The dynamic evolution of indolent γδT-cell clones in Felty syndrome (FS) and their relationship with progressive splenomegaly remain unclear. This paper reports a case of an FS patient followed for ten years. Serial assessments of γδT-cell clone burden, spleen size, and blood cell levels were performed. The results revealed that the γδT-cell clone burden showed minimal fluctuation over the decade, while the spleen demonstrated progressive enlargement, and blood cells progressively decreased. A newly identified nasopharyngeal hypermetabolic lesion (SUVmax 10.7) on PET-CT was pathologically confirmed as reactive plasmacytosis. This study suggests that indolent proliferation of γδT-cell clones may exist in FS, and the mechanism underlying the progression of splenomegaly might be independent of the lymphocyte clone. 惰性γδT细胞克隆在Felty综合征（FS）中的动态演变及其与脾进行性肿大之间的关系尚未明确。本文通过十年的随访，报道一例FS患者病例资料，动态监测γδT细胞克隆负荷、脾大小及血细胞水平，发现患者十年间γδT细胞克隆负荷波动幅度小，而脾呈进行性增大，血细胞进行性减少，PET-CT新发现的鼻咽部高代谢灶（SUVmax 10.7）经病理检验证实为反应性浆细胞增生。本研究提示FS中可能存在γδT细胞克隆惰性增殖现象，其脾肿大进展机制或独立于淋巴细胞克隆。.

Atrial fibrillation (AF) is a common and increasing arrhythmia posing major public health challenges. While management has improved, long-term efficacy and safety remain limited. Felty Syndrome, a severe rheumatoid arthritis (RA) subtype with splenomegaly and neutropenia, offers a chance to examine the autoimmune inflammation-AF link. We employed five Mendelian randomization (MR) approaches using genome-wide association study (GWAS) data to investigate whether Felty Syndrome causes AF. We analyzed data from the FinnGen biobank and a separate AF GWAS, selecting 17 independent SNPs as genetic instruments. We applied five MR methods, including inverse-variance weighted and MR-Egger, to estimate causal effects. Although no statistical significance was observed (e.g., weighted median beta = 0.028, P = 0.064; weighted mode beta = 0.033, P = 0.077; IVW beta = 0.021, P = 0.086; simple mode beta = 0.039, P = 0.087), a consistent trend suggested Felty Syndrome may increase AF risk. Sensitivity analyses showed robust results, with no significant heterogeneity or pleiotropy. In summary, while statistical significance was not achieved, our findings indicate a potential biological association that merits further investigation. This study highlights the need to identify new risk factors to improve AF prevention and management. The lack of significance may reflect a common challenge in MR studies of rare exposures like Felty Syndrome, where weak instruments can dilute causal estimates. Future research requires larger genetic datasets and should investigate the underlying molecular mechanisms for targeted therapies. Key Points • This study first applies Mendelian randomization to explore the Felty Syndrome-atrial fibrillation link, finding a consistent positive trend across multiple methods. • By focusing on Felty Syndrome-a condition linked to high-titer rheumatoid factor-we address prior RA study heterogeneity and offer a more precise causal model. • The results highlight the need to assess AF risk specifically in seropositive rheumatoid arthritis subgroups in future research.

Leishmaniasis is a potentially life-threatening protozoan infection that presents with many clinical manifestations, including cutaneous, mucocutaneus and visceral forms. In patients with rheumatoid arthritis (RA), cutaneous leishmaniasis can persist or re-emerge due to treatment-induced immunosuppression. However, it remains unclear whether this severe opportunistic infection is primarily driven by medication-induced immunosuppression or other poorly understood immune-mediated mechanisms that increase susceptibility. We describe an unusual case of disseminated leishmaniasis in a 50-year-old Italian man from Apulia, diagnosed with RA two years earlier. Following 15 months of unsuccessful immunosuppressive therapies, he developed severe multilineage pancytopenia, moderate hypertransaminasemia, elevated inflammatory markers, monoclonal gammopathy, clinically significant hepatosplenomegaly, and an ulcerated skin lesion. Initial diagnostic efforts excluded common infectious agents, primary hematological disorders, Felty syndrome, and amyloidosis. The non-specific histopathological findings from the pyoderma gangrenosum-like lesion and the transient clinical response to empirical steroids, broad-spectrum antibiotics, and granulocyte colony-stimulating factors further complicated the diagnostic process. The breakthrough came when a liver biopsy, performed to investigate persistent hypertransaminasemia, revealed Leishmania amastigotes within macrophages. This finding triggered a re-evaluation of the ulcerated skin lesion, and histological analysis confirmed concurrent cutaneous leishmaniasis. Subsequent bone marrow biopsy also identified Leishmania amastigotes, clinching the diagnosis of disseminated leishmaniasis. A holistic re-assessment of the patient's clinical presentation, developmental history, and laboratory, radiologic, and pathological data led to the definitive diagnosis. Treatment with standard intravenous amphotericin B resulted in clinical resolution. A follow-up bone marrow biopsy a few weeks later confirmed the infection had been completely eradicated. In patients with rheumatological conditions, the overlapping symptoms of systemic diseases and infections like leishmaniasis can lead to significant diagnostic delays. This case underscores the importance of comprehensive and meticulous diagnostic evaluations in immunosuppressed individuals to prevent potentially fatal outcomes.

