2010/02/26 by Gijs W.D. Landman, Gijs W Landman, Kornelis JJ van Hateren +7
Medicine · #Diabetes Treatment and Management #Diabetes, Cardiovascular Risks, and Lipoproteins #Hyperglycemia and glycemic control in critically ill and hospitalized patients
paper · pdf · doi:10.3399/bjgp10x483517
openalex publication_date 2010/02/26 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/31
BACKGROUND: The relationship between the degree of glycaemic control and mortality remains an important topic of discussion. AIM: This study aimed to investigate this relationship. DESIGN OF STUDY: Prospective cohort study. SETTING: Primary care. METHOD: A total of 1145 patients with type 2 diabetes were enrolled in the Zwolle Outpatient Diabetes project Integrating Available Care (ZODIAC) in 1998. Their survival status was recorded in September 2004. Mortality ratios were calculated using standardised mortality ratios (SMRs). Associations between haemoglobin A(1c) (HbA(1c)) levels and mortality were studied with a Cox proportional hazard model. HbA(1c) levels were studied as continuous and as categorical variables. RESULTS: A total of 335 patients died after a median follow-up period of 5.8 years. The SMR (95% confidence interval [CI]) for total mortality was 1.86 (95% CI = 1.66 to 2.06) and 2.24 (95% CI = 1.91 to 2.61) for cardiovascular mortality. For each 1% increase in HbA(1c) there was a 21% increase in the hazard ratio for total mortality. When compared with the target HbA(1c) group (HbA(1c) 6.5-7%), the group with very poor glycaemic control (HbA1c >9%) had a hazard ratio of 2.21 (95% CI = 1.42 to 3.42) for total mortality. The group with normal glycaemic control (HbA(1c) <6.5%) had a hazard ratio of 1.00 (95% CI = 0.46 to 2.19) for total mortality. CONCLUSION: HbA(1c) level was associated with mortality and this effect seemed largely attributable to patients who were in really poor glycaemic control. The absence of differences in mortality in the groups with lower HbA(1c) levels supports the position that there is no basis for continually decreasing the therapeutic target HbA(1c) level in patients with type 2 diabetes mellitus.