Background/Aims: This nationwide cohort study aimed to evaluate (1) whether primary Sjogren’s syndrome (pSS) can contribute to the development of dementia and (2) whether the use of hydroxychloroquine (HCQ) can decrease the incidence of dementia in patients with pSS using the Health Insurance Review and Assessment database. Methods: We established a cohort between 2008 and 2020 of 20,160 patients with pSS without a history of dementia. The control group comprised sex- and age-matched individuals with no history of autoimmune disease or dementia. Cox proportional hazard analyses were performed to identify the association between pSS and dementia development. We also assessed the hazard ratio (HR) of dementia in early users of HCQ (within 180 days of the diagnosis of pSS) compared to non-users, adjusted for age, sex, and comorbidities. Results: The incidence of dementia was 0.68 (95% CI 0.64–0.72) cases per 100 person-years in pSS, and it was 0.58 (0.56–0.60) in the controls. The adjusted HR (aHR) of developing dementia was 1.16 (1.09–1.25) times greater in the pSS group than in the controls. The risk of dementia did not increase in HCQ users (aHR 1.07 [0.94–1.21]), but HCQ non-users had a 1.22 (1.12–1.33) higher risk of developing dementia than the matched controls. The use of HCQ lowered the risk of dementia in comparison with non-users in patients with pSS (aHR 0.82 [0.71–0.94]). Conclusions Our results suggest that pSS is associated with an increased risk of dementia. HCQ may prevent dementia in patients with pSS.

Background/Aims: This nationwide cohort study aimed to evaluate (1) whether primary Sjogren’s syndrome (pSS) can contribute to the development of dementia and (2) whether the use of hydroxychloroquine (HCQ) can decrease the incidence of dementia in patients with pSS using the Health Insurance Review and Assessment database. Methods: We established a cohort between 2008 and 2020 of 20,160 patients with pSS without a history of dementia. The control group comprised sex- and age-matched individuals with no history of autoimmune disease or dementia. Cox proportional hazard analyses were performed to identify the association between pSS and dementia development. We also assessed the hazard ratio (HR) of dementia in early users of HCQ (within 180 days of the diagnosis of pSS) compared to non-users, adjusted for age, sex, and comorbidities. Results: The incidence of dementia was 0.68 (95% CI 0.64–0.72) cases per 100 person-years in pSS, and it was 0.58 (0.56–0.60) in the controls. The adjusted HR (aHR) of developing dementia was 1.16 (1.09–1.25) times greater in the pSS group than in the controls. The risk of dementia did not increase in HCQ users (aHR 1.07 [0.94–1.21]), but HCQ non-users had a 1.22 (1.12–1.33) higher risk of developing dementia than the matched controls. The use of HCQ lowered the risk of dementia in comparison with non-users in patients with pSS (aHR 0.82 [0.71–0.94]). Conclusions Our results suggest that pSS is associated with an increased risk of dementia. HCQ may prevent dementia in patients with pSS.

Background/Aims: This nationwide cohort study aimed to evaluate (1) whether primary Sjogren’s syndrome (pSS) can contribute to the development of dementia and (2) whether the use of hydroxychloroquine (HCQ) can decrease the incidence of dementia in patients with pSS using the Health Insurance Review and Assessment database. Methods: We established a cohort between 2008 and 2020 of 20,160 patients with pSS without a history of dementia. The control group comprised sex- and age-matched individuals with no history of autoimmune disease or dementia. Cox proportional hazard analyses were performed to identify the association between pSS and dementia development. We also assessed the hazard ratio (HR) of dementia in early users of HCQ (within 180 days of the diagnosis of pSS) compared to non-users, adjusted for age, sex, and comorbidities. Results: The incidence of dementia was 0.68 (95% CI 0.64–0.72) cases per 100 person-years in pSS, and it was 0.58 (0.56–0.60) in the controls. The adjusted HR (aHR) of developing dementia was 1.16 (1.09–1.25) times greater in the pSS group than in the controls. The risk of dementia did not increase in HCQ users (aHR 1.07 [0.94–1.21]), but HCQ non-users had a 1.22 (1.12–1.33) higher risk of developing dementia than the matched controls. The use of HCQ lowered the risk of dementia in comparison with non-users in patients with pSS (aHR 0.82 [0.71–0.94]). Conclusions Our results suggest that pSS is associated with an increased risk of dementia. HCQ may prevent dementia in patients with pSS.

