Abstract
Aim
This study aims to test the hypothesis that vascular dysfunction is present early in pregnancy in women with type 1 diabetes who subsequently develop preeclampsia.
Methods
Eighty-three women with type 1 diabetes of more than 10 years duration were followed up prospectively during pregnancy. External ultrasound was used to measure the dilatory response of the brachial artery to postischemic increased blood flow (endothelium-dependent, flow-associated dilatation) and to nitroglycerin (NTG) [endothelium-independent, NTG-induced dilatation (NID)] at Gestational Weeks 11 and 29. Plasma concentrations of the vascular markers vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and von Willebrand factor antigen were also measured together with 24-h urinary albumin excretion (UAE), blood pressure (BP), and HbA1C.
Results
Fourteen (17%) of the 83 women developed preeclampsia. NID was significantly impaired at Week 29 in women prone to preeclampsia (108.8±7.0% vs. 116.8±8.9%, mean±S.D., P<.05), and the plasma concentrations of VCAM-1 and ICAM-1 were significantly elevated at Gestational Week 11 (612±82 vs. 516±109 µg/l, P<.005 and 293±67 vs. 255±57 µg/l, P<.05, respectively). Women who later developed preeclampsia were also characterized by higher UAE, higher BP, and higher HbA1C than women who did not [Gestational Week 11: 194 (3–1104) vs. 7 (0–412) mg/24 h, median (range), P=.0003; 122±12/75±6 vs. 111±11/69±9 mmHg, mean±S.D., P<.01; and 8.2% (5.9–10.5%) vs. 7.2% (5.3–10.9%), P=.008, respectively].
Conclusion
This prospective study indicates that signs of maternal vascular dysfunction precede development of preeclampsia in women with type 1 diabetes.
This study aims to test the hypothesis that vascular dysfunction is present early in pregnancy in women with type 1 diabetes who subsequently develop preeclampsia.
Methods
Eighty-three women with type 1 diabetes of more than 10 years duration were followed up prospectively during pregnancy. External ultrasound was used to measure the dilatory response of the brachial artery to postischemic increased blood flow (endothelium-dependent, flow-associated dilatation) and to nitroglycerin (NTG) [endothelium-independent, NTG-induced dilatation (NID)] at Gestational Weeks 11 and 29. Plasma concentrations of the vascular markers vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and von Willebrand factor antigen were also measured together with 24-h urinary albumin excretion (UAE), blood pressure (BP), and HbA1C.
Results
Fourteen (17%) of the 83 women developed preeclampsia. NID was significantly impaired at Week 29 in women prone to preeclampsia (108.8±7.0% vs. 116.8±8.9%, mean±S.D., P<.05), and the plasma concentrations of VCAM-1 and ICAM-1 were significantly elevated at Gestational Week 11 (612±82 vs. 516±109 µg/l, P<.005 and 293±67 vs. 255±57 µg/l, P<.05, respectively). Women who later developed preeclampsia were also characterized by higher UAE, higher BP, and higher HbA1C than women who did not [Gestational Week 11: 194 (3–1104) vs. 7 (0–412) mg/24 h, median (range), P=.0003; 122±12/75±6 vs. 111±11/69±9 mmHg, mean±S.D., P<.01; and 8.2% (5.9–10.5%) vs. 7.2% (5.3–10.9%), P=.008, respectively].
Conclusion
This prospective study indicates that signs of maternal vascular dysfunction precede development of preeclampsia in women with type 1 diabetes.
| Original language | English |
|---|---|
| Journal | Journal of Diabetes and its Complications |
| Volume | 21 |
| Issue number | 5 |
| Pages (from-to) | 288-93 |
| Number of pages | 6 |
| ISSN | 1056-8727 |
| DOIs | |
| Publication status | Published - 2007 |
