Colorectal neoplasia in veterans is associated with Barrett's esophagus but not with proton-pump inhibitor or aspirin/NSAID use.

BACKGROUND: It has been suggested that Barrett's esophagus (BE) is associated with an increased risk of developing colorectal neoplasia, but this has not been reported consistently. AIM: To study whether BE is associated with an increased risk of colorectal neoplasia, and if it is, whether it is dependent on use of proton-pump inhibitors (PPIs) or aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). DESIGN: Case-control study. SETTING: Endoscopic database of the Palo Alto Veterans Affairs Health Care System. POPULATION: 268 veterans with BE were matched with 268 controls without BE. INTERVENTION: Controls had undergone upper GI endoscopy within 14 days of the corresponding case. Colonoscopy was performed within 6 months in cases and controls. MAIN OUTCOME MEASURE: Development of colorectal neoplasia. RESULTS: Colorectal neoplasia was present in 162 of 268 (60%) BE patients and in 105 of 268 (40%) controls (p < 0.001). The presence of BE (odds ratio [OR] 2.02: 95% CI [1.35, 3.04]), but also increasing age (OR 1.24 per decade: 95% CI [1.04, 1.48]) and alcohol use (OR 1.70: 95% CI [1.16, 2.50]) were associated with an increased risk of colorectal neoplasia in multivariable logistic regression analysis, whereas PPIs (OR 0.99: 95% CI [0.66, 1.48]) and aspirin/NSAIDs (OR 0.90: 95% CI [0.61, 1.33]) had no meaningful effect. LIMITATIONS: This was a retrospective study in mostly male veterans. CONCLUSIONS: Veterans with BE are at an increased risk of developing colorectal neoplasia. This association is independent from the use of PPIs or aspirin/NSAIDs.

Prophylaxis against chemotherapy-induced reactivation of hepatitis B virus infection with Lamivudine.

The results of lamivudine therapy in 4 patients with chemotherapy-induced hepatitis B virus (HBV) reactivation are reported. Cancer chemotherapy-induced reactivation is a known complication in patients with chronic HBV infection or history of HBV infection with recovery. Reactivation of HBV infection has a broad spectrum of manifestations ranging from mild elevation of aminotransferase levels to fatal fulminant hepatitis. Lamivudine is a nucleoside analogue and a potent inhibitor of HBV reverse transcription. The 4 patients treated with lamivudine included 1 woman with breast cancer and 3 men with non-Hodgkin lymphoma, ranging from 41 to 63 years of age. All 4 patients were undergoing standard, multi-agent chemotherapy when they presented with HBV reactivation manifested by sudden onset of fatigue, jaundice, and HBV serology consistent with active HBV infection (detectable serum HBV DNA) in the absence of other known causes of acute hepatitis. Lamivudine therapy (100 mg/d in 3 patients and 150 mg/d in 1 patient) was initiated from 1 to 18 days following the diagnosis of HBV reactivation. All 4 patients showed rapid decrease in aminotransferase levels within 2 weeks after initiating lamivudine therapy. Unfortunately, hepatic synthetic function failed to improve in 2 patients, who both died. The remaining 2 patients had suppression of HBV DNA to undetectable levels after 1 and 4 months of treatment and had biochemical and clinical improvement. The 2 patients who died received lamivudine therapy for 8 days and for 3 weeks. There have been no randomized clinical trials to study the role of lamivudine for prophylaxis or treatment of HBV reactivation associated with chemotherapy. However, based on our limited experience, lamivudine may be efficacious in suppressing potentially fatal HBV reactivation secondary to chemotherapy in patients with chronic HBV infection or prior infection with recovery. Patients who undergo chemotherapy should be screened for the presence of markers of chronic hepatitis B infection or previous HBV infection. We recommend that patients with chronic HBV infection (positive HBV DNA and/or positive HBsAg) or history of HBV infection with recovery (positive hepatitis B core antibody with or without HBsAb) be considered for prophylactic lamivudine use to prevent chemotherapy-induced HBV reactivation.

Racial differences in effectiveness of alpha-fetoprotein for diagnosis of hepatocellular carcinoma in hepatitis C virus cirrhosis.

alpha-Fetoprotein (AFP) is frequently used as a diagnostic marker for hepatocellular carcinoma (HCC). Most available data concerning AFP come from studies of patients with chronic hepatitis B or other chronic liver diseases of mixed etiologies. Limited data concerning the diagnostic value of AFP for hepatitis C virus (HCV)-related HCC have to date come only from Asian and European studies, and results are conflicting. There may be significant differences in AFP levels depending on racial backgrounds and etiologies of primary liver disease. We conducted a multicenter, retrospective, case-control study of 163 HCC patients with HCV infection and 149 control patients with HCV-related cirrhosis. The positive likelihood ratios for AFP at 0 to 20, 21 to 50, 51 to 100, and 101 to 200 ng/mL were 0.46, 1.31, 1.15, and 6.90, respectively. No controls had AFP greater than 200 ng/mL. The sensitivity of AFP for the diagnosis of HCC in African Americans with HCV infection was lower than that of patients of all other ethnic groups combined (57.1% vs. 81.6% for AFP > 10 ng/mL, P =.02, and 42.9% vs. 66.0% for AFP > 20 ng/mL, P =.05). The area under the receiver operating characteristics curve was 0.81 for non-African Americans but only 0.56 for African Americans. In conclusion, AFP greater than 200 ng/mL can be used to confirm HCC in patients with HCV-related cirrhosis and a hepatic mass. However, AFP is insensitive for the diagnosis of HCC in African Americans.