Editorial Board: Emmet B. Keeffe, MD (Chair); M. Eric Gershwin, MD;

Ira S. Goldman, MD; John L. Gollan, MD, PhD; Kris V. Kowdley, MD;

Paul Martin, MD; Marion G. Peters, MD

HEPATOLOGY WATCH^®

JANUARY 2004

CHRONIC HEPATITIS C VIRUS (HCV) INFECTION

Prevalence in porphyria cutanea tarda (PCT). PCT is caused by reduced activity of the uroporphyrinogen decarboxylase. When exposed to triggering factors (e.g., alcohol abuse, iron overload, viral infection), clinical manifestations include cutaneous lesions and liver disease. Previous epidemiologic studies have indicated that there is an increased prevalence of HCV infection among patients with PCT. Thus, Javier Gisbert et al. performed a meta-analysis of 50 studies investigating HCV prevalence in patients with PCT (N = 2,167). The mean prevalence of HCV infection was 47% by serologic tests and 50% by PCR assays. HCV prevalence varied by geographic region and type of PCT (57% in sporadic PCT and 26% in familial PCT). In the 7 studies that included healthy controls, HCV prevalence was 40% in PCT patients versus 0.24% in controls. This meta-analysis suggests a possible causal relationship between HCV infection and PCT, which is discussed further by Silvia Fargion and Anna Fracanzani in an editorial. (Gisbert JP, et al. J Hepatol 2003;39:620-627 and Fargion S and Fracanzani AL. J Hepatol 2003;39:635-638)

END-STAGE LIVER DISEASE

Osteopenia. Osteopenia is a well-recognized complication of cholestatic liver disease. Orthotopic liver transplantation (OLT) further accelerates the rate of bone loss resulting in a high incidence of post-transplant fractures in patients with primary biliary cirrhosis and primary sclerosing cholangitis. Elizabeth Carey et al. report the results of a study of osteopenic bone disease in the following groups of consecutive patients (N = 207) with noncholestatic liver disease who underwent OLT at the Mayo Clinic in Rochester between January 1991 and September 2001: 1) HCV alone (n = 68); 2) alcoholic liver disease (ALD) alone (n = 66); and 3) HCV and ALD (n = 73). Although ALD patients had more advanced liver disease, baseline mean bone densitometry T scores prior to OLT were lower in the HCV group. Patients in the HCV and ALD group had intermediate T scores. The pattern of bone loss after OLT was similar for the 3 study groups. Fractures occurred in 17% of patients within the first year after OLT. The majority of fractures were vertebral compression fractures. These data showed that osteopenic bone disease is also a frequent complication of noncholestatic liver disease and that these patients should be screened for osteopenia prior to OLT. (Carey EJ, et al. Liver Transpl 2003;9:1166-1173)

CHOLANGICARCINOMA

Photodynamic therapy (PDT). Nonresectable cholangiocarcinoma is an incurable malignancy refractory to chemotherapy and irradiation; biliary stenting is the palliative treatment of choice. Recently, several pilot studies have suggested that PDT is feasible palliative treatment for these patients. PDT incorporates the administration of hematoporphyrin derivatives as nontoxic photosensitizers that are preferentially retained by neoplastic tissue. Energy from the absorption of light is transferred to molecular oxygen, resulting in tumor cell death. Marianne Ortner and others conducted an open-label, multicenter (4 centers) study in which patients with nonresectable cholangiocarcinoma were randomized to receive PDT and stenting (n = 20) or stenting alone (n = 19). PDT was associated with improved biliary drainage and quality of life. In addition, the median overall survival time was prolonged in patients treated with PDT plus stenting compared to those who received stenting alone (493 vs. 98 days). In an accompanying editorial, Gregory Gores emphasized that stenting alone failed to relieve bile duct obstruction in the patient population of this trial. Thus, PDT extended the survival of cholangiocarcinoma patients who did not respond to stenting alone. (Ortner MEJ, et al. Gastroenterology 2003;125:1355-1363 and Gores GJ. Gastroenterology 2003;125:1536-1538)

HEPATOCELLULAR CARCINOMA (HCC)

Increasing incidence in the US. Hashem El-Serag and coworkers performed a retrospective cohort study to update the trends in HCC incidence using data from the National Cancer Institute Surveillance, Epidemiology, and End Results registries. The patient population consisted of persons given a diagnosis of HCC between 1975 and 1998. The age-adjusted incidence rate of HCC increased from 1.4/100,000 in 1975 to 1977 to 3.0/100,000 in 1996 to 1998. Furthermore, there was a 25% increase in HCC incidence during 1996 to 1998 compared to 1993 to 1995. The greatest increase in HCC incidence occurred in white men aged 45 to 49 years. A multivariate regression model confirmed that there was an almost 2-fold increase in the incidence ratio for HCC for 1996 to 1998 compared to 1975 to 1978. These findings are consistent with a true increase in the incidence of HCC in the US, which may be due to HCV infection acquired during the 1960s and 1970s. (El-Serag HB, et al. Ann Intern Med 2003;139:817-823)

PRIMARY SCLEROSING CHOLANGITIS (PSC)

Epidemiology in Olmsted County, Minnesota. Kiran Bambha et al. from the Mayo Clinic in Rochester reported a descriptive epidemiologic study of patients with a confirmed diagnosis of PSC utilizing the Rochester Epidemiologic Project, a medical records linkage system in Olmsted County from 1976 to 2000, in which 22 patients met the diagnostic criteria for PSC. The age-adjusted incidences of PSC were 1.25 and 0.54 per 100,000 person-years for men and women, respectively. The prevalences of PSC in the year 2000 were 20.9/100,000 for men and 6.3/100,000 for women. Inflammatory bowel disease was associated with PSC in 73% of these cases. Survival among the PSC patients was significantly less than expected for the Minnesota white population adjusted for age and gender. These data are the first population-based estimates of PSC incidence and prevalence in the US. The results suggest that the prevalence of PSC in the US may be greater than previously estimated. (Bambha K, et al. Gastroenterology 2003;125:1364-1369)

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