Participating providers reported very high rates of surveillance utilization and use of a biannual interval. It is likely that the sample is composed of providers who are very engaged and informed about HCC surveillance. However, their surveillance imaging practices largely deviated from practice guidelines, which all recommend only using US. Providers affiliated with transplant centers tend to use additional imaging modalities such as computed tomography and MRI, instead of US only.

In this review we critically assess the literature to evaluate the level of risk posed by alcohol as both a primary etiology of hepatocellular carcinoma (HCC) and as a cofactor in its development. Although there have been conflicting findings, based on the body of evidence to date, it appears that the linkage between compensated alcoholic liver disease-associated cirrhosis and HCC is best characterized as medium-high risk, with the risk increasing with age and with quantity and duration of alcohol consumption and is more pronounced in females. While abstinence is the most effective way to reduce HCC risk, its effect seems largely dependent on the severity of liver damage at the point of cessation. Alcohol clearly interacts with other etiologies and conditions including viral hepatitis B and C, hereditary hemochromatosis, diabetes, and obesity to increase the risk for developing HCC, either synergistically or additively. Continued progress in genetics, especially through mechanistic-based and genome-wide association studies may ultimately identify which single nucleotide polymorphisms are risk factors for the onset of alcoholic liver disease and its progression to HCC and lead to the development of targeted therapeutics which may help providers better manage at-risk patients.

Background Treatment for chronic hepatitis C virus (HCV) has rapidly evolved to simple, well-tolerated, all-oral regimens of direct-acting antivirals (DAAs). There are few data on the epidemiology of HCV in American Indians/Alaska Natives (AI/ANs), a population disproportionately affected by HCV. Methods In this retrospective cohort study, all HCV-infected AI/AN patients treated with DAA therapies between January 1, 2014, and February 24, 2016, in specialty clinics or by primary care clinicians participating in Extension for Community Healthcare Outcomes (ECHO) were included. Demographic, clinical, and virologic data on all patients treated for HCV from pretreatment through sustained virologic response at 12 weeks (SVR12) were collected. Results Two hundred eighty patients were included; 71.1% of patients (n = 199) were infected with genotype 1 (GT1), 18.2% (n = 51) with GT2, and 10.7% with (n = 30) GT3. At baseline, 26.1% (n = 73) patients had cirrhosis and 22.6% (n = 56) had active substance use disorder; eighty-eight percent (n = 232) of patients achieved SVR12. Among the 165 GT1 patients treated with sofosbuvir (SOF)/ledipasvir for 8, 12, and 24 weeks, SVR12 was achieved by 91.5% (n = 54), 92.2% (n = 71), and 100% (n = 13), respectively. Among GT2 patients, 87.2% (n = 34) and 71.4% (n = 5) treated with 12 and 16 weeks of SOF/ribavirin (RBV) achieved SVR12, respectively. Among GT3 patients, 100% (n = 2) and 83.3% (n = 20) treated with 12 and 24 weeks of SOF/RBV achieved SVR12, respectively. SVR12 rates remained high among patients with active substance use disorder. Conclusions DAA therapies are highly efficacious in HCV-infected AI/ANs. SVR12 rates remained high among patients with active substance use disorder. More steps must be taken to increase access to treatment for this underserved, vulnerable population.