Relative glucose tolerance and subsequent development of hypertension in pregnancy

Citation
Ke. Innes et al., Relative glucose tolerance and subsequent development of hypertension in pregnancy, OBSTET GYN, 97(6), 2001, pp. 905-910
Citations number
40
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
OBSTETRICS AND GYNECOLOGY
ISSN journal
00297844 → ACNP
Volume
97
Issue
6
Year of publication
2001
Pages
905 - 910
Database
ISI
SICI code
0029-7844(200106)97:6<905:RGTASD>2.0.ZU;2-9
Abstract
Objective: To test the hypothesis that relative carbohydrate tolerance, an indicator of insulin resistance, predicts subsequent risk for hypertension of pregnancy among previously normoglycemic, normotensive women. Methods: We conducted a nested case-control study in women enrolled at a la rge Colorado urban health maintenance organization. Subjects were previousl y healthy pregnant women who tested abnormal on their initial 50-g glucose screens and subsequently completed 3-hour, 100-g oral glucose tolerance tes ts. Cases were 54 previously normotensive women who subsequently developed hypertension and controls were 51 subjects with normotensive pregnancies, m atched to cases on parity. Subjects diagnosed with gestational diabetes (17 cases, six controls) were excluded from the main analyses. Results: Among the 82 normoglycemic women (45 controls, 37 cases, 13 preecl ampsia, 24 gestational hypertension), mean post-load glucose levels and tot al glucose area under the curve were significantly higher in cases than in controls (P less than or equal to .04) and were positively correlated with peak mean arterial pressure. After adjustment for potential confounders, P- hour post-load glucose levels remained strongly related to risk for hyperte nsion (adjusted odds ratios = 1.48; 95% confidence interval 1.13, 1.92 per 10 mg/dL increase) and to peak mean arterial blood pressure (r = .23, P = . 04), as did total glucose area under the curve (P less than or equal to .04 ). Cases were also more likely to have had one abnormal glucose tolerance t est (28% versus 5%, P = .004). Stratifying analyses by case severity (preec lampsia and gestational hypertension) yielded similar results. Among all su bjects, more cases than controls were also diagnosed with gestational diabe tes (31% versus 12%, P = .008). Conclusion: These findings are consistent with the hypothesis that insulin resistance precedes the clinical onset of hypertension in pregnancy, and ma y be important in the etiology of hypertension. (Obstet Gynecol 2001;97:905 -10. (C) 2001 by The American College of Obstetricians and Gynecologists.).