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Hepatitis C testing is rarely initiated in primary care clinics based on physician-identified risk factors. Interventions should be developed to optimize early diagnosis of hepatitis C as significant liver disease may be present despite the absence of symptoms.

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The question of possible earlier and more aggressive recurrence of hepatitis C virus (HCV) infection after living donor liver transplantation (LDLT) compared to deceased donor liver transplantation (DDLT) remains unanswered. To address this issue we retrospectively reviewed virological, histological, and clinical data in 67 patients (52 DDLT and 15 LDLT) who underwent liver transplant for their HCV-related cirrhosis since April 2001. Our data indicate that there is no statistical difference between LDLT and DDLT groups in mean age, Child-Turcotte-Pugh score, model for end-stage liver disease score, and gender distribution. The mean follow-up was 749 Ϯ 371 days in LDLT and 692 Ϯ 347 days in DDLT. The predominant genotype in the LDLT and DDLT are genotype 1 (LDLT, 91%; DDLT, 70%). All patients with histologically confirmed recurrent HCV had detectable HCV-RNA in serum. The histological recurrence rate of hepatitis C was 58% at 4 months, 90% at 1 year, and 100% at 2 years in LDLT patients vs. 71% at 4 months, 94% at 1 year, and 95% at 2 years in DDLT patients (not significant) Comparison of the activity of inflammation and fibrosis score at all time points failed to show a statistical difference. Kaplan-Meier survival analysis showed similar patient and graft survival rates between the 2 groups. Our data indicate that histological recurrence of HCV is an early event and virtually universal 2 years' posttransplantation, regardless of modality of donor procurement. Liver Transpl 12: 560-565, 2006.

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Vitamin A toxicity has been reported to cause severe liver disease and, occasionally, liver failure. Herein we present the case of a 60-year-old male with symptoms of muscle soreness, alopecia, nail dystrophy, and ascites. He continued to deteriorate with the development of refractory ascites, renal insufficiency, encephalopathy, and failure to thrive. In this era of natural supplements, medication toxicity remains a major cause of concern. Biotransformation of drugs is a major function of the liver. Drug-induced liver injury can be serious enough to cause fulminant hepatic failure resulting in death or liver transplantation. We report a case of liver injury from subacute vitamin A toxicity leading to liver transplantation. To our knowledge, there is no prior published report of liver transplantation for vitamin A toxicity in the United States. CASE REPORTThe case was that a 60-year-old gentleman whose initial complaint was muscle soreness of 1-month duration. He also noticed increased shedding of his scalp hair (Fig. 1). He developed cold intolerance, chapped lips, dystrophy of his fingernails, and a skin rash with pruritus within 2 months (Figs. 2 and 3) His past medical history was significant for dyslipidemia, hypertension, and possibly celiac sprue, which was untreated. A comprehensive metabolic profile showed liver injury with aminotransferases elevated to 2 times the upper limit of normal, with alkaline phosphatase slightly above normal. Total bilirubin was normal. The patient was on atorvastatin at that time, and it was discontinued. His alcohol intake was minimal, and he stopped soon after the development of symptoms. When the liver injury tests remained persistently abnormal, he underwent an evaluation for chronic liver disease. This evaluation was essentially normal with a ferritin 26 g/mL, iron serum 43 g/dL, iron binding capacity 348 g/dL, iron saturation 12%, and lactate dehydrogenase 177 U/L. His serologies for hepatitis A, B, and C were negative. Antinuclear antibody and antimitochondrial antibody were negative, and ceruloplasmin and alpha-1 antitrypsin levels and phenotype were normal as well. In the meantime, the patient developed ascites. He was afebrile and anicteric with an erythematous skin rash on the abdomen and extremities. He also had nonscarring alopecia, decreased pubic and axillary hair, and dystrophic nail changes.An abdominal Doppler ultrasound showed ascites and normal Doppler waveforms of the hepatic artery and portal veins. The echogenicity and appearance of the liver were within normal limits. The spleen was normal in size. The patient's laboratory values at this time were as follows: hemoglobin, 11.6 mg/dL; white

The 69th World Health Assembly endorsed the Global Health Sector Strategy for Viral Hepatitis, embracing a goal to eliminate hepatitis infection as a public health threat by 2030. This was followed by the World Health Organization's (WHO) global targets for the care and management of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. These announcements and targets were important in raising awareness and calling for action; however, tracking countries’ progress towards these elimination goals has provided insights to the limitations of these targets. The existing targets compare a country's progress relative to its 2015 values, penalizing countries who started their programmes prior to 2015, countries with a young population, or countries with a low prevalence. We recommend that (1) WHO simplify the hepatitis elimination targets, (2) change to absolute targets and (3) allow countries to achieve these disease targets with their own service coverage initiatives that will have the maximum impact. The recommended targets are as follows: reduce HCV new chronic cases to ≤5 per 100 000, reduce HBV prevalence among 1‐year‐olds to ≤0.1%, reduce HBV and HCV mortality to ≤5 per 100 000, and demonstrate HBV and HCV year‐to‐year decrease in new HCV‐ and HBV‐related HCC cases. The objective of our recommendations is not to lower expectations or diminish the hepatitis elimination standards, but to provide clearer targets that recognize the past and current elimination efforts by countries, help measure progress towards true elimination, and motivate other countries to follow suit.