OBJECTIVE: Recently, lipoprotein(a) [Lp(a)] has been identified as a major risk factor for coronary heart disease. There are few data available on the influence of metabolic control on plasma Lp(a) concentrations in subjects with insulin-dependent diabetes mellitus (IDDM), a group at high risk for coronary heart disease. RESEARCH DESIGN AND METHODS: We examined the effects of improved metabolic control on plasma lipid and lipoproteins and Lp(a) concentrations in 12 subjects before and after 21 days of tight metabolic control. RESULTS: Glycosylated hemoglobin declined from 8.4 to 6.9% (P less than 0.001), and Lp(a) declined from 29.7 to 27.1 mg/dl (P = 0.022). There were no significant differences in total, low-density lipoprotein, or high-density lipoprotein cholesterol, although the decline in triglyceride concentrations were borderline statistically significant. The distribution of apolipoprotein(a) isoforms in IDDM patients was not unusual, and the apolipoprotein(a) isoform phenotypes did not change with improved metabolic control. Lp(a) concentrations were also significantly higher than in a population-based control group of nondiabetic subjects from the San Antonio Heart Study. CONCLUSIONS: Although the number of subjects was small and the degree of improvement in metabolic control was modest, the results suggest that improved metabolic control may decrease the risk of coronary heart disease mediated by Lp(a) in IDDM.
OBJECTIVE: Recently, lipoprotein(a) [Lp(a)] has been identified as a major risk factor for coronary heart disease. There are few data available on the influence of metabolic control on plasma Lp(a) concentrations in subjects with insulin-dependent diabetes mellitus (IDDM), a group at high risk for coronary heart disease. RESEARCH DESIGN AND METHODS: We examined the effects of improved metabolic control on plasma lipid and lipoproteins and Lp(a) concentrations in 12 subjects before and after 21 days of tight metabolic control. RESULTS: Glycosylated hemoglobin declined from 8.4 to 6.9% (P less than 0.001), and Lp(a) declined from 29.7 to 27.1 mg/dl (P = 0.022). There were no significant differences in total, low-density lipoprotein, or high-density lipoprotein cholesterol, although the decline in triglyceride concentrations were borderline statistically significant. The distribution of apolipoprotein(a) isoforms in IDDMpatients was not unusual, and the apolipoprotein(a) isoform phenotypes did not change with improved metabolic control. Lp(a) concentrations were also significantly higher than in a population-based control group of nondiabetic subjects from the San Antonio Heart Study. CONCLUSIONS: Although the number of subjects was small and the degree of improvement in metabolic control was modest, the results suggest that improved metabolic control may decrease the risk of coronary heart disease mediated by Lp(a) in IDDM.
Authors: J Q Purnell; S M Marcovina; J E Hokanson; H Kennedy; P A Cleary; M W Steffes; J D Brunzell Journal: Diabetes Date: 1995-10 Impact factor: 9.461
Authors: A Császár; H Dieplinger; C Sandholzer; I Karádi; E Juhász; H Drexel; T Halmos; L Romics; J R Patsch; G Utermann Journal: Diabetologia Date: 1993-01 Impact factor: 10.122