title: Diabetic retinopathy in two patients with congenital IGF-I deficiency (Laron syndrome).
abstract: OBJECTIVE
  Animal and clinical studies have shown that excessive amounts of growth hormone or insulin-like growth factor-I (IGF-I) promote the development of diabetes and diabetic retinopathy. Forthwith, we present two patients with congenital IGF-I deficiency who developed type II diabetes and subsequently retinopathy.
  
  
  METHODS
  Eighteen adult patients with classical Laron syndrome (8 males, 10 females, aged 20-62 years) were followed by us since childhood or underwent fundus photography with a Nikon NF 505 instrument. Three had been treated in childhood with IGF-I, the rest were never treated, including the two patients reported.
  
  
  RESULTS
  Two never-treated patients were diagnosed with type II diabetes (DM) at ages 39 and 41 respectively. There was no diabetes in the families. Oral treatment was followed by insulin injections. Metabolic control was not optimal and one patient developed proliferative diabetic retinopathy, necessitating laser surgery. He also has nephropathy and severe neuropathy. The other patient has background diabetic retinopathy and has developed, progressively, exudates, microaneurisms, hemorrhages and clinically significant macular edema. He also has subacute ischemic heart disease.
  
  
  CONCLUSIONS
  Our findings show that congenital IGF-I deficiency, similar to excess, causes vascular complications of DM, denoting also that vascular endothelial growth factor can induce neovascularization in the presence of congenital IGF-I deficiency.
authors.affiliation: Endocrinology and Diabetes Research Unit, Schneider Children's Medical Center, Petah Tikva, Israel. laronz@clalit.org.il
authors.forename: Zvi
authors.initials: Z
authors.lastname: Laron
authors.forename: Dov
authors.initials: D
authors.lastname: Weinberger
mesh_terms: D000328:Adult; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000235:genetics* / Q000503:physiopathology; D003930:Diabetic Retinopathy / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000172:deficiency* / Q000235:genetics*; D008297:Male; D009389:Neovascularization, Pathologic / Q000209:etiology / Q000235:genetics / Q000503:physiopathology
chemical_list: D007334:Insulin-Like Growth Factor I