Elevated long-term glycated haemoglobin precedes proliferative retinopathy and nephropathy in Type 1 (insulin-dependent) diabetic patients

Abstract

The importance of glycaemic control for the development of proliferative retinopathy and nephropathy was assessed by monitoring glycated haemoglobin for 5 years or more before the diagnosis of these complications. The study comprised Type 1 (insulin-dependent) diabetic patients diagnosed at an age less than 31 years, and with diabetes duration 25 years or less. They were followed for an average of 7.9 years with 3.3 measurements per year. Of 172 patients screened for retinopathy 60 had no retinopathy, 104 had background retinopathy, and 8 had proliferative retinopathy The mean HbAlc (95% confidence intervals) of the groups was 6.4% (6.2-6.7%), 7.3% (7.1-7.5%) and 8.9% (8.1-9.6%), respectively (p < 0.0001); the mean duration of diabetes was 12, 18, and 17 years. Of 186 patients 7 had nephropathy (albuminuria > 200 mg/l). Mean HbAlc in patients without nephropathy was 7.0% (6.8-7.1%) and in patients with nephropathy 8.8% (7.8-9.9%, p < 0.001). Mean diabetes duration was 16 years in both groups. Multiple logistic regression including mean HbAlc, age at onset, duration, sex, and hypertension, was for both proliferative retinopathy and nephropathy significant only for mean HbAlc. In all cases, proliferative retinopathy and nephropathy were preceded by poor glycaemic control over several years, suggesting that these complications are caused by poor glycaemic control.

Early changes in glomerular size selectivity in young adults with type 1 diabetes and retinopathy. Results from the Diabetes Incidence Study in Sweden

“…The association between glycemic control and development or progression of retinopathy has been described in several clinical long-term studies in patients with type 1 diabetes (Nørgaard et al 1989;Chase et al 1990;Kullberg and Arnqvist 1993;Klein, Klein and Moss 1995;Rossing et al 1998;Porta et al 2001;Lövestam-Adrian et al 2001;Voutilainen-Kaunisto et al 2001). The results in this study confirm these observations; HbA 1c levels were higher in patients with retinopathy than in patients without retinopathy.…”

“…However, as a clinical classification is uncertain (Arnqvist et al 1993;Littorin et al 1999), the results of islet antibody analysis, at diagnosis 1987-88, were used to KDISS9out.doc/WORD/WINXP/KDISStyp1_eye.sav/Torffvit2007-09-26 6 make a more accurate classification (Landin-Olsson et al 1992;Schölin et al 2004). Patients reported as having type 1 diabetes at follow-up and patients clinically considered as having type 2 or unclassifiable diabetes but displaying islet antibodies at diagnosis were all classified as having type 1 diabetes.…”

Subclinical nerve dysfunction in children and adolescents with IDDM

“…Since 1993 a DCA 2000 is used. The normal range for the HbAl~-method in use from 1986-1993 was 3.2-6.0 %, and the normal ranges for the other methods correspond well with this interval when transformed [27]. Fasting serum C-peptide [28] was examined in blood collected within a year of the examination.…”

Nerve conduction defects are retarded by tight metabolic control in type I diabetes

“…The development of nephropathy and retinopathy is delayed by modern treatment when HbA1c values are kept at <7.5% and <7.0%, respectively. 1,13 The finding that nerve dysfunction develops at lower HbA1c suggests that long-term hyperglycemia not only causes microangiopathy but may have a direct metabolic effect on nerve conduction. A decrease in MCV can be reversed after improved metabolic control, 16,19 and thus the changes observed in the present study may also be reversible.…”