HEPATOLOGY WATCH®
AUGUST
2002
PRIMARY SCLEROSING CHOLANGITIS
(PSC)
Small-duct PSC. Patients with small-duct PSC have hepatic
histology that is compatible with PSC, but normal findings on
cholangiography. The natural history of
small-duct PSC, particularly progression to large-duct PSC or
cholangiocarcinoma, is unknown. Paul
Angulo and colleagues performed a longitudinal cohort study of 18 patients with
small-duct PSC and 36 age- and sex-matched patients with classic PSC (follow-up
of 32.5 years). Death or liver
transplantation occurred in 3 (17%) small-duct PSC patients and 15 (42%)
classic PSC patients.
Transplantation-free survival was greater in the small-duct vs. the
classic PSC group. Compared to the
general US population, the overall survival of patients with small-duct PSC was
similar, while that of patients with classic PSC was lower. None of the small-duct PSC patients,
compared to 4 classic PSC patients, developed hepatobiliary malignancy. Follow-up cholangiography showed that 3
small-duct PSC patients had progressed to typical PSC at 4, 5.5, and 21
years. In a second study, Ulrika Broomé
et al. followed 32 Swedish patients with small-duct PSC for a median of 63
months (range, 1-194 months). No
patient developed cholangiocarcinoma and 4 were found to have progressed to
classic PSC. These findings suggest
that small-duct PSC frequently has a benign course and few patients progress to
classic PSC or develop hepatobiliary malignancies. An accompanying editorial by Roger Chapman provides a concise
literature review and discussion.
(Angulo P, et al. Hepatology 2002;35:1494-1500; Broomé U, et al. J
Hepatol 2002; 36:586-589; and Chapman RW. J Hepatol 2002;36:692-694)
LIVER Transplantation: Evolution in Outcomes
Chronic hepatitis C virus (HCV). Lisa Forman et al. conducted a retrospective
cohort study of 11,036 patients who had undergone 11,791 liver transplants
between 1992 and 1998 (data from United Network for Organ Sharing). HCV-positive recipients were found to have an
increased rate of death (hazard ratio [HR] = 1.23; 95% CI: 1.12-1.35) and
allograft failure (HR = 1.30; 95% CI: 1.21-1.39) compared to HCV-negative
recipients. The effect of HCV on
survival was most pronounced in females.
These data show that HCV infection adversely affects post-transplant outcomes. (Forman LM, et al. Gastroenterology
2002;122:889-896)
Chronic hepatitis B virus (HBV). Thomas Steinmüller and coworkers at Humboldt
University in Berlin analyzed their experience with liver transplantation of
HBV-related liver disease (228 liver transplantations in 206 HBV patients from
1988 to 2000). Overall, the 1-, 5-, and
10-year survival rates were 91%, 81%, and 73%, respectively. Decreased survival rates were seen in
patients with hepatocellular carcinoma, HBV reinfection, or preoperative
positive HBeAg. Compared to patients
transplanted prior to 1993, patients who underwent transplantation after
effective antiviral drugs became available had a greater 2-year survival rate
(44% vs. 85%) and a lower 2-year recurrence rate (42% vs. 8%). These observations show that current
strategies can achieve long-term survival results in HBV patients following
liver transplantation. (Steinmüller T,
et al. Hepatology 2002;35:1528-1535)
Alcoholic liver disease (ALD). Liver transplantation is standard therapy
for end-stage ALD. Santiago Tomé and
associates reviewed survival data from 68 patients transplanted for alcoholic
cirrhosis and 101 patients transplanted for other miscellaneous causes. Survival rates for these 2 transplantation
groups were found to be similar. In
addition, there were no differences in survival rates between patients with
superimposed acute alcoholic hepatitis and patients with liver cirrhosis
alone. Return to alcohol consumption
(n=7) was not associated with alcoholic hepatitis or graft loss. An accompanying editorial by Michael Lucy
discusses whether it is appropriate to perform liver transplantation in
patients with acute alcoholic hepatitis and concludes that prospective
randomized controlled trials are needed.
(Tomé S, et al. J Hepatol 2002;36:793-798 and Lucey MR. J
Hepatol 2002;36:829-831)
CHRONIC
HEPATITIS B
HBeAg seroconversion. The presence of HBeAg is associated with
active liver disease while HBeAg seroconversion to anti-HBe antibody often
coincides with clinical remission.
Yao-Shih Hsu and colleagues followed 283 chronic HBV patients for at
least 1 year after HBeAg seroconversion to obtain long-term outcome data
(median follow-up of 8.6 years; range, 1 to 18.4 years). A sustained biochemical remission was maintained
in 189 (66.8%) patients. Elevated serum
ALT levels developed in 94 patients (33.2%) and were associated with HBeAg
reversion (n=12), detectable serum HBV DNA without HBeAg reversion, (n=68) or
undetermined causes (n=14).
Hepatocellular carcinoma occurred in only 6 patients (2.2%) and
cirrhosis developed in only 21 (7.8%) of 269 patients without cirrhosis at the
time of HBeAg seroconversion. In
addition, a retrospective analysis conducted by Chi-Jen Chu et al. of stored
sera from 332 Chinese patients with chronic HBV revealed that HBeAg
seroconversion occurred approximately 1 decade earlier in HBV genotype B
patients than in HBV genotype C patients.
These studies indicate that HBeAg seroconversion confers a favorable
long-term outcome and may be responsible for the better prognostic liver
disease observed in patients infected with genotype B. (Hsu Y-S, et al. Hepatology
2002;35:1522-1527 and Chu C-J, et al. Gastroenterology 2002;
122:1756-1762)
brief
REPORTS
Alagille syndrome. Karan Emerick and Peter Whitington reviewed
the results of partial external biliary diversion in 9 patients with Alagille
syndrome, a disorder marked by chronic cholestasis in children, to report the
effectiveness of this surgical procedure in the treatment of pruritus and xanthomas. (Emerick KM and Whitington PF. Hepatology
2002;35:1501-1506)
Cirrhosis and obesity. A retrospective analysis by Vlad Ratziu et
al. showed that obesity-related cryptogenic cirrhosis is a distinct disease
entity that can cause severe liver disease, liver cancer and death. (Ratziu V, et al. Hepatology 2002;35:1485-1493)
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