Increased risk of sudden sensory neural hearing loss in patients with rheumatoid arthritis: a longitudinal follow-up study using a national sample cohort

Self Cite

Psoriasis is a well-known immune-mediated disease. Its autoimmune pathophysiology is consistent with the immune-mediated systemic vascular hypothesis regarding the pathogenesis of sudden sensorineural hearing loss (SSNHL). The purpose of our study was to investigate whether psoriasis affects the prevalence of SSNHL in all age groups matched by age, sex, income, and region of residence. Korean Health Insurance Review and Assessment Service-National Patient Samples were collected from 2002 to 2013. A 1:4 matched psoriasis group (n = 12,864) and control group (n = 51,456) were selected. The crude (simple) and adjusted (Charlson comorbidity index) hazard ratios (HR) for psoriasis and SSNHL were analyzed using the stratified Cox proportional hazard model. The incidence of SSNHL was significantly higher in the psoriasis group than in the control group (0.5% vs. 0.4%, p = 0.004). Psoriasis increased the risk of SSNHL (adjusted HR = 1.44, 95% confidence interval (CI) = 1.09–1.90, p = 0.010). In the stratification analysis, the incidence of SSNHL was significantly higher in the 30–59-year-old group than other group SSNHL (adjusted HR = 1.50, 95% CI = 1.06–2.12, p = 0.023). In addition, SSNHL occurred significantly more frequently in men with psoriasis (adjusted HR = 1.70, 95% CI = 1.17–2.49, p = 0.006). Psoriasis increased the risk of SSNHL, and SSNHL was more prevalent in between the age of 30–59-year-olds and men with psoriasis.

Section: Participant Selectionmentioning

confidence: 99%

Psoriasis Increases the Risk of Sudden Sensorineural Hearing Loss: A Longitudinal Follow Up Study Using a National Sample Cohort

Choi

Park

Hong

et al. 2020

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“…Age groups were divided into 5-year intervals: 50–54, 55–59, 60–64…, and 85+ years old. Income and region of residence were determined following our previous studies [ 29 , 30 ].…”

Section: Methodsmentioning

confidence: 99%

High Risk of Hip and Spinal Fractures after Distal Radius Fracture: A Longitudinal Follow-Up Study Using a National Sample Cohort

Choi

Kim

Lee

et al. 2021

The purpose of the present study was to estimate the risk of hip and spinal fracture after distal radius fracture. Data from the Korean National Health Insurance Service—National Sample Cohort were collected between 2002 and 2013. A total of 8013 distal radius fracture participants who were 50 years of age or older were selected. The distal radius fracture participants were matched for age, sex, income, region of residence, and past medical history in a 1:4 ratio with control participants. In the subgroup analysis, participants were stratified according to age group (50–59, 60–69, or ≥70 years) and sex (male or female). Distal radius fracture patients had a 1.51-fold and 1.40-fold higher incidence of hip fracture and spinal fracture in the adjusted models, respectively. Among males, patients of all ages had a significantly higher incidence of hip fracture, and those who were 50 to 69 years of age had a significantly higher incidence of spinal fracture. Among females, those older than 70 years had a significantly higher incidence of hip fracture, and patients of all ages had a significantly higher incidence of spinal fracture. Previous distal radius fracture has a significant impact on the risk of subsequent hip and spinal fractures.

“…Besides age and sex, we also considered the insurance fee and area of residence of the subjects. The common comorbidities including HT (ICD-9-CM codes 401-405) [30,31], DM (ICD-9-CM code 250) [32,33], stroke (ICD-9-CM codes 430-438) [34], head injury (ICD-9-CM codes 850-854) [22,23], CKD (ICD-9-CM code 585) [35,36], IHD (ICD-9-CM codes 410-414) [37,38], alcoholism (ICD-9-CM codes 305.0 and 303) [39,40], nicotine dependence (ICD-9-CM code 305.1) [41,42], asthma (ICD-9-CM code 493) [43][44][45], COPD (ICD-9-CM codes 490-492, 494, and 496) [46], and RA (ICD-9-CM code 714) [47] were considered as potential confounders.…”

Section: Main Outcome and Covariatesmentioning

confidence: 99%

“…Several etiological factors can cause SHL, such as loud noise [17,18], viral infection [14,19], genetic mutations [20,21], accidental events [22,23], ototoxicity [24][25][26], autoimmune diseases [27] and unknown illness-induced sudden SHL [28,29]. Several diseases such as hypertension (HT) [30,31], diabetes mellitus (DM) [32,33], stroke [34], chronic kidney disease (CKD) [35,36], ischemic heart disease (IHD) [37,38], alcoholism [39,40], nicotine dependence [41,42], asthma [43][44][45], chronic obstructive pulmonary disease (COPD) [46], and rheumatoid arthritis (RA) [47] are associated with SHL. Notably, some of these diseases can cause defects in the vascular system and microcirculation in the cochlea, subsequently resulting in hypoxia [48][49][50].…”

Section: Introductionmentioning

confidence: 99%

Increased Risk of Sensorineural Hearing Loss as a Result of Exposure to Air Pollution

Chang

Tsai

Lee

et al. 2020

Whether exposure to air pollution is associated with developing sensorineural hearing loss (SHL) remains controversial. Using data from the National Health Insurance Research Database, we recruited a total of 75,767 subjects aged older than 20 years with no history of SHL from 1998 to 2010, and they were followed up until SHL was observed, they withdrew from the National Health Insurance program, or the study ended. The subjects were evenly exposed to low-level, mid-level, and high-level carbon monoxide (CO) and nitrogen dioxide (NO2). The incidence rate ratio of SHL for patients exposed to high-level CO was 1.24 (95% confidence interval (CI) = 1.14–1.36). The NO2 pollutants increased the incidence rate ratios of SHL in mid-level NO2 and high-level NO2 exposures by 1.10 (95% CI = 1.10–1.32) and 1.36 (95% CI = 1.24–1.49) times, respectively. The adjusted hazard ratio (adj. HR) of SHL in patients exposed to high-level CO was 1.45 (95% CI = 1.31–1.59), relative to that of patients exposed to low-level CO. Compared to patients exposed to low-level NO2, patients exposed to mid-level NO2 (adj. HR = 1.40, 95% CI = 1.27–1.54) and high-level NO2 (adj. HR = 1.63, 95% CI = 1.48–1.81) had a higher risk of developing SHL. The increased risk of SHL following the increased concentrations of air pollutants (CO and NO2) was statistically significant in this study. In conclusion, the subjects’ exposure to air pollution exhibited a significantly higher risk of developing SHL in Taiwan.