PURPOSE: There are 2 common alleles for Hp (Hp-1 and Hp-2) and 3 common Hp genotypes: Hp1-1, Hp2-1, and Hp2-2. The haptoglobin genotype may play a dual role in morbidities of diabetes: Hp1-1, protective and Hp2-2, provocative. This study investigated the possible association of haptoglobin genotypes with onset of retinopathy in Type 2 diabetes (DM2). METHODS: The sample included 98 consecutive adults with DM2 under routine outpatient follow-up from 2007 to 2009 who met the criteria for either no retinopathy at ≥10 years after diagnosis (Group 1) or proliferative retinopathy at ≤10 years after diagnosis (Group 2). Blood samples were collected for haptoglobin genotyping by polymerase chain reaction. Findings were compared between and within groups. RESULTS: Eighty-four patients had no retinopathy and 14 had early proliferative retinopathy. The distributions of the Hp genotypes were as follows: no-retinopathy group: 28.6% Hp1-1, 35.7% Hp2-1, and 35.7% Hp2-2 and proliferative retinopathy group: 22.6% Hp1-1, 27.4% Hp2-1, and 50% Hp2-2 (NS). On statistical analysis (limited to the larger no-retinopathy group), a predominance of Hp1-1 was noted in older patients; Hp2-2 was associated with an increased rate of stroke. CONCLUSION: The Hp genotype apparently plays no role in the development or worsening of proliferative retinopathy in DM2. Hp1-1 may be involved in delaying the onset of diabetes. Hp2-2 may pose a microvascular risk.
PURPOSE: There are 2 common alleles for Hp (Hp-1 and Hp-2) and 3 common Hp genotypes: Hp1-1, Hp2-1, and Hp2-2. The haptoglobin genotype may play a dual role in morbidities of diabetes: Hp1-1, protective and Hp2-2, provocative. This study investigated the possible association of haptoglobin genotypes with onset of retinopathy in Type 2 diabetes (DM2). METHODS: The sample included 98 consecutive adults with DM2 under routine outpatient follow-up from 2007 to 2009 who met the criteria for either no retinopathy at ≥10 years after diagnosis (Group 1) or proliferative retinopathy at ≤10 years after diagnosis (Group 2). Blood samples were collected for haptoglobin genotyping by polymerase chain reaction. Findings were compared between and within groups. RESULTS: Eighty-four patients had no retinopathy and 14 had early proliferative retinopathy. The distributions of the Hp genotypes were as follows: no-retinopathy group: 28.6% Hp1-1, 35.7% Hp2-1, and 35.7% Hp2-2 and proliferative retinopathy group: 22.6% Hp1-1, 27.4% Hp2-1, and 50% Hp2-2 (NS). On statistical analysis (limited to the larger no-retinopathy group), a predominance of Hp1-1 was noted in older patients; Hp2-2 was associated with an increased rate of stroke. CONCLUSION: The Hp genotype apparently plays no role in the development or worsening of proliferative retinopathy in DM2. Hp1-1 may be involved in delaying the onset of diabetes. Hp2-2 may pose a microvascular risk.