Background/Aims: This nationwide cohort study aimed to evaluate (1) whether primary Sjogren’s syndrome (pSS) can contribute to the development of dementia and (2) whether the use of hydroxychloroquine (HCQ) can decrease the incidence of dementia in patients with pSS using the Health Insurance Review and Assessment database. Methods: We established a cohort between 2008 and 2020 of 20,160 patients with pSS without a history of dementia. The control group comprised sex- and age-matched individuals with no history of autoimmune disease or dementia. Cox proportional hazard analyses were performed to identify the association between pSS and dementia development. We also assessed the hazard ratio (HR) of dementia in early users of HCQ (within 180 days of the diagnosis of pSS) compared to non-users, adjusted for age, sex, and comorbidities. Results: The incidence of dementia was 0.68 (95% CI 0.64–0.72) cases per 100 person-years in pSS, and it was 0.58 (0.56–0.60) in the controls. The adjusted HR (aHR) of developing dementia was 1.16 (1.09–1.25) times greater in the pSS group than in the controls. The risk of dementia did not increase in HCQ users (aHR 1.07 [0.94–1.21]), but HCQ non-users had a 1.22 (1.12–1.33) higher risk of developing dementia than the matched controls. The use of HCQ lowered the risk of dementia in comparison with non-users in patients with pSS (aHR 0.82 [0.71–0.94]). Conclusions Our results suggest that pSS is associated with an increased risk of dementia. HCQ may prevent dementia in patients with pSS.

Background/Aims: This nationwide cohort study aimed to evaluate (1) whether primary Sjogren’s syndrome (pSS) can contribute to the development of dementia and (2) whether the use of hydroxychloroquine (HCQ) can decrease the incidence of dementia in patients with pSS using the Health Insurance Review and Assessment database. Methods: We established a cohort between 2008 and 2020 of 20,160 patients with pSS without a history of dementia. The control group comprised sex- and age-matched individuals with no history of autoimmune disease or dementia. Cox proportional hazard analyses were performed to identify the association between pSS and dementia development. We also assessed the hazard ratio (HR) of dementia in early users of HCQ (within 180 days of the diagnosis of pSS) compared to non-users, adjusted for age, sex, and comorbidities. Results: The incidence of dementia was 0.68 (95% CI 0.64–0.72) cases per 100 person-years in pSS, and it was 0.58 (0.56–0.60) in the controls. The adjusted HR (aHR) of developing dementia was 1.16 (1.09–1.25) times greater in the pSS group than in the controls. The risk of dementia did not increase in HCQ users (aHR 1.07 [0.94–1.21]), but HCQ non-users had a 1.22 (1.12–1.33) higher risk of developing dementia than the matched controls. The use of HCQ lowered the risk of dementia in comparison with non-users in patients with pSS (aHR 0.82 [0.71–0.94]). Conclusions Our results suggest that pSS is associated with an increased risk of dementia. HCQ may prevent dementia in patients with pSS.

