The Case for Biennial Retinopathy Screening in Children and Adolescents

Response to Maguire et al.

I have read the article by Maguire et al. (1) with interest. In a large, longitudinal cohort of type 1 diabetic children and adolescents, the study describes the natural history and prevalence of retinopathy. Although not the main focus of the article, their data also highlight two important points. First, Maguire et al. highlight the relationship between puberty and microvascular complications, as evidenced by the significantly increased incidence of retinopathy after 2 years’ follow-up in subjects aged >11 years and after 5 years’ follow-up in subjects aged <11 years. These findings were independent of glycemic control. Second, the study reveals that in 136 subjects with evidence of retinopathy at outset, 64 (47%) regressed, after a median of 3.1 years, to either lower-grade retinopathy or to normal at the end of follow-up, although the median age at which this occurs is not given.

These data are comparable to the natural history of microalbuminuria as described in longitudinal studies of children and adolescents, including the Oxford Regional Prospective Study in the U.K. (2). In this study, puberty (using age 11 years as a surrogate marker for onset of puberty) conferred a threefold increased risk of microalbuminuria, independent of poor glycemic control, and these data have been in part confirmed by previous studies from Couper et al. (3). This may relate in part to pubertal hormonal variables, as recent evidence suggests that microalbuminuria risk in this age-group is associated with growth hormone hypersecretion and insulin resistance, particularly in females (4). Furthermore, in ∼60% of subjects, microalbuminuria subsequently regressed, and in these subjects compared with those with persistent microalbuminuria, mean HbA_1c levels were similar before onset of microalbuminuria (median age 15.8 years) but were lower thereafter. Thus, adolescent subjects with regression may be individuals in whom microalbuminuria initially manifests during the poor glycemic control and insulin resistant state associated with puberty but demonstrate regression when glycemic control improves in the postpubertal period. One may hypothesize that microalbuminuria may subsequently reappear in these “at risk” subjects in later life; however, this remains unproven.

These same mechanisms may apply to the pathogenesis and natural history of retinopathy during adolescence. We hope Maguire et al. will further detail the demographic details and risk factors for progression and regression of retinopathy, as adequate longitudinal data in this age-group are currently lacking.