Impact of HbA(1c), Followed From Onset of Type 1 Diabetes, on the Development of Severe Retinopathy and Nephropathy: The VISS Study (Vascular Diabetic Complications in Southeast Sweden)
2015 (English)In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 38, no 2, 308-315 p.Article in journal (Refereed) Published
OBJECTIVEHbA(1c) is strongly related to the development of diabetes complications, but it is still controversial which HbA(1c) level to strive for in the treatment of type 1 diabetes. The aim of the current study was to evaluate HbA(1c), followed from diagnosis, as a predictor of severe microvascular complications and to formulate HbA(1c) target levels for treatment.RESEARCH DESIGN AND METHODSA longitudinal observation study followed an unselected population of 451 patients diagnosed with type 1 diabetes during 1983-1987 before the age of 35 years in a region of Southeast Sweden. Retinopathy was evaluated by fundus photography and nephropathy data collected from medical records. HbA(1c) was measured starting from diagnosis and during the whole follow-up period of 20-24 years. Long-term weighted mean HbA(1c) was then calculated. Complications were analyzed in relation to HbA(1c) levels.RESULTSThe incidence of proliferative retinopathy and persistent macroalbuminuria increased sharply and occurred earlier with increasing long-term mean HbA(1c). None of the 451 patients developed proliferative retinopathy or persistent macroalbuminuria below long-term weighted mean HbA(1c) 7.6% (60 mmol/mol); 51% of the patients with long-term mean HbA(1c) above 9.5% (80 mmol/mol) developed proliferative retinopathy and 23% persistent macroalbuminuria.CONCLUSIONSLong-term weighted mean HbA(1c), measured from diagnosis, is closely associated with the development of severe complications in type 1 diabetes. Keeping HbA(1c) below 7.6% (60 mmol/mol) as a treatment target seems to prevent proliferative retinopathy and persistent macroalbuminuria for up to 20 years.
Place, publisher, year, edition, pages
American Diabetes Association , 2015. Vol. 38, no 2, 308-315 p.
Endocrinology and Diabetes
IdentifiersURN: urn:nbn:se:liu:diva-114569DOI: 10.2337/dc14-1203ISI: 000348461400032PubMedID: 25510400OAI: oai:DiVA.org:liu-114569DiVA: diva2:791631
Funding Agencies|Swedish Child Diabetes Foundation (Barndiabetesfonden); Medical Research Council of Southeast Sweden (Forskningsradet I Sydostra Sverige)2015-03-022015-02-262016-03-29Bibliographically approved