OBJECTIVES: In this study, we sought to evaluate the association between smoking status and subclinical coronary atherosclerosis, as detected by coronary computed tomography angiography (CCTA), in asymptomatic individuals. METHODS: We retrospectively analyzed 9,285 asymptomatic participants (mean age, 53.7±8.0 years; n=6,017, 64.8% male) with no history of coronary artery disease (CAD) who had undergone self-referred CCTA. Of these participants, 4,333 (46.7%) were considered never smokers, 2,885 (31.1%) former smokers, and 2,067 (22.3%) current smokers. We assessed the degree and characteristics of subclinical coronary atherosclerosis using CCTA, with obstructive CAD defined as a diameter stenosis of at least 50%. RESULTS: Compared with never-smokers, former smokers exhibited no significant differences in the probabilities of obstructive CAD, any coronary plaque, calcified plaque, or mixed plaque, as determined using adjusted odds ratios (aORs; p>0.05 for all). However, the risk of non-calcified plaque was significantly higher in former smokers (aOR, 1.34; 95% confidence interval [CI], 1.00 to 1.78; p=0.048). Current smokers had significantly higher rates of obstructive CAD (aOR, 1.46; 95% CI, 1.10 to 1.96; p=0.010), any coronary plaque (aOR, 1.41; 95% CI, 1.20 to 1.65; p<0.001), calcified plaque (aOR, 1.32; 95% CI, 1.13 to 1.55; p=0.001), non-calcified plaque (aOR, 1.72; 95% CI, 1.28 to 2.32; p<0.001), and mixed plaque (aOR, 2.00; 95% CI, 1.39 to 2.86; p<0.001) compared to never smokers. CONCLUSIONS This cross-sectional study revealed a significant association between current smoking and subclinical coronary atherosclerosis, as detected on CCTA. Additionally, former smoking demonstrated an association with non-calcified plaque, indicating elevated cardiovascular risk.

OBJECTIVES: In this study, we sought to evaluate the association between smoking status and subclinical coronary atherosclerosis, as detected by coronary computed tomography angiography (CCTA), in asymptomatic individuals. METHODS: We retrospectively analyzed 9,285 asymptomatic participants (mean age, 53.7±8.0 years; n=6,017, 64.8% male) with no history of coronary artery disease (CAD) who had undergone self-referred CCTA. Of these participants, 4,333 (46.7%) were considered never smokers, 2,885 (31.1%) former smokers, and 2,067 (22.3%) current smokers. We assessed the degree and characteristics of subclinical coronary atherosclerosis using CCTA, with obstructive CAD defined as a diameter stenosis of at least 50%. RESULTS: Compared with never-smokers, former smokers exhibited no significant differences in the probabilities of obstructive CAD, any coronary plaque, calcified plaque, or mixed plaque, as determined using adjusted odds ratios (aORs; p>0.05 for all). However, the risk of non-calcified plaque was significantly higher in former smokers (aOR, 1.34; 95% confidence interval [CI], 1.00 to 1.78; p=0.048). Current smokers had significantly higher rates of obstructive CAD (aOR, 1.46; 95% CI, 1.10 to 1.96; p=0.010), any coronary plaque (aOR, 1.41; 95% CI, 1.20 to 1.65; p<0.001), calcified plaque (aOR, 1.32; 95% CI, 1.13 to 1.55; p=0.001), non-calcified plaque (aOR, 1.72; 95% CI, 1.28 to 2.32; p<0.001), and mixed plaque (aOR, 2.00; 95% CI, 1.39 to 2.86; p<0.001) compared to never smokers. CONCLUSIONS This cross-sectional study revealed a significant association between current smoking and subclinical coronary atherosclerosis, as detected on CCTA. Additionally, former smoking demonstrated an association with non-calcified plaque, indicating elevated cardiovascular risk.

