Background and Aims Chronic HBV is the predominant cause of HCC worldwide. Although HBV coinfection is common in HIV, the determinants of HCC in HIV/HBV coinfection are poorly characterized. We examined the predictors of HCC in a multicohort study of individuals coinfected with HIV/HBV. Approach and Results We included persons coinfected with HIV/HBV within 22 cohorts of the North American AIDS Cohort Collaboration on Research and Design (1995‐2016). First occurrence of HCC was verified by medical record review and/or cancer registry. We used multivariable Cox regression to determine adjusted HRs (aHRs [95% CIs]) of factors assessed at cohort entry (age, sex, race, body mass index), ever during observation (heavy alcohol use, HCV), or time‐updated (HIV RNA, CD4+ percentage, diabetes mellitus, HBV DNA). Among 8,354 individuals coinfected with HIV/HBV (median age, 43 years; 93% male; 52.4% non‐White), 115 HCC cases were diagnosed over 65,392 person‐years (incidence rate, 1.8 [95% CI, 1.5‐2.1] events/1,000 person‐years). Risk factors for HCC included age 40‐49 years (aHR, 1.97 [1.22‐3.17]), age ≥50 years (aHR, 2.55 [1.49‐4.35]), HCV coinfection (aHR, 1.61 [1.07‐2.40]), and heavy alcohol use (aHR, 1.52 [1.04‐2.23]), while time‐updated HIV RNA >500 copies/mL (aHR, 0.90 [0.56‐1.43]) and time‐updated CD4+ percentage <14% (aHR, 1.03 [0.56‐1.90]) were not. The risk of HCC was increased with time‐updated HBV DNA >200 IU/mL (aHR, 2.22 [1.42‐3.47]) and was higher with each 1.0 log10 IU/mL increase in time‐updated HBV DNA (aHR, 1.18 [1.05‐1.34]). HBV suppression with HBV‐active antiretroviral therapy (ART) for ≥1 year significantly reduced HCC risk (aHR, 0.42 [0.24‐0.73]). Conclusion Individuals coinfected with HIV/HBV on ART with detectable HBV viremia remain at risk for HCC. To gain maximal benefit from ART for HCC prevention, sustained HBV suppression is necessary.

Background Despite increasing incidence of hepatocellular carcinoma (HCC) among HIV-infected patients, it remains unclear if HIV-related factors contribute to development of HCC. We examined if higher or prolonged HIV viremia and lower CD4+ cell percentage were associated with HCC. Methods We conducted a cohort study of HIV-infected individuals who had HIV RNA, CD4+, and CD8+ cell counts and percentages assessed in the Veterans Aging Cohort Study (1999–2015). HCC was ascertained using Veterans Health Administration cancer registries and electronic records. Cox regression was used to determine hazard ratios (HR, 95% confidence interval [CI]) of HCC associated with higher current HIV RNA, longer duration of detectable HIV viremia (≥500 copies/mL), and current CD4+ cell percentage less than 14%, adjusting for traditional HCC risk factors. Analyses were stratified by previously validated diagnoses of cirrhosis prior to start of follow-up. Results Among 35 659 HIV-infected patients, 302 (0.8%) developed HCC over 281 441 person-years (incidence rate = 107.3 per 100 000 person-years). Among patients without baseline cirrhosis, higher HIV RNA (HR = 1.25, 95% CI = 1.12 to 1.40, per 1.0 log10 copies/mL) and 12 or more months of detectable HIV (HR = 1.47, 95% CI = 1.02 to 2.11) were independently associated with higher risk of HCC. CD4+ percentage less than 14% was not associated with HCC in any model. Hepatitis C coinfection was a statistically significant predictor of HCC regardless of baseline cirrhosis status. Conclusion Among HIV-infected patients without baseline cirrhosis, higher HIV RNA and longer duration of HIV viremia increased risk of HCC, independent of traditional HCC risk factors. This is the strongest evidence to date that HIV viremia contributes to risk of HCC in this group.

Nonrespiratory extrapulmonary tuberculosis is less likely than pulmonary tuberculosis to be a result of recent infection. Pleural tuberculosis is not an appropriate indicator for recent transmission among our population.

IMPORTANCE Hepatitis C virus (HCV) screening has been recommended for patients born between 1945 and 1965, but rates remain low.OBJECTIVE To evaluate whether a default order within the admission order set increases HCV screening compared with a preexisting alert within the electronic health record. DESIGN, SETTING, AND PARTICIPANTSThis stepped-wedge randomized clinical trial was conducted from June 23, 2020, to April 10, 2021, at 2 hospitals within an academic medical center.Hospitalized patients born between 1945 and 1965 with no history of screening were included in the analysis. INTERVENTIONSDuring wedge 1 (a preintervention period), both hospital sites had an electronic alert prompting clinicians to consider HCV screening. During wedge 2, the first intervention wedge, the hospital site randomized to intervention (hospital B) had a default order for HCV screening implemented within the admission order set. During wedge 3, the second intervention wedge, the hospital site randomized to control (hospital A) had the default order set implemented. MAIN OUTCOMES AND MEASURES Percentage of eligible patients who received HCV screeningduring the hospital stay. RESULTSThe study included 7634 patients (4405 in the control group and 3229 in the intervention group). The mean (SD) age was 65.4 (5.8) years; 4246 patients (55.6%) were men; 2142 (28.1%) were Black and 4625 (60.6%) were White; and 2885 (37.8%) had commercial insurance and 3950 (51.7%) had Medicare. The baseline rate of HCV screening in wedge 1 was 585 of 1560 patients (37.5% [95% CI, 35.1%-40.0%]) in hospital A and 309 of 1003 patients (30.8% [95% CI, 27.9%-33.7%]) in hospital B. The main adjusted model showed an increase of 31.8 (95% CI, 29.7-33.8) percentage points in test completion in the intervention group compared with the control group (P <. 001). CONCLUSIONS AND RELEVANCEThis stepped-wedge randomized clinical trial found that embedding HCV screening as a default order in the electronic health record substantially increased ordering and completion of testing in the hospital compared with a conventional interruptive alert. TRIAL REGISTRATION Clinicaltrials.gov: NCT04525690