Effect of Concurrent Metabolic Dysfunction-Associated Steatotic Liver Disease on Serial Non-invasive Fibrosis Markers in Chronic Hepatitis B.

BACKGROUND & AIMS: Concurrent hepatic steatosis has diverse effects on chronic hepatitis B (CHB), however the combined effects of metabolic dysfunction-associated steatotic liver disease (MASLD) and CHB on liver fibrosis progression remains unclear. The primary aim of this study was to utilize serial fibrosis measurements to compare the dynamic change in fibrosis in CHB patients with/without concurrent MASLD. The secondary aim was to investigate factors associated with steatosis development and regression in CHB patients. METHODS: This was a retrospective cohort study of all non-cirrhotic CHB patients identified from 1/1/2011 to 31/12/2016. Hepatic steatosis was diagnosed by ultrasound. Fibrosis markers included liver stiffness (LSM) by transient elastography, APRI and FIB-4. General linear mixed effects modelling was used to fit polynomial and linear estimates. RESULTS: Of 810 CHB patients (n = 2,373 LSM measurements; median age 44.4y; 48% male; 24% HBeAg positive), 14% had concurrent MASLD. LSM was higher at baseline but decreased in MASLD patients over time, while LSM remained stable in non-MASLD patients, such that all patients had similar LSM beyond 4-5 years. MASLD patients had lower APRI compared to non-MASLD patients, which was predominately due to a higher platelet count and higher ALT over time. There was substantial discordance between LSM, APRI and FIB-4. Baseline BMI was the only factor that predicted steatosis development and regression. CONCLUSIONS: We found no evidence of an association between concurrent MASLD and fibrosis progression amongst CHB patients without baseline advanced liver disease. APRI and FIB-4 may have reduced accuracy in MASLD patients.

Antisynthetase syndrome with rare EJ-1 antibodies with antiphospholipid syndrome.

We describe the first case of antisynthetase syndrome (ASS) with antibodies to anti-glycyl tRNA synthetase (EJ-1) with antiphospholipid syndrome (APLS). A 66-year-old man presented with progressive dyspnoea, fever, dry cough and proximal muscle weakness over several months on a background of cryptogenic organizing pneumonia. Examination revealed bibasal fine chest crackles, proximal muscle weakness of the upper and lower limbs, digital skin thickening and facial telangiectasias. Creatine kinase was elevated and autoimmune screening was positive for anti-EJ-1, anti-beta-2-glycoprotein, anti-Ro and anti-La antibodies. Computed tomography of the chest revealed a usual interstitial pneumonia pattern and a ventilation-perfusion scan demonstrated scintigraphic evidence of bilateral pulmonary emboli. A diagnosis of ASS and APLS was made. Immunosuppressive therapy including pulsed methylprednisolone, rituximab and mycophenolate was commenced with improvement in symptoms. This case highlights the importance of evaluation for ASS in idiopathic interstitial pneumonia, and APLS in ASS patients.