Jung Sun Lee

So Hye Nam, M.D., Byeongzu Ghang, M.D., Ph.D., Jungsun Lee, M.D., Ph.D., Doo-Ho Lim, M.D., Ph.D., Soo Min Ahn, M.D., Ji Seon Oh, M.D., Ph.D., Seokchan Hong, M.D., Ph.D., Yong-Gil Kim, M.D., Ph.D., Chang-Keun Lee, M.D., Ph.D., Soo Jeong Nam, M.D., Ph.D., Bin Yoo, M.D., Ph.D.. J Rheum Dis -0001;0:. https://doi.org/10.4078/jrd.2026.0078

Jung Sun Lee, M.D., Ph.D.. J Rheum Dis -0001;0:. https://doi.org/10.4078/jrd.2025.0158

Objectives This study aimed to assess the association between obesity or changes in body mass index (BMI) and the risk of RA considering the abdominal obesity status. Methods We included individuals aged 23 to 60 who underwent a national health examination in 2012–2013 (baseline) and four years prior. Obesity was defined by a BMI ≥ 25 kg/m². The change in BMI over 4 years was divided into quartiles. Cox proportional hazard analysis was performed to assess the association of obesity and BMI change with the risk of RA. Results A total of 6,207,246 subjects were included, and 7,859 incident cases of RA were identified. Obesity was associated with a reduced risk of RA in males (HR 0.78, 95% CI 0.71–0.85) and females (HR 0.91, 95% CI 0.85–0.97). In subgroup analysis according to abdominal obesity status, the associations were observed for obesity with normal waist circumference (WC) in males (HR 0.75, 95% CI 0.67–0.84) and females (HR 0.88, 95% CI 0.81–0.95). In terms of BMI change, compared to the stable BMI group (quartile 2), the third (HR 0.92, CI 0.85–0.99) and highest quartile (HR 0.89, CI 0.83–0.96) showed an inverse association with the risk of RA in females, particularly in those with normal WC. Conclusion Obesity was associated with a lower risk of RA, especially among individuals with a normal WC. Increased BMI was also associated with a lower risk of RA, but this association was mainly observed in females and specifically for those with normal WC.

Background: Several studies have identified factors associated with the development of interstitial lung disease (ILD) in patients with idiopathic inflammatory myopathies (IIMs). However, few have assessed the association between ILD and muscle biopsy findings, including inflammatory marker expressions analyzed using immunohistochemistry (IHC). Methods: Muscle biopsies from patients who were newly diagnosed with IIMs between 2000 and 2017 were reviewed. ILD was diagnosed based on chest computed tomography findings at the time of diagnosis of IIMs. IHC staining was performed for CD3, CD4, CD8, CD20, CD68, CD163, MX1, MHC class I, and HLA-DR. The factors associated with the presence of ILD were evaluated by logistic regression analysis. Results: Of the 129 patients with IIM, 49 (38%) had ILD. In the muscle biopsy findings, CD4 expression, MX1 expression on immune cells, and expression of MHC class I and HLA-DR on myofibers were more common in patients with ILD than those without. In the logistic regression analysis, the HLA-DR expression on myofibers was significantly associated with the risk of ILD (OR, 2.39; 95% CI, 1.24–4.90, p = 0.012) after adjusting for pathologic findings, clinical features, and autoantibodies. Conclusion: The expression of HLA-DR on myofibers was associated with the presence of ILD in patients with IIM.

Objectives: To investigate the frequency of monosodium urate (MSU) crystal deposits on dual-energy computed tomography (DECT) in patients with clinical diagnosis of gout and the factors associated MSU crystal positivity. Methods: This study was conducted in patients with clinical diagnosis of gout who underwent DECT. Clinical features were compared between patients with positive and those with negative DECT results. A logistic regression analysis was performed to determine the factors associated with MSU crystal positivity on DECT. Results: A total of 148 patients with clinical diagnosis of gout were included, and MSU crystal deposition on DECT was observed in 64 patients (43.3%). The patients with positive DECT results were more likely to have renal insufficiency, longer disease duration, and higher serum urate level than those with negative. In the multivariable analysis, first gout attack (odds ratio 0.462; 95% confidence interval 0.229–0.931, p = 0.031) was associated with a less likely MSU crystal deposit-positive DECT result. In the subgroup analysis of patients with first attack, serum urate level > 8 mg/dL was associated with DECT positivity. Conclusion: Of the patients with clinical diagnosis of gout, those with renal insufficiency, longer disease duration, and high serum urate level were more likely to be positive of gout on DECT. First gout attack was associated with less likely to be positive for MSU crystal on DECT. Thus, performing DECT scan in the selected patients who had characteristics that highly probability of DECT positivity could increase positive predictive value.

Background: Patients with ankylosing spondylitis (AS) have increased levels of protein phosphatase magnesium-dependent 1A (PPM1A) and autoantibodies. We evaluated the usefulness of serum anti-PPM1A antibodies as a biomarker for AS. Methods: Serum samples from 58 AS patients were obtained from a multicenter registry prior to the initiation of anti-TNF agents. The serum levels of anti-PPM1A antibodies were measured using ELISA. Spinal radiographic progression was defined as an increase in the modified stoke ankylosing spondylitis spinal score (mSASSS) by ≥2 units or a newly developed syndesmophyte. The role of exogenous PPM1A on bone mineralization was evaluated using primary osteoprogenitors acquired from patients with AS and non-inflammatory controls. Results: The baseline levels of anti-PPM1A antibodies and mSASSS were higher in the radiographic progression group than in the non-progression group. In logistic regression analysis, baseline mSASSS and serum anti-PPM1A antibodies were associated with a higher risk of progression. The level of anti-PPM1A antibodies for predicting progression had an AUC of 0.716 (cut-off value: 43.77 ng/mL). PPM1A stimulation increased matrix mineralization in AS-osteoprogenitors but not in controls. Conclusion: Along with mSASSS, the serum levels of anti-PPM1A antibodies might be useful as a predictor of radiographic progression after treatment with anti-TNF agents.

