Handbook of Nutrition, Diet, and the Eye

Abstract

Diabetic retinopathy (DR) results from vascular injury and leakage of blood. Genetic risk factors may play a role. Free hemoglobin is a potent oxidant protein. Haptoglobin protects from hemoglobin potential oxidative damage. Haptoglobin binds to hemoglobin during its transport and facilitates its removal from the extravascular compartment. Hp1-1, Hp2-1, and Hp2-2 differ markedly in their antioxidant ability. Patients who are Hp1-1 form dimeric haptoglobin molecules, whereas those who are Hp1-2 or Hp2-2 form multimers of two or more haptoglobin molecules. Haptoglobin multidimers are sterically hindered from binding to hemoglobin and have less access to the extravascular space. Hp2-2 genotype and diabetes mellitus may carry a higher risk of microvascular and macrovascular complications. Hp1-1 has a possible role in delaying the onset of retinopathy. Heterozygotes (Hp 2-1) are protected from both diabetes and DR. A few studies showed that haptoglobin genotype plays no role in the development or severity of proliferative retinopathy in type 2 diabetes. Type 2 diabetes may be independent of haptoglobin phenotype.