Summary Background and Aim Bulevirtide (BLV) blocks the uptake of the hepatitis D virus (HDV) into hepatocytes via the sodium/bile acid cotransporter NTCP. BLV was conditionally approved by the EMA but real‐life data on BLV efficacy are limited. Methods Patients were treated with BLV monotherapy. Patients who did not achieve further decreases in HDV‐RNA after 24 weeks were offered PEG‐IFN as an add‐on therapy in a response‐guided manner. Results Twenty‐three patients (m: 10, f: 13; mean age: 47.9 years, cirrhosis: 16; median ALT: 71 IU/ml; median HDV‐RNA: 2.1 × 105copies/ml) started BLV monotherapy (2 mg/day: 22; 10 mg/day: 1). Twenty‐two completed ≥24 weeks of treatment (24–137 weeks): Ten (45%) were classified as BLV responders at week 24. BLV was stopped in two patients with >6 months HDV‐RNA undetectability, but both became HDV‐RNA positive again. One patient was transplanted at week 25. One patient terminated treatment because of side effects at week 60. Ten patients are still on BLV monotherapy. Adding PEG‐IFN in eight patients induced an HDV‐RNA decrease in all (1.29 ± 0.19 [SD] log within 12 weeks). HDV‐RNA decreased by >2log or became undetectable in 45%(10/22), 55%(11/20), 65% (13/20) and 69% (9/13); and ALT levels normalised in 64% (14/22), 85% (17/20), 90% (18/20) and in 92% (12/13) patients at weeks 24, 36, 48 and 60, respectively. Portal pressure decreased in 40% (2/5) of patients undergoing repeated measurement under BLV therapy. Conclusion Long‐term BLV monotherapy is safe and effectively decreases HDV‐RNA and ALT—even in patients with cirrhosis. The optimal duration of BLV treatment alone or in combination with PEG‐IFN remains to be established. An algorithm for a response‐guided BLV treatment approach is proposed.

Background Hepatitis D virus (HDV) coinfection aggravates the course of hepatitis B virus (HBV). The prevalence of HDV in Austria is unknown. Objective This national study aimed at (i) recording the prevalence of HDV‐infection in Austria and (ii) characterizing the “active” HDV cohort in Austria. Methods A total of 10 hepatitis treatment centers in Austria participated in this multicenter study and retrospectively collected their HDV patients between Q1/2010 and Q4/2020. Positive anti‐HDV and/or HDV‐RNA‐polymerase chain reaction (PCR) results were retrieved from local database queries. Disease severity was assessed by individual chart review. Viremic HDV patients with clinical visits in/after Q1/2019 were considered as the “active” HDV cohort. Results A total of 347 anti‐HDV positive patients were identified. In 202 (58.2%) patients, HDV‐RNA‐PCR test was performed, and 126/202 (62.4%) had confirmed viremia. Hepatocellular carcinoma was diagnosed in 7 (5.6%) patients, 7 (5.6%) patients underwent liver transplantation, and 11 (8.7%) patients died during follow‐up. The “active” Austrian HDV cohort included 74 (58.7%) patients: Evidence for advanced chronic liver disease (ACLD, i.e., histological F3/F4 fibrosis, liver stiffness ≥10 kPa, varices, or hepatic venous pressure gradient ≥6 mmHg) was detected in 38 (51.4%) patients, including 2 (5.3%) with decompensation (ascites/hepatic encephalopathy). About 37 (50.0%) patients of the “active” HDV cohort had previously received interferon treatment. Treatment with the sodium‐taurocholate cotransporting polypeptide inhibitor bulevirtide was initiated in 20 (27.0%) patients. Conclusion The number of confirmed HDV viremic cases in Austria is low (<1% of HBV patients) but potentially underestimated. Testing all HBV patients will increase the diagnostic yield. More than half of viremic HDV patients had ACLD. Improved HDV testing and workup strategies will facilitate access to novel antiviral therapies.

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