis. To date, the mainstay of NAFLD treatment is weight loss and increased exercise. In the February 2006 Journal of Hepatology, Larter and Farrell examined the interactions among insulin resistance, adiponectin, and other cytokines (chemical messengers) in people with NASH, asking, “which is the best target to treat?” Finally, in the January 2006 issue of Alimentary Pharmacology & Therapeutics, K.M. Comar and Richard Sterling presented an overview of drug therapy for NAFLD using insulin sensitizing and antidiabetic medications (e.g., metformin [Glucophage], pioglitazone [Actos], rosiglitazone [Avandia]), antioxidants such as vitamins C and E, and liver-protective agents (e.g., betaine, ursodeoxycholic acid, pentoxyfylline). They concluded that treatment for NAFLD ideally should focus on correcting the underlying metabolic disorders. “Promising pharmacological treatments have been demonstrated with antioxidants, insulin sensitizers, hepatoprotectants, and lipid-lowering agents,” they wrote. “However, without larger randomized studies, no pharmacological treatments can be recommended at this time.”

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Retinal Damage as a Side Effect of Interferon

Along with more common side effects such as depression, interferon-based therapy for hepatitis C has also been linked to eye problems including retinal lesions and visual impairment. As reported in the January 2006 Journal of Hepatology, Louis D’Alteroche and colleagues from France assessed ophthalmologic complications in 156 HCV patients treated with conventional or pegylated interferon alpha, with or without ribavirin; none had signs of retinopathy (retinal damage) before starting therapy. The researchers observed retinal lesions in about one-quarter of the patients during treatment: 31 with “cotton wool spots” (patches of white discoloration on the retina) and nine with retinal hemorrhage. About 20% of patients experienced visual impairment before treatment, increasing to 47% during treatment. Retinopathy was significantly associated with history of arterial hypertension (high blood pressure), age above 45 years, and use of pegylated interferon. The authors concluded that, “signs of retinopathy and neurovisual impairment were common in patients receiving alpha interferon therapy.” However, lesions were rarely symptomatic and disappeared in all patients, leading the researchers to suggest that interferon therapy “may usually be continued in asymptomatic patients as long as there is careful fundoscopic examination” (using a lighted instrument to view the rear portion of the eyeball).

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