Increased Risk of Age-Related Macular Degeneration with Chronic Hepatitis C Virus Infection: A Nationwide Population-Based Propensity Score-Matched Cohort Study in Taiwan

Abstract

Studies evaluating the association between age-related macular degeneration (AMD) risk and HCV infection are scant. In this population-based cohort study, 13,300 patients newly diagnosed as having HCV (HCV cohort) and 26,600 propensity score-matched patients without HCV (non-HCV cohort) were identified from the Taiwan National Health Insurance Research Database between 2000 and 2013. Furthermore, 1,983 patients with HCV who received pegylated interferon and ribavirin treatment (HCV-treated cohort) and propensity score-matched patients with HCV (matched at a ratio of 1:2) who did not receive this treatment (HCV-untreated cohort) were selected from the HCV cohort. Cox proportional hazards regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) associated with the risk of AMD in the HCV and non-HCV cohorts. The adjusted HR (aHR) for AMD in the HCV cohort was 1.22 (95% CI = 1.09–1.35). This significant association was observed only for nonexudative AMD (aHR = 1.22, 95% CI = 1.09–1.37). Compared with the HCV-untreated cohort, the HCV-treated cohort showed no significant association with any type of AMD (aHR = 1.07, 95% CI = 0.81–1.43). Age and sex did not modify AMD development after the exposure and treatment of chronic HCV infection. Our findings revealed that patients with chronic HCV infection had an increased risk of AMD.

Dust Storms Increase the Risk of Age-Related Macular Degeneration

“…Surprisingly, a positive and significant association between dry AMD outpatient visits 2 days after DSs appeared among people under 50 years old. Even though dry AMD is the most common type of AMD, incurring almost no vision loss, it can progress to wet AMD [ 4 , 5 , 6 ]. However, a younger age of getting dry AMD results in a sooner transition into wet AMD and a subsequent risk of visual impairment.…”

“…One is dry (also called nonexudative) AMD, and the other is wet (also called exudative) AMD. Although the latter only accounts for 10–15% of all AMD cases, wet AMD can lead to severe visual impairment and blindness, dramatically affecting an individual’s independence and quality of life [ 1 , 3 , 4 , 5 , 6 , 7 ]. Moreover, AMD treatments are costly and may not be affordable to everyone in both developed and developing countries, thus potentially imposing a substantial burden on the healthcare sector, society, and global economy.…”

Gout as a Risk Factor for Age-Related Macular Degeneration in Taiwanese Adults—A Population-Based Study in Taiwan

“…The number of patients with AMD is predicted to reach 288 million by 2040 [ 2 ]. Unfortunately, the etiology of AMD remains unknown, but risk factors include an age greater than 60, smoking, Caucasian ethnicity, obesity, the presence of comorbidities (such as cardiovascular or other systemic diseases), and a family history of or genetic predisposition to AMD [ 3 ]. AMD is clinically classified as early or late stage based on drusen size, drusen numbers, retinal pigmentation around the macula and non-macular retina, neovascularization, and outer retinal thinning.…”

“…The complement pathway, which includes CFH (Complement Factor H), CFI (Complement Factor I), C2 (Complement Component 2), CFB (Complement Component Factor B), and C3 (Complement Component 3), accounts for a large proportion of these loci, as well as (to a lesser extent) the age-related maculopathy susceptibility (ARMS2) locus, which acts through a matrix metalloproteinase inhibitor. The association between AMD and inflammation has been determined based on this hypothesis, particularly when it occurs with a background of cardiovascular disease, chronic hepatitis C, or dementia [ 3 ]. No cure has yet been found for AMD, and no treatment is available for the geographic or atrophic subtypes.…”

“…NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) is one of the key players in this response. It encodes the NOD-, LRR-, and pyrin domain-containing protein [ 3 ], which causes inflammation through a two-signal initiation system [ 9 ]. The first signal results in the galvanization of NF-κB through TLR4 and TLR2, with the formation of pro-IL-1β [ 10 ] and inflammasome elements.…”