OBJECTIVES: In this study, we sought to evaluate the association between smoking status and subclinical coronary atherosclerosis, as detected by coronary computed tomography angiography (CCTA), in asymptomatic individuals. METHODS: We retrospectively analyzed 9,285 asymptomatic participants (mean age, 53.7±8.0 years; n=6,017, 64.8% male) with no history of coronary artery disease (CAD) who had undergone self-referred CCTA. Of these participants, 4,333 (46.7%) were considered never smokers, 2,885 (31.1%) former smokers, and 2,067 (22.3%) current smokers. We assessed the degree and characteristics of subclinical coronary atherosclerosis using CCTA, with obstructive CAD defined as a diameter stenosis of at least 50%. RESULTS: Compared with never-smokers, former smokers exhibited no significant differences in the probabilities of obstructive CAD, any coronary plaque, calcified plaque, or mixed plaque, as determined using adjusted odds ratios (aORs; p>0.05 for all). However, the risk of non-calcified plaque was significantly higher in former smokers (aOR, 1.34; 95% confidence interval [CI], 1.00 to 1.78; p=0.048). Current smokers had significantly higher rates of obstructive CAD (aOR, 1.46; 95% CI, 1.10 to 1.96; p=0.010), any coronary plaque (aOR, 1.41; 95% CI, 1.20 to 1.65; p<0.001), calcified plaque (aOR, 1.32; 95% CI, 1.13 to 1.55; p=0.001), non-calcified plaque (aOR, 1.72; 95% CI, 1.28 to 2.32; p<0.001), and mixed plaque (aOR, 2.00; 95% CI, 1.39 to 2.86; p<0.001) compared to never smokers. CONCLUSIONS This cross-sectional study revealed a significant association between current smoking and subclinical coronary atherosclerosis, as detected on CCTA. Additionally, former smoking demonstrated an association with non-calcified plaque, indicating elevated cardiovascular risk.

OBJECTIVES: In this study, we sought to evaluate the association between smoking status and subclinical coronary atherosclerosis, as detected by coronary computed tomography angiography (CCTA), in asymptomatic individuals. METHODS: We retrospectively analyzed 9,285 asymptomatic participants (mean age, 53.7±8.0 years; n=6,017, 64.8% male) with no history of coronary artery disease (CAD) who had undergone self-referred CCTA. Of these participants, 4,333 (46.7%) were considered never smokers, 2,885 (31.1%) former smokers, and 2,067 (22.3%) current smokers. We assessed the degree and characteristics of subclinical coronary atherosclerosis using CCTA, with obstructive CAD defined as a diameter stenosis of at least 50%. RESULTS: Compared with never-smokers, former smokers exhibited no significant differences in the probabilities of obstructive CAD, any coronary plaque, calcified plaque, or mixed plaque, as determined using adjusted odds ratios (aORs; p>0.05 for all). However, the risk of non-calcified plaque was significantly higher in former smokers (aOR, 1.34; 95% confidence interval [CI], 1.00 to 1.78; p=0.048). Current smokers had significantly higher rates of obstructive CAD (aOR, 1.46; 95% CI, 1.10 to 1.96; p=0.010), any coronary plaque (aOR, 1.41; 95% CI, 1.20 to 1.65; p<0.001), calcified plaque (aOR, 1.32; 95% CI, 1.13 to 1.55; p=0.001), non-calcified plaque (aOR, 1.72; 95% CI, 1.28 to 2.32; p<0.001), and mixed plaque (aOR, 2.00; 95% CI, 1.39 to 2.86; p<0.001) compared to never smokers. CONCLUSIONS This cross-sectional study revealed a significant association between current smoking and subclinical coronary atherosclerosis, as detected on CCTA. Additionally, former smoking demonstrated an association with non-calcified plaque, indicating elevated cardiovascular risk.

Interstitial lung disease (ILD) is often observed in connective tissue diseases (CTDs), frequently in rheumatoid arthritis, systemic sclerosis, primary Sjögren’s syndrome, and inflammatory myositis. Early detection of ILDs secondary to rheumatic diseases is important as timely initiation of proper management affects the prognosis. Among many imaging modalities, high-resuloution computed tomography (HRCT) serves the gold standard for finding early lung inflammatory and fibrotic changes as well as monitoring afterwards because of its superior spatial resolution. Additionally, lung ultrasound (LUS) and magnetic resonance imaging (MRI) are the rising free-radiation imaging tools that can get images of lungs of CTD-ILD. In this review article, we present the subtypes of ILD images found in each CTD acquired by HRCT as well as some images taken by LUS and MRI with comparative HRCT scans. It is expected that this discussion would be helpful in discussing recent advances in imaging modalities for CTDILD and raising critical points for diagnosis and tracing of the images from the perspective of rheumatologists.