{"id":"01f1a809dfca","type":"article","url":"https://hartvaat.nl/2020/02/11/haptoglobinefenotype-wijzigt-het-effect-van-intensieve-glycemische-controle-op-c/","title":"Haptoglobinefenotype wijzigt het effect van intensieve glycemische controle op CV-uitkomsten","title_en":"Haptoglobin Phenotype Modifies the Influence of Intensive Glycemic Control on Cardiovascular Outcomes.","category":"preventie","category_label":"Preventie","professions":["cardioloog","internist"],"tags":["diabetes-type-2","select-trial"],"journal":"Journal of the American College of Cardiology","doi":"10.1016/j.jacc.2019.11.051","source_url":"https://doi.org/10.1016/j.jacc.2019.11.051","authors":["Allie S Carew","Andrew P Levy","Henry N Ginsberg","Steven Coca","Orit Lache","Thomas Ransom","Robert Byington","Eric B Rimm","John Sapp","Martin Gardner","Leah E Cahill"],"significance":5,"published":"2020-02-11","source_date":"2020-02-11","image":"","kennis":["https://hartvaat.nl/kennis/cardiometabool/diabetes-type-1-en-hart/","https://hartvaat.nl/kennis/cardiometabool/diabetes-en-cardiovasculair-risico/"],"congress":"","summary_en":"This study showed that haptoglobin phenotype modifies the cardiovascular benefit of intensive glycemic control in diabetes, identifying a pharmacogenomic factor that may explain the variable outcomes of glucose-lowering trials.","created":"2026-07-03T10:28:25Z","updated":"2026-07-03T13:27:36Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Studie die aantoont dat het haptoglobinefenotype het cardiovasculaire effect van intensieve glycemische controle bij diabetes modificeert.","abstract_original":"BACKGROUND: Whereas there exists a direct relationship between glycated hemoglobin and cardiovascular disease (CVD), clinical trials targeting glycated hemoglobin to near-normal levels using intensive therapy have failed to prevent CVD and have even increased mortality, making clinical decision making difficult. A common polymorphism at the haptoglobin (Hp) genetic locus is associated with CVD, especially coronary heart disease, in the setting of hyperglycemia. OBJECTIVES: This study sought to determine whether the treatment difference of intensive versus standard glucose-lowering therapy on risk of CVD events in the ACCORD (Action to Control Cardiovascular Risk in Diabetes) study depended on Hp phenotype. METHODS: Hp phenotype was measured within 5,806 non-Hispanic white ACCORD participants using a validated assay. Adjusted hazard ratios (aHR) with 95% confidence intervals (CI) estimated from stratified Cox regression models were used to quantify the association between intensive therapy and incident CVD for the 2 different Hp phenotype groups (Hp2-2, Hp1 carriers). RESULTS: Compared with standard therapy, intensive therapy was associated with a lower risk of incident coronary heart disease among participants with the Hp2-2 phenotype (n = 2,133; aHR: 0.71; 95% CI: 0.55 to 0.91; p = 0.006), but not among the other 2 phenotypes (Hp1 allele carriers) (n = 3,673; aHR: 0.95; 95% CI: 0.79 to 1.13; p = 0.550). The same pattern was observed for CVD. Conversely, intensive therapy was associated with an increased risk of fatal CVD (aHR: 1.50; 95% CI: 1.00 to 2.25; p = 0.049) and total mortality (aHR: 1.40; 95% CI: 1.08 to 1.81; p = 0.011) among the Hp1 carriers, whereas this risk was not increased in the Hp2-2 phenotype (fatal CVD: aHR: 1.02; 95% CI: 0.59 to 1.77; p = 0.931; total mortality: aHR: 0.98; 95% CI: 0.68 to 1.41; p = 0.908). CONCLUSIONS: Intensive glucose-lowering therapy was effective at preventing incident coronary heart disease and CVD events in ACCORD study participants with the Hp2-2 phenotype but not in Hp1 carriers, who had increased mortality risk from intensive therapy."}