Abstract
PurposeTo study the association between retinitis pigmentosa (RP) and the progression of diabetic retinopathy (DR).MethodsUsing the Longitudinal Health Insurance Database 2000 of Taiwan, we identified individuals with an initial diagnosis for RP during the period of 1997–2008. A non-RP comparison group, 10-fold frequency matched by sex, age, index year and the year of diabetes diagnosed, were randomly selected from the same database. The occurrence of DR was observed for all subjects until the end of 2009. The Kaplan-Meier curves were used to illustrate the cumulative probability of developing DR for the RP group and comparison groups. The hazard ratio (HR) of DR for the RP group relative to the comparison group was estimated using Cox proportional hazards model after adjusting for potential confounders.ResultsThe Kaplan-Meier curves were not statistically significant different between the RP group and the comparison group. However, the RP group had a higher cumulative probability of developing DR during the first six to seven years. The cumulative probability kept increasing and became higher in the comparison group but remained unchanged in the RP group. The HR for the RP patients comparing with the comparison group was 0.96 (95% confidence interval (CI) = 0.43–2.14). Stratified by severity, RP was associated with a non-statistically significant reduced risk of proliferative DR (PDR) (HR = 0.70, 95% CI = 0.16–3.14). The HR for non-proliferative DR (NPDR) was 1.08 (95% CI = 0.40–2.86).ConclusionIn this study, RP was not statistically significant associated with the incidence of DR.
Highlights
The capillary endothelial cells in the retina are insulin-insensitive and so cannot regulate glucose well. [12,13] Hyperglycemia hastens the production of reactive oxygen species (ROS), which leads to cell death
During the follow-up period, the incidence density of diabetic retinopathy (DR) per 1000 person-years was 28.49 in the Retinitis pigmentosa (RP) group (8 events) and 27.68 (80 events) in the comparison group; the hazard ratio (HR), adjusted for age, sex, residential area, glaucoma, cataracts, heart disease, and hypertension, was 0.96 (Table 2)
Relative to the comparison group, the HR for the RP patients was 1.08 for developing nonproliferative diabetic retinopathy (NPDR) and 0.70 for proliferative diabetic retinopathy (PDR)
Summary
Retinitis pigmentosa (RP) was first described by Donders in 1857 as an inflammatory disorder characterized by night blindness and pigmentary deposits in the retinae. [1] In 1861, Lirbreich determined this disorder to be hereditary rather than caused by inflammation and characterized PR as causing retinal ‘‘bonespicule’’ pigmentary changes, a ‘‘waxy’’ pallor of the optic disc, and attenuated retinal vessels. [2] In 1872, Landolt found this condition was primarily due to photoreceptor degeneration and the vascular change was more likely the effect rather than the cause. [3] There has been increasing evidence to support Landolt’s opinion that vasoconstriction results from increased oxygen tension due to reduced oxygen consumption by the degenerated photoreceptors as well as retinal circulation closer to the choroid in the thinned retinae [4,5,6].The incidence of diabetic retinopathy (DR) in patients with RP, in which the photoreceptor cells are apoptotic due to mutations of rhodopsin and other proteins, is very interesting from clinical and pathophysiological points of view. Hypoxia induces vascular endothelial growth factor (VEGF), which increases vascular permeability, damages endothelial cells, and causes neovascularization [10]. Based on the severity of the retinal vascular changes, DR can be categorized into an earlier nonproliferative diabetic retinopathy (NPDR) stage and a more advanced proliferative diabetic retinopathy (PDR) stage. Vascular abnormalities in the former stage include capillary nonperfusion, dot hemorrhages, and microaneurysms, while the latter stage is characterized by neovascularization. The capillary basement membrane thickens in response to hyperglycemia and causes tissue hypoxia, which induces new vessel growth [16]
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