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2.2% Liver Cancer developed Among SVRs; Sexual Dysfunction among HCV+
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Reported by Jules Levin
http://www.natap.org
from AASLD
Nov 13, 2005, San Francisco
The AASLD conference opened today. It’s a beautiful day in SF, sunny & warm. Still, the only city in the USA where you can get real pizza is NYC, nowhere else has good pizza. There are several posters this morning on using non-invasive fibrosis tests instead of liver biopsy. At the current time I think there is not enough evidence that the tests have anymore than at best limited utility and very well may mislead on decision making. The real news out of this meeting is HCV new drug pipeline with new data on new HCV drugs pouring out of this meeting and the new data here on HBV drugs. This AASLD is alandmark because it’s the first liver conference with so many new HCV drugs being presented on with new study data. There are about 10 new HCV drugs being reported on here at AASLD. As well, there are so many HBV drugs available now or in clinical development. How to use HBV drugs is a key question. The treatment guidelines are inadequate and we have yet to research combination therapy in HBV. This will be the next major research horizon, how to & if we can combine HBV drugs. Here are two interesting posters from this morning’s poster session. In the first 2.2% of SVRs developed liver cancer (HCC) & in talking with the study authors they told me steatosis appears to be the cause & not genotype 3-related steatosis. The second poster reports from study in NYC at Bellevue on a finding of sexual dysfunction in HCV+ individuals. The important HCV & HBV drug data will be reported Monday & Tuesday.
Jules Levin
DEVELOPMENT OF HEPATOCELLULAR CARCINOMA LONG AFTER SUSTAINED VIRAL RESPONSE TO INTERFERON THERAPY IN PATIENTS WITH CHRONIC HEPATITIS C -FAT ACCUMULATION MAY CONTRIBUTE
TO THE CARCINOGENESIS-
Hiroko Kurihara, Teikyo University, School of Medicine, Tokyo, Japan; Atsushi Tanaka, Teikyo University, School of Medicine, Tokyo, Japan; Satoko Uegaki, Teikyo University, School of Medicine, Tokyo, Japan; Jou Aida, Ikuo Nagashima, Junji Shiga, Hajime Takikawa, Teikyo University, School of Medicine,
Tokyo, Japan
Background: It has been well established that continuous eradication of hepatitis C virus (HCV) by interferon (IFN) therapy (sustained viral response; SVR) significantly inhibits development of hepatocellular carcinoma (HCC). However, we sporadically encounter occurrence of HCC even in patients with SVR, and it is of clinical importance to identify patients who are at risk for HCC
after achievement of SVR.
Aim: We examined whether HCV still remained in the liver and was related to carcinogenesis in patients who developed HCC long after SVR. Next, we evaluated clinical and histopathological profiles of the patients to identify factors which could contribute to development of HCC.
Patients and Methods: Since 1985, one-thousand and ninety-eight patients with chronic hepatitis C have been treated by interferon therapy with and without ribavirin in our hospital. Among 1,098 patients, SVR was achieved in 265 patients (24.1%). HCC developed in 6 patients out of 265 SVR patients (2.3%). In 4 patients, total RNA was isolated from liver specimens taken before IFN therapy as well as at the development of HCC. HCV-RNA was sought by RT-PCR using these liver derived cDNA. To assess the quality of RNA, we also amplified beta-actin as positive control. In addition, clinical and histopathological characteristics were evaluated in these patients to identify risk factors for development of HCC.
Results:
All 6 patients were male. The time interval between termination of IFN and HCC occurrence was on average 5-6 yrs. Undetectable serum HCV-RNA and normal
ALT had been continuously maintained since IFN therapy in all patients. Excess intake of alcoholic beverage was denied by all patients. Since it is likely that latent HCC might be already present during IFN therapy in patients who developed HCC soon after IFN, we focused on 4 patients who developed HCC more than 5 years after termination of IFN for further investigation.
HCV-RNA in liver specimens, which was present before IFN, was undetected both in cancerous and non-cancerous tissue. Betaactin was well amplified in all specimens. Of note, liver histology demonstrated moderate to severe fat accumulation in 3 out of 4 patients, and resembled non-alcoholic steatohepatitis in one patient.
