Anemia in elderly rheumatoid arthritis patients: a cohort study.

Introduction: Anemia is common in elderly patients with rheumatoid arthritis (RA). This study aimed to evaluate the current status and influencing factors of anemia in RA patients, to provide insights for clinical RA treatment and care. Material and methods: This study included elderly patients with high RA activity treated in our hospital from June 1, 2021 to December 31, 2022 for analysis. The characteristics of RA patients were analyzed. Pearson correlation and logistic regression analysis were conducted to analyze the influencing factors of anemia in elderly patients with RA. Results: A total of 285 RA patients were included. The incidence of anemia in high RA activity patients was 62.46%. There were significant differences in the course of RA, hemoglobin (Hb), low-density lipoprotein cholesterol (LDL-C), platelet/lymphocyte rate (PLR) and albumin (Alb) between RA patients with anemia and without anemia (all p < 0.05). Pearson correlation analysis indicated that course of RA (r = 0.522), Hb (r = 0.797), LDL-C (r = 0.558), PLR (r = 0.615) and Alb (r = 0.604) were correlated with anemia in patients with high RA activity (all p < 0.05). Logistic regression analysis indicated that course of RA ≥ 8 years (OR = 2.584, 95% CI: 1.822-3.647), LDL-C ≤ 2.8 mmol/l (OR = 3.202, 95% CI: 2.804-3.431), PLR ≥ 8 (OR = 2.183, 95% CI: 1.744-2.457), Alb ≤ 35 g/l (OR = 1.716, 95% CI: 1.401-2.006) were the risk factors of anemia in elderly patients with high RA activity (all p < 0.05). Conclusions: Anemia in elderly patients with high RA activity is closely related to the course of RA, LDL-C, PLR and Alb. Close attention should be paid to the monitoring of those indicators to take early intervention measures to improve the prognosis of RA patients.

LncRNA HOTTIP promotes inflammatory response in acute gouty arthritis via miR-101-3p/BRD4 axis.

INTRODUCTION: Acute gouty arthritis (AGA) is characterized by the accumulation of pro-inflammatory factors. This research aimed to examine the regulation of long non-coding RNA HOXA distal transcript antisense RNA (HOTTIP) in AGA on inflammation and its potential mechanisms. METHODS: Serum levels of HOTTIP in AGA patients were examined by reverse-transcription quantitative polymerase chain reaction. The receiver operating characteristic curve was performed in the diagnosis of AGA patients. Monosodium urate (MSU) stimulation of THP-1-derived macrophages was used to establish an in vitro AGA model. Enzyme-linked immunosorbent assay was carried out to assess the levels of pro-inflammatory cytokines. Pearson correlation was applied to examine the correlation. RNA immunoprecipitation assay and dual-luciferase reporter assay were employed to identify the targeting relationship between miR-101-3p and HOTTIP or bromodomain-containing 4 (BRD4). RESULTS: HOTTIP and BRD4 were statistically overexpressed in AGA patients compared with controls, while miR-101-3p was reduced (P < 0.05). Serum HOTTIP can significantly distinguish AGA patients from healthy controls. HOTTIP bound with miR-101-3p then augmented BRD4 via a competing endogenous RNA mechanism. Additionally, HOTTIP levels were elevated in a dose-dependent manner by MSU (P < 0.05). Weakened HOTTIP significantly inhibited MSU-induced release of pro-inflammatory factors interleukin (IL)-1ß, IL-8, and transforming growth factor-α in macrophages (P < 0.05), but this inhibition was reversed by silencing miR-101-3p (P < 0.05). CONCLUSION: In short, HOTTIP contributes to inflammation via miR-101-3p/BRD4 axis, and serves as a new diagnostic biomarker. This study offers a renewed perspective on the diagnosis and treatment of AGA.

H19 is involved in the regulation of inflammatory responses in acute gouty arthritis by targeting miR-2-3p.

A great number of studies have confirmed that long noncoding RNA (lncRNA) are involved in the regulation of inflammatory response in acute gouty arthritis (AGA). This paper aimed to survey the regulatory mechanism of H19 on AGA. The expression of serum H19 in all subjects was examined by qRT-PCR. The ROC curve was used to estimate the diagnostic value of H19 for AGA. THP-1 cells were induced by MSU to establish in vitro AGA cell model. The concentrations of cytokines such as IL-1ß, IL-8, and TNF-α were tested by ELISA. Luciferase reporter gene analysis was used to verify the interaction between H19 and the 3'-UTR of miR-22-3p. Expressions of serum H19 in AGA patients were significantly higher than that in controls. The ROC curve indicated the potential of H19 as a diagnostic marker for AGA. Cell experiments revealed that the downregulation of H19 significantly inhibited the expressions of IL-1ß, IL-8, and TNF-α. The luciferase reporter gene assay manifested that miR-22-3p is the target gene of H19. And knockdown of miR-22-3p overturned the downregulation of inflammatory factors caused by H19 inhibition. H19 aggravated MSU-induced THP-1 inflammation by negatively targeting miR-22-3p, suggesting a new regulatory mechanism and potential therapeutic target for AGA.