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Rheumatology
5th Nov, 2025
The Lancet
Qian Wang and colleagues assessed the feasibility of HN2301, an engineered CD8 T-cell-targeted lipid nanoparticle encapsulating CD19 chimeric antigen receptor (CAR) messenger RNA, in five patients with refractory systemic lupus erythematosus (SLE). Patients received an infusion of HN2301 at a dose of 2 mg or 4 mg. CD8+ CD19 CAR T cells and CAR mRNA peaked at 6 h after infusion, decreasing to baseline levels within 2–3 days. Within 6 h after infusion, circulating B cells were substantially decreased in the two patients who received the 2 mg dose and were completely depleted for 7–10 days after administration in the three patients who received the 4 mg dose.
Benjamin S, Vi L, Chatterjee D, et al. Maternal autoantibodies to the sodium potassium pump α1 subunit AT1A1 and fetal autoimmune congenital heart block: a case-control study. Lancet Rheumatology 2025; 7: e554–64—In this Article, the last sentence of the Summary Findings should read “Anti-AT1A1 autoantibodies were absent in all unaffected pregnancies of women with no history of fetal heart block (autoimmune congenital heart block-naive, 54 [100%] of 54) and in 61 (94%) of 65 of unaffected pregnancies”.
I read with interest the Article by Dennis A Ton and colleagues1 comparing MRI findings in patients with rheumatoid arthritis, at-risk populations, and healthy individuals. Using well defined cohorts, the authors provide valuable insights into the specificity of MRI findings in rheumatoid arthritis. However, the findings also highlight the need for caution in how MRI results are interpreted across different clinical contexts.
Aikeremujiang Muheremu and Kan Jiang raise insightful and thought-provoking points on our recent paper1 on CNS activation in patients with rheumatoid arthritis. We are pleased to hear that the key thesis of the study—that the CNS is a key determinant of therapeutic responses to TNF inhibitors in patients with rheumatoid arthritis—has been recognised by Muheremu and Jiang. Indeed, these findings challenge the conventional, peripherally focused view of rheumatoid arthritis by providing evidence for a crucial joint–brain axis that might influence therapeutic responses to cytokine inhibition.
The landmark study by Hess and colleagues1 represents a paradigm shift in rheumatoid arthritis therapeutics by positioning the CNS as a key predictor of TNF inhibitor response. The authors' randomised trial compellingly shows that patients with high baseline functional MRI (fMRI)-measured CNS pain activation have substantially better clinical outcomes with certolizumab pegol than individuals with low activation. This work challenges the peripheral–centric view of rheumatoid arthritis, reframing subjective symptoms such as pain as active therapeutic targets rather than mere byproducts of joint inflammation.
A recent series of studies on Sjögren's disease have shown clustering of patients that share clinical features, such as pain, fatigue, and dryness.1–3 Although these delineations might aid patient stratification for a more personalised approach, patient heterogeneity remains considerable within groups, and the overlap in symptoms between groups is substantial. Hence, stratification and a more targeted treatment approach might lead to increased effectiveness and prevention of unnecessary drug exposure for patients.
Serum biomarkers have increasingly been studied to aid in the diagnosis, prognosis, disease monitoring, and treatment response in patients with juvenile idiopathic arthritis (JIA). One might think that by now we would have found biomarkers for diagnosis and treatment. Ideally, a biomarker that can assist in deciding which treatment would be effective for which patients. However, in 2025, JIA remains a clinical diagnosis, taking into account presenting symptoms, imaging findings, and blood test results (such as rheumatoid factor and antinuclear antibodies).
Non-specific low back pain remains one of the leading global causes of disability, substantially diminishing productivity and quality of life among working-age adults. A subset of individuals develop chronic non-specific low back pain, characterised by persistent functional limitations.1 This group accounts for a disproportionate share of health-care resource use compared with people experiencing acute or subacute episodes.2 When symptoms persist for longer than 12 weeks, neurophysiological adaptations can alter pain processing pathways, leading to a shift in the pain profile from predominantly nociceptive or neuropathic to nociplastic.
In The Lancet Rheumatology, Gabriele De Marco and colleagues1 present their study on the benefit of using methotrexate with golimumab in patients with early psoriatic arthritis. On average, the median time from symptom onset to diagnosis was 10 months. All patients received an intramuscular dose of methylprednisolone 120 mg (or an equivalent intra-articular dose), and methotrexate (increased to 25 mg orally weekly within 28 days) and were randomly assigned to either the golimumab and methotrexate group or the placebo and methotrexate group, stratified by oligoarticular or polyarticular involvement.
Management of psoriatic arthritis has advanced substantially in recent years, with emerging targeted therapies and disease-specific studies redefining patient outcomes. The high burden of comorbidities associated with the disease—the theme of World Psoriasis day 2025—alongside limited understanding of disease pathogenesis, highlights the continued need for optimised care and innovative therapies.
Gastroenterology & Hepatology
Psychogastroenterology encompasses both basic mechanistic research, which identifies psychological mechanisms (eg, fear-learning) that contribute to disorders of gut–brain interaction (DGBIs), and clinical applied research, which evaluates the efficacy of gut–brain behavioural therapies in DGBIs. However, progress in the field is hindered by inadequate communication between these areas, such that mechanistic processes are rarely translated into clinical targets, and interventions are developed with an incomplete understanding of the potential mechanisms by which they work or for whom they work.
Recompensation of decompensated cirrhosis has been defined by the Baveno consensus as control or cure of the main underlying cause; resolution of clinical manifestations, including ascites and hepatic encephalopathy, without the use of prophylactic medications, and without variceal bleeding for 12 months; and restoration of hepatic function. Cure and recompensation are usually associated with regression of liver fibrosis. Recompensation can occur when hepatitis C virus is eradicated, if hepatitis B virus infection (without hepatitis D co-infection) is suppressed, and following persistent alcohol abstinence in patients with alcohol-associated cirrhosis.
Considerable attrition was seen across the chronic hepatitis B care cascade, with low rates of retention especially in patients not on antiviral therapy. Assessment for treatment eligibility and initiation of antiviral therapy were lower in primary versus hospital-based specialist care models. Chronic hepatitis B services need to adopt strategies to optimise linkage to care after diagnosis, initiation of antiviral therapy if eligible, adherence to antiviral therapy and retention in care, as promoted in 2024 WHO hepatitis B guidelines.
MetALD might be associated with a higher risk of liver-related events, hepatocellular carcinoma, and extrahepatic cancers than MASLD, whereas all-cause mortality, extrahepatic cancer-related mortality, and cardiovascular events seem similar between the two conditions. These findings emphasise the need for distinct clinical strategies for these related yet different entities within the steatotic liver disease spectrum and highlight the importance of conducting pharmacological clinical trials in this context.
Torp N, Bech KT, Schnefeld HL, et al Phosphatidylethanol and self-reported alcohol intake to subclassify individuals at risk of steatotic liver disease: an analysis of data from a prospective cohort study. Lancet Gastroenterol Hepatol 2025; published online Sept 10. https://doi.org/10.1016/S2468-1253(25)00187-6—The title of this Article has been corrected. This correction has been made as of Sept 16, 2025.
Medical Journal
15th Jan, 2026
Wiley
Nature Medicine's Advance Online Publication (AOP) table of contents.
Medical News
phys.org
