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Br J Ophthalmol 1998;82:725-730 doi:10.1136/bjo.82.7.725
  • Original Article
    • Clinical science

Evidence that upregulation of serum IGF-1 concentration can trigger acceleration of diabetic retinopathy

  1. E Chantelau
  1. Medical Department, Heinrich-Heine-Universität Düsseldorf, Germany
  1. Ernst Chantelau, MD, PhD, Diabetesambulanz MNR-Klinik, Heinrich-Heine-Universität Düsseldorf, Postfach 10 10 07, D-40001 Düsseldorf, Germany.
  • Accepted 22 January 1998

Abstract

BACKGROUND Acute reduction of chronic hyperglycaemia can accelerate early diabetic retinopathy. In adolescent patients with Mauriac’s syndrome, this phenomenon is related to an upregulation of subnormal serum IGF-1 levels.

AIM To obtain longitudinal data on serum IGF-1 and retinopathy status in poorly controlled adult insulin dependent (type 1) diabetic patients without Mauriac’s syndrome, in whom hyperglycaemia is reduced by intensive insulin therapy.

METHODS Four patients with chronic severe insulin deficiency and early microangiopathy were studied prospectively. Changes in plasma glucose, HbA1c, serum IGF-1 levels, proteinuria, retinopathy, and clinical status were followed up closely.

RESULTS Reducing hyperglycaemia from >16 mmol/l (equivalent to HbA1c>11%) to <10 mmol/l (HbA1c <8%) within 5 months increased serum IGF-1 levels by 70–220%. While proteinuria and symptomatic neuropathy regressed, retinopathy progressed from the mild to the severe non-proliferative stage with maculopathy (n=4), and to the proliferative stage (n=1). Laser coagulation was commenced upon the appearance of sight threatening macular oedema (n=4).

CONCLUSION Upregulation of serum IGF-1 preceding retinal deterioration in these patients suggests a cause-effect relation, consistent with earlier experimental and clinical data.

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