There are limited studies regarding the safety of methotrexate (MTX) in patients with reduced renal function. This study aimed to investigate methotrexate (MTX)-related toxicity in patients with rheumatoid arthritis (RA) and renal dysfunction. This retrospective cohort study included patients with RA and renal dysfunction. Renal dysfunction was defined as an estimated glomerular filtration rate (eGFR) of < 60 mL/min/1.73 m². We classified the patients into two groups according to the onset of renal dysfunction: newly and previously developed group. MTX-associated toxicity included renal toxicity, hepatotoxicity, serious infection, pancytopenia, leukopenia, thrombocytopenia and mucositis. Cox analysis was performed to determine the factors associated with toxicity. The study included 120 patients with RA and renal dysfunction receiving MTX (66: newly developed; 54: previously developed). The median eGFR was 52.1 mL/min/1.73 m² [IQR 47.1–57.3]. Thirty-five patients (29.2%) experienced toxicity, and the median time to toxicity events was 23 months (IQR 10–57). Toxicity was distributed as follows: leukopenia (10%, 12/120), renal toxicity (5.8%, 7/120), hepatotoxicity (7.5%, 9/120), serious infection (8.3%, 10/120), pancytopenia (5.0%, 6/120), thrombocytopenia (5.8%, 7/120), and mucositis (5.8%, 7/120). The toxicity rate did not differ significantly between newly and previously developed group [23/66 (34.8%) vs. 12/54 (22.2%), P = 0.130]. Multivariate analysis revealed that hydroxychloroquine use (HR 0.425, 95% CI 0.212–0.853, P = 0.016), baseline eGFR (HR 0.938, 95% CI 0.890–0.988, P = 0.015) and being female (HR 10.538, 95% CI 1.375–80.793, P = 0.023) were associated with MTX-related toxicity. Toxicity occurred in approximately 30% of patients with RA and renal dysfunction receiving MTX treatment. Hydroxychloroquine use exhibited a protective effect against MTX-associated toxicity development.

A substantial portion of gout patients have normal serum urate levels during an acute attack but data on the clinical characteristics and risk of recurrence compared with hyperuricemic patients are limited. In this retrospective cohort study, clinical features of normouricemic and hyperuricemic patients were compared. Multivariate analysis was performed to determine whether normouricemic patients were less likely to have a recurrent attack. Among a total of 221 gout patients, 88 (39.8%) had normouricemia during an acute attack. Postsurgical gout (22.7% vs. 6.0%, p < 0.001), hemodialysis initiation (9.1% vs. 2.3%, p = 0.029) and inflammatory activity were higher in normouricemic patients than in hyperuricemic patients. The frequency of renal insufficiency was lower in normouricemic patients (25.0% vs. 53.4%, p < 0.001). However, the recurrence rate of gout attack was not different between the two groups (24.7% vs. 33.0%, p = 0.220). In multivariate analysis, female sex, history of urinary stone, presence of tophi, and use of thiazide were associated with increase of recurrent gout attack, but not with serum urate status during an acute attack (hazard ratio, 1.075; 95% confidence interval, 0.972 to 1.190; p = 0.159). Normouricemia during an acute gout attack was more frequently observed in postsurgical episodes, hemodialysis initiation and patients with preserved renal function. While higher inflammatory activity was observed in normouricemic patients, recurrent attack was not associated with serum urate levels during an acute attack. Thus, careful follow-up should be considered in gout patients regardless of serum urate levels during an acute attack.

We aimed to determine whether tumor necrosis factor inhibitors (TNFi) have beneficial effects on bone mineral density (BMD) in rheumatoid arthritis (RA) patients with osteoporosis receiving bisphosphonate. A total of 199 RA patients, who were newly diagnosed with osteoporosis and receiving bisphosphonate between January 2005 and March 2017, were reviewed. Changes in BMD after 1 year were compared between patients treated with and without TNFi. The inverse probability of treatment weighting (IPTW) method using the propensity score was performed to minimize confounding factors, and logistic regression analysis was applied to identify any factors associated with significant BMD improvement (≥ 3%) at the lumbar spine and femur neck. Among patients receiving bisphosphonate, 29 were exposed to TNFi, and 170 patients were not exposed. The percentage change in BMD and the proportion of significant improvements at the lumbar spine and femur neck were similar between patients treated with and without TNFi, before and after IPTW adjustment. In addition, the disease activity score 28 (DAS28) with three variables [adjusted odds ratio (OR) 0.741, 95% confidence interval (CI) 0.592–0.927, p = 0.009] and cumulative steroid dose (adjusted OR 0.639, 95% CI 0.480–0.851, p = 0.002) were inversely associated with an improvement in BMD. Conversely, TNFi use was not associated with any improvement in BMD after adjustment by IPTW using the propensity score. TNFi did not influence BMD improvement in RA patients with osteoporosis receiving bisphosphonate, suggesting that TNFi cannot be considered as a preferred therapeutic option for increasing BMD.