Felty syndrome (FS) is a rare type of rheumatoid arthritis, and its combined occurrence with liver cirrhosis was rarely reported. FS was easily misdiagnosed as autoimmune cirrhosis or myelodysplastic syndrome, which led to improper medication and serious consequences. A 72-year-old male patient was admitted to Shuguang Hospital Affiliated with the Shanghai University of Traditional Chinese Medicine due to recurrent fatigue associated with a cough. Imaging suggested liver cirrhosis and splenomegaly, according to imaging diagnosis, laboratory tests, ultrasound, magnetic resonance, and history of rheumatoid arthritis, we considered the diagnosis of liver cirrhosis due to FS. Immunomodulatory and anti-liver fibrosis therapy was carried out, combined with Chinese patent medicines, and the patient's condition was stable in the future years. FS, liver cirrhosis, and chronic renal insufficiency. Routine immunomodulation, liver protection, and anti-liver fibrosis treatment, moreover Traditional Chinese Medicine was used to protect the liver and promote bile excretion, and regulate immunity. The patient's symptoms improved and his subsequent condition stabilized. Physicians should have a better understanding of FS and know that it can lead to liver cirrhosis, to avoid misdiagnosis and poor response to glucocorticoids, delay the disease, and increase the burden on patients.

Neutropenia in rheumatoid arthritis (RA) is a problem that often needs to be addressed. Side effects of basic antirheumatic treatment, infections or substrate deficiencies are common causes; however, T‑cell large granular lymphocytic (T-LGL) leukemia, a mature T‑cell neoplasm, can also lead to autoimmune cytopenia. The T‑LGL leukemia can be associated not only with RA but also with other autoimmune diseases or neoplasms. Correspondingly, increases in clonal T cells, natural killer T (NKT) cells and LGL cells are found in the peripheral blood. A T‑cell receptor PCR and flow cytometry (or at least a blood smear) are therefore necessary to diagnose T‑LGL leukemia. The presence of clonal T cells alone is usually not pathological. A distinction must be made from Felty's syndrome (consisting of the clinical triad of arthritis, leukopenia, splenomegaly), which does not require the two T‑LGL leukemia criteria mentioned. The treatment for both entities (with underlying RA) is methotrexate and, if insufficiently effective, rituximab. Neutropenien bei rheumatoider Arthritis (RA) sind ein häufig abzuklärendes Problem. Nebenwirkungen der antirheumatischen Basistherapie, Infektionen oder Substratmangel sind häufige Ursachen. Aber auch eine „T-large granular lymphocytic“(T-LGL)-Leukämie – eine reife T‑Zell-Neoplasie – kann zu autoimmunen Zytopenien führen. T‑LGL-Leukämien können nicht nur mit einer RA vergesellschaftet sein, sondern auch mit anderen Autoimmunerkrankungen oder Neoplasien. Im peripheren Blut findet sich zytologisch eine Vermehrung der LGL-Zellen, die klonalen T‑ oder NKT-Zellen (natürliche Killer-T-Zellen) entsprechen. Zur Abklärung einer T‑LGL-Leukämie sind somit eine T‑Zell-Rezeptor-PCR (Polymerasekettenreaktion) und eine Durchflusszytometrie (oder mindestens ein Blutausstrich) nötig. Das Vorhandensein von klonalen T‑Zellen alleine ist meist nicht pathologisch. Abzugrenzen ist ein Felty-Syndrom (bestehend aus der klinischen Trias Arthritis, Leukopenie, Splenomegalie), das die beiden genannten T‑LGL-Leukämie-Kriterien nicht fordert. Für die Therapie der beiden Entitäten (bei zugrunde liegender RA) stehen Methotrexat und bei unzureichender Wirksamkeit Rituximab zur Verfügung.