Conclusion: HCV-RNA was undetectable in the liver in patients who developed HCC long after SVR, suggesting that HCV does not directly contribute to occurrence of HCC. Fat accumulation was noted in 3 out of 4 patients, and thus the carcinogenic process, leading to HCC formation in NASH liver, may play a crucial role as well after eradication of HCV.
SEXUAL DYSFUNCTION IS HIGHLY PREVALENT AMONG MEN WITH CHRONIC HEPATITIS C VIRUS INFECTION AND NEGATIVELY IMPACTS HEALTH-RELATED QUALITY OF LIFE
".....Sexually dysfunction is highly prevalent in men with chronic HCV infection, is independent of depression, and is associatedwith a marked reduction in HRQOL (quality of life survey)....".
David Wan, NYU School of Medicine, New York, NY; Ann Danoff, VA New York Harbor Healthcare System and NYU School of Medicine, New York, NY; Oona Khan, NYU School of Medicine, NYU, NY; Lainie Hurst, Daniel Cohen, NYU School of Medicine, New York, NY; Craig T. Tenner, Edmund J. Bini, VA New York Harbor Healthcare System and NYU School of Medicine, New York,
NY
Background: Sexual dysfunction has been reported in patients with hepatitis C virus (HCV) infection, yet little is known about this association. The aim of this study was to determine the prevalence of sexual dysfunction among men with chronic HCV infection and to evaluate the impact of sexual dysfunction on
health-related quality of life (HRQOL).
Methods: We prospectively enrolled 112 HCV men without decompensated
cirrhosis who were not taking interferon/ribavirin and 239 HCV negative controls from our GI and Primary Care clinics. Patients were excluded if they had diabetes, HIV, prostate or other cancer, prostate surgery, thyroid disease, alcohol or drug abuse, or were on methadone. A medical history was obtained, and all patients completed validated questionnaires to assess sexual function (Brief Male Sexual Function Inventory [BMSFI]), depression (Beck Depression Inventory), and HRQOL (Medical Outcomes Study SF-36). The BMSFI assessed sexual drive (0-8), erection (0-12), ejaculation (0-8), sexual problem assessment (0-12), and overall sexual satisfaction (0-4), with lower scores indicating
greater dysfunction.
Results:
Although HCV+ patients were younger than control subjects (median age, 55.0 vs 62.0 years, P 0.001), they had significantly more sexual dysfunction across all BMFSI domains: sex drive (3.4 ± 2.5 vs 4.6 ± 2.2, < 0.001), erection (5.1 ± 3.9 vs 7.2 ± 3.8, P<0.001), ejaculation (4.4 ± 3.0 vs 5.7 ± 2.6, P<0.001), sexual
problem assessment (5.6 ± 4.6 vs 8.6 ± 3.9, P<0.001), and overall sexual satisfaction (1.5 ± 1.4 vs 2.2 ± 1.3, P<0.001).
For overall sexual satisfaction, the proportion of subjects who were not sexually
satisfied was higher in the HCV patients than in controls (53.6% vs 28.9%, P<0.001) and this remained significant after adjusting for age, race, and other potential confounding variables (OR =2.56; 95% CI, 1.49–4.41).
In addition, HCV+ patients were more likely to use sildenafil citrate within the last 30 days as compared with control subjects (19.6% vs 9.6%, P =0.009).
Among HCV+ patients, the proportion of subjects who were not sexually
satisfied did not differ (P=0.52) among those with none (47.5%),
mild-moderate (64.0%), moderate-severe (59.1%), and severe depression
(50.0%).
HCV+ patients who were not sexually satisfied scored significantly worse in 6 of 8 domains of HRQOL as compared with HCV+ patients who did not report being sexually dissatisfied.
Conclusions: Sexually dysfunction is highly prevalent in men with chronic HCV infection, is independent of depression, and is associated
with a marked reduction in HRQOL. Future studies to investigate the mechanisms of sexual dysfunction in this population are needed.
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