Objectives
Systemic rheumatic disease is characterized by autoimmunity and systemic inflammation and affects multiple organs. Few studies have investigated whether autoimmune diseases increase the risk of dementia. Herein, we evaluate the relationship between systemic rheumatic disease and dementia through a population-based study using the Korean National Health Insurance Service (NHIS) claims database.
Methods
We conducted a nationwide population-based study using the Korean NHIS database, consisting of individuals who submitted medical claims from 2002–2013. Dementia was defined as having an acetylcholinesterase inhibitors (AChEIs) prescription along with symptoms satisfying the Alzhemier’s disease (AD) International Classification of Diseases (ICD)-10 codes (F00 or G30), or vascular dementia (VaD; ICD-10 or F01) criteria. Control subjects were matched to the dementia patients by age and sex. The study group was limited to those diagnosed with rheumatic disease at least 6 months prior to diagnosis of dementia. Rheumatic disease was defined by the following ICD-10 codes: Rheumatoid arthritis (RA: M05), Sjögren’s syndrome (SS: M35), systemic lupus erythematosus (SLE: M32), and Behcet’s disease (BD: M35.2).
Results
Of the 6,028 dementia patients, 261 (4.3%) had RA, 108 (1.6%) had SS, 12 (0.2%) had SLE, and 6 (0.1%) had BD. SLE history was significantly higher in dementia patients (0.2%) than in controls (0.1%) and was associated with dementia (odds ratio [OR], 2.48; 95% confidence interval [CI], 1.19–5.15). In subgroup analysis, SLE significantly increased dementia risk, regardless of dementia type (AD: OR, 2.29; 95% CI, 1.06–4.91; VaD: OR, 4.54; 95% CI, 1.36–15.14). However, these associations were not sustained in the mild CCI or elderly group.
Conclusion
SLE was independently associated with a higher risk of dementia, including AD and VaD when compared to the control group, even after adjustment. SLE patients (<65 years old) are a high-risk group for early vascular dementia and require screening for early detection and active prevention.
Abstract1-Nitropyrene (1-NP) is a major nitro-polycyclic aromatic hydrocarbon (nitro-PAH), and a common constituent in diesel exhaust particles (DEPs). Absorbed 1-nitropyrene is partly metabolized to 1-aminopyrene and excreted in urine. Recently, the number of diesel cars has been increasing, which could be a major cause of air pollution, resulting elevated levels of traffic-related DEPs around cities. The aim of this study was to investigate the usability of 1-aminopyrene (1-AP) as a biomarker for DEP exposure by examining the association between urinary 1-AP concentration and the amount of exposure to atmospheric 1-NP. The study subjects included 65 individuals who work on vehicular roads or bus terminals. Their 24 h urine samples were collected, and atmospheric air was sampled using a personal air sampler for 24 h. Urinary 1-AP and atmospheric nitro-PAH levels were measured using a high-pressure liquid chromatography-fluorescence detector (HPLC-FD). The average urine 1-AP concentration was 0.334 pg/g creatinine. Urinary 1-AP levels were significantly correlated with 1-NP level exposure (r = 0.385, p = 0.002) but not with the other nitro-PAHs. When the subjects were classified into high-and low-exposure groups, a significant association was only found in the high exposure group (r = 0.357, p = 0.045). In conclusion, there was a significant correlation between 1-NP exposure and urinary 1-AP concentration; therefore, urinary 1-AP level could be used as an exposure biomarker for DEP.
Polycyclic aromatic hydrocarbons (PAHs) have been reported to cause oxidative stress in metabolic processes. This study aimed to evaluate the relationship between exposure to PAHs, including benzo[a]pyrene (BaP) and 1-nitropyrene (1-NP), in the atmosphere and oxidative stress levels in the human body. This study included 44 Korean adults who lived in Cheongju, South Korea. Atmospheric BaP and 1-NP concentrations and urinary 6-hydroxy-1-nitropyrene (6-OHNP), N-acetyl-1-aminopyrene (1-NAAP), and 1-hydroxypyrene (1-OHP) concentrations were measured. The oxidative stress level was assessed by measuring urinary thiobarbituric acid reactive substances (TBARS) and 8-hydroxydeoxyguanosine (8-OHdG) concentrations. Urinary TBARS and 6-OHNP concentrations significantly differed between winter and summer. BaP exposure was significantly associated with urinary 8-OHdG concentrations in summer. However, atmospheric 1-NP did not show a significant correlation with oxidative stress marker concentrations. Urinary 1-NAAP concentration was a significant determinant for urinary 8-OHdG concentration in summer. Oxidative stress in the body increases in proportion to inhalation exposure to BaP, and more 8-OHdG is produced in the body as the amount of 1-NP, which is metabolized to 1-AP or 1-NAAP, increases.
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