Dataset Information

Age at onset and the risk of proliferative retinopathy in type 1 diabetes.

ABSTRACT:

Objective

Age at onset of type 1 diabetes influences the risk of microvascular complications. However, the long-term risk of proliferative retinopathy within the wide spectrum of age at onset of type 1 diabetes is less well known.

Research design and methods

A sample of 1,117 consecutively recruited patients was drawn from the FinnDiane Study population (4,800 patients). Type 1 diabetes was defined as age at onset ResultsThe mean durations to proliferative retinopathy were 24.3 (22.7-25.9) years in the 0-4 years group, 20.1 (19.2-21.1) years in the 5-14 years group, and 21.6 (19.8-23.3) years in the 15-40 years group (P < 0.001). In a Cox regression model, with A1C, blood pressure, sex, and BMI as covariates, the highest risk of proliferative retinopathy was observed in the 5-14 years group (hazard ratio 1.90 [95% CI 1.45-2.48], P < 0.001). Diabetes onset 0-4 vs. 5-14 years made no difference in the long-term risk of proliferative retinopathy (P = 0.2). When split into two groups, age at onset <15 years was associated with a higher long-term risk than age at onset >or=15 years (1.82 [1.40-2.36], P < 0.001).

Conclusions

Age at onset significantly modifies the long-term risk of proliferative retinopathy. The highest risk is in age-at-onset group 5-14 years, whereas the lowest risk is in age-at-onset group 15-40 years.

SUBMITTER: Hietala K

PROVIDER: S-EPMC2875446 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Age at onset and the risk of proliferative retinopathy in type 1 diabetes.

Hietala Kustaa K Harjutsalo Valma V Forsblom Carol C Summanen Paula P Groop Per-Henrik PH

Diabetes care 20100225 6

<h4>Objective</h4>Age at onset of type 1 diabetes influences the risk of microvascular complications. However, the long-term risk of proliferative retinopathy within the wide spectrum of age at onset of type 1 diabetes is less well known.<h4>Research design and methods</h4>A sample of 1,117 consecutively recruited patients was drawn from the FinnDiane Study population (4,800 patients). Type 1 diabetes was defined as age at onset <or=40 years, insulin treatment initiated within 1 year, and C-pept ...[more]

PMID: 20185730

Similar Datasets

Project description:BackgroundType 2 diabetes diagnosed during youth and early adulthood is aggressive and associated with a high burden of vascular complications. The increase in complications is often attributed to long disease duration and poor metabolic control. Whether people with young-onset type 2 diabetes are inherently more susceptible to long-term complications than those diagnosed in later adulthood is unclear.MethodsProspective data from 3322 individuals, diagnosed between the age of 15 and 70 years and collected 10-25 years after diabetes diagnosis, were analysed. The cross-sectional associations between age at diagnosis and microvascular and macrovascular complications were analysed using logistic regression models, adjusted for duration of diabetes exposure and metabolic risk factors including blood pressure, cholesterol and updated mean HbA1c .ResultsThe prevalence of retinopathy was highest in those with young-onset type 2 diabetes (diagnosed at age 15 to <40 years). After 10-15 years' diabetes duration, the adjusted odds ratio for retinopathy in this population was 2.8 (95% CI 1.9-4.1; reference group those diagnosed at 60 to <70 years of age). The odds of retinopathy remained higher in people with young-onset type 2 diabetes after longer durations of diabetes exposure; the odds decreased with increasing age at diagnosis. This pattern was not observed in models of other complications: after 10-15 years' diabetes exposure, the adjusted odds ratios for albuminuria, peripheral neuropathy and macrovascular disease in people with young-onset type 2 diabetes were 0.5 (95% CI 0.4-0.8), 0.7 (95% CI 0.5-1.1) and 0.2 (95% CI 0.1-0.3), respectively.ConclusionAfter accounting for disease duration and other important confounders, people with type 2 diabetes diagnosed in youth and early adulthood (or with a younger current age) appeared to be inherently more susceptible to retinopathy. For other complications, adjusted risk appears highest in the oldest age of diagnosis group. These data have screening and treatment target implications.

Project description:PurposeTo perform a prospective epigenome-wide association study of DNA methylation (DNAm) and 28-year proliferative diabetic retinopathy (PDR) incidence in type 1 diabetes (T1D).DesignProspective observational cohort study.ParticipantsThe Pittsburgh Epidemiology of Diabetes Complications (EDC) study of childhood-onset (< 17 years) T1D.MethodsStereoscopic fundus photographs were taken in fields 1, 2, and 4 at baseline, 2, 4, 6, 8, 16, 23, and 28 years after DNAm measurements. The photos were graded using the modified Airlie House System. In those free of PDR at baseline (n = 265; mean T1D duration of 18 years at baseline), whole blood DNAm (EPIC array) at 683 597 CpGs was analyzed in Cox models for time to event. Associations between significant CpGs and clinical risk factors were assessed; genetic variants associated with DNAm were identified (methylation quantitative trait loci [meQTLs]). Mendelian randomization was used to examine evidence of causal associations between DNAm and PDR. Post hoc regional and functional analyses were performed.Main outcome measuresProliferative diabetic retinopathy was defined as the first instance of a grade of ≥ 60 in at least 1 eye or pan-retinal photocoagulation for PDR. Follow-up time was calculated from the study visit at which DNAm data were available (baseline) until PDR incidence or censoring (December 31, 2018 or last follow-up).ResultsPDR incidence was 53% over 28-years' follow-up. Greater DNAm of cg27512687 (KIF16B) was associated with reduced PDR incidence (P = 6.3 × 10-9; false discovery rate [FDR]: < 0.01); 113 cis-meQTLs (P < 5 × 10-8) were identified. Mendelian randomization analysis using the sentinel meQTL as the instrumental variable supported a potentially causal association between cg27512687 and PDR. Cg27512687 was also associated with lower pulse rate and albumin excretion rate and higher estimated glomerular filtration rate, but its association with PDR remained independently significant after adjustment for those factors. In regional analyses, DNAm of FUT4, FKBP1A, and RIN2 was also associated with PDR incidence.ConclusionsDNA methylation of KIF16B, FUT4, FKBP1A, and RIN2 was associated with PDR incidence, supporting roles for epigenetic regulation of iron clearance, developmental pathways, and autophagy in PDR pathogenesis. Further study of those loci may provide insight into novel targets for interventions to prevent or delay PDR in T1D.Financial disclosuresProprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Dataset Information

Age at onset and the risk of proliferative retinopathy in type 1 diabetes.

Objective

Research design and methods

Conclusions

Publications

Age at onset and the risk of proliferative retinopathy in type 1 diabetes.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets