Nonthyroidal illness syndrome (NTIS), also known as low triiodothyronine (T3) syndrome, frequently affects patients with systemic lupus erythematosus (SLE) and may affect lipid metabolism. Dyslipidemia is highly prevalent and associated with the long-term prognosis of SLE. The aim of the present study was to explore the clinical significance of NTIS on disease activity and dyslipidemia in patients with SLE. Clinical and laboratory data were collected retrospectively from 223 patients with SLE. The correlation between free triiodothyronine (FT3), SLE disease activity, and lipid profiles were estimated. The correlation coefficient (r) was calculated using a Pearson’s regression model. Univariate and multivariate logistic regression analyses were performed to identify the risk factors for dyslipidemia in SLE. Serum FT3 levels were negatively correlated with the levels of 24 h urine protein (UP), blood urea nitrogen (BUN), creatinine (Cr) and SLE disease activity index (SLEDAI) (all p < 0.001) in NTIS patients but not in euthyroid patients. ApoB/ApoA1 was significantly correlated with SLEDAI (p < 0.01) in NTIS patients and CRP (p < 0.001) and ESR (p < 0.01) in euthyroid patients. A multivariate analysis revealed that only FT3 exhibited an independent negative association with dyslipidemia (P = 0.01; OR = 0.48; 95% CI 0.27–0.85). NTIS frequently occurs in patients with SLE. Low FT3 is associated with disease activity in SLE patients complicated with NTIS. Low FT3 is an independent risk factor for dyslipidemia in patients with SLE.

To evaluate the clinical significance of the HScore and MS score in the prognosis of anti-melanoma differentiation-associated gene 5 (MDA5) positive patients with dermatomyositis (DM) and interstitial lung disease (ILD). The clinical features as well as HScore and MS score were compared between the survivors (n = 61) and nonsurvivors (n = 36) among 97 anti-MDA5-positive DM-ILD patients. Potential prognostic factors were analysed. Compared with survivors, nonsurvivors had significantly older age, tended to be male, and had a significantly higher frequency of fever at disease onset, higher levels of aspartate transaminase, lactate dehydrogenase, and serum ferritin, as well as higher values of HScore and MS score but had a significantly lower frequency of arthritis at disease onset. Multivariate analysis revealed that age ≥50 years [hazard ratio (HR) = 2.70, p = .040, 95% confidence interval (CI) 1.05–6.97)], male gender (HR = 3.20, p = .017, 95% CI 1.23–8.28), and higher HScore (HR = 3.72, p = .003, 95% CI 1.56–8.86) were independent risk factors for mortality. Patients with more risk factors had significantly poorer survival (p < .001). Older age, high HScore, and male gender are risk factors for poor survival among anti-MDA5-positive DM-ILD patients, suggesting the potential role of macrophage activation in the pathogenesis.

Neutrophils respond rapidly to inflammation and infection via defense mechanisms, including degranulation, reactive oxygen species production, and neutrophil extracellular trap formation (known as "NETosis"). As the most abundant neutrophil components, granule proteins constitute the major mediators of neutrophil effector functions and likely orchestrate their functional diversity. However, a systematic profile of these proteins, particularly their temporal release dynamics during inflammatory responses, remains uncharacterized. Here, we performed a "multistate" proteomic study to explore circulating neutrophils' dynamic responses to diverse infectious and inflammatory signals over time. Circulating neutrophils exhibited both conserved and stimulus-specific protein expression programs. Through integrated characterization of the cellular and secretory proteome landscapes, we delineated the release patterns of canonical granule proteins and identified inflammatory mediators, including soluble membrane receptors. Notably, granule membrane receptors were translocated to the cell surface and shed via proteolytic cleavage, highlighting their dynamic regulation and diversity. These findings revealed the complexity of the neutrophil degranulation program, demonstrating its stimulus-dependent and temporally layered nature. Our study provides a functional atlas of neutrophil degranulation upon inflammation, which would strengthen our understanding of neutrophil activation in inflammation and facilitate the exploration of inflammation management therapies.

Dear Editor, OA is classically considered as a non-inflammatory degenerative joint disease [ 1]. However, accumulating evidence suggests that the presence of inflammatory features in synovium occurs in up to 21% of patients with OA [ 2]. The inflammatory phenotype is characterized by evident synovitis and increased proinflammatory factors [ 3]. Generally, the effective treatments for OA are very scarce. As the first-line pharmacologic choice for knee OA, NSAIDs are inadequate for the control of the inflammation and the disease progression of inflammatory OA. Neither TNF inhibitor nor IL-1 inhibitor have shown clinical efficacy in inflammatory OA [ 4, 5]. A Janus kinase (JAK) 2 inhibitor was demonstrated to protect cartilage damage in an OA model, indicating that the JAK pathway might be a potential target in OA treatment [ 6]. Baricitinib, a highly selective JAK1 and JAK2 inhibitor, can block the signals of a wide array of proinflammatory cytokines. Based on the pathologic characteristics of inflammatory knee OA, we conducted a prospective, single-centre, open-label clinical study (Chinese Clinical Trial Registry number, ChiCTR2100050394) to evaluate the efficacy of baricitinib in inflammatory knee OA refractory to NSAIDs. The study had been approved by the ethics committee of Shanghai sixth people’s hospital. [No. 2020–244-(1)].