Pregnancy Normalized Familial Hyperaldosteronism Type I: A Novel Role for Progesterone?
Presentation Number: SUN-0790
Date of Presentation: June 22nd, 2014
Carmen Campino*1, Pamela Trejo1, Cristian A Carvajal1, Andrea Vecchiola1, Carolina Valdivia1, Cristobal A Fuentes1, Jose F Delgado1, Carlos F Lagos1, Carmen A Carrasco1, Alejandro Martínez-Aguayo1, Marlene Aglony2, Hernan Garcia Bruce2, Carolina A Loureiro2 and Carlos E Fardella1
1Pontificia Universidad Catolica de Chile, Santiago, Chile, 2Pontificia Universidad Católica de Chile, Santiago, Chile
Familial hyperaldosteronism Type I (FH-I) is caused by the presence of a chimeric CYP11B1/CYP11B2 gene that produces high amounts of aldosterone in response to ACTH and hypertension. We have recently reported the inhibitory actions of progesterone on aldosterone synthesis via the chimeric or native aldosterone synthase enzymes using an in vitro assay (1). Objective: To investigate the changes of blood pressure, progesterone, aldosterone and plasma renin activity (PRA) in a woman with FH-I during the third trimester of pregnancy and postpartum. Patient and Methods: A hypertensive woman belonging to a family with FH-I who was 16 years old at the time of diagnosis with a blood pressure of 120/95 mmHg, a Na+-K+ level of 142-4.1 mEq/L, an aldosterone level of 11.3 ng/dl, plasma renin activity (PRA) of <0.2 ng/ml/h and an aldosterone/PRA ratio (ARR) of >56.5 (2). She was normotensive and normokalemic under treatment with dexamethasone (0.25 mg/day). At 21 years of age, she became pregnant and discontinued treatment. Blood pressure and aldosterone, PRA, Na+, K+ and progesterone levels were measured at pregnancy (28 and 36 weeks) and postpartum (45 days). Normal values of hormones (3-5) are in brackets [X±SE]. The blood sample drawn at 36 weeks of gestation was obtained 2 hours prior to cesarean delivery. Results: Patient’s values at pregnancy (28 and 36 weeks) and postpartum (45 days) were as follows: blood pressure (mmHg): 103/69, 110/70 and 136/94, respectively; Na+-K+ level (mEq/L): 138-4.3, 137-4.0 and 143-4.2, respectively; aldosterone level (ng/dl): 63.9 [44±5], 44.1[58±6] and 39.4 [6.5±1], respectively; PRA level (ng/ml*h): 4.6 [5.5±1], 1.57[5.4±0.9] and <0.2 [1.4±0.1], respectively; ARR: 13.9 [8.8±5.8]; 28.1[ 16.6±7.9] and >197 [4.9±0.7], respectively; and progesterone level (ng/ml): 103.7 [105±1], 306.7 [140±20] and 0.31 [0.38±0.06], respectively. The increases in blood pressure and ARR were concomitant with a decrease in progesterone levels. Conclusions: 1. Our results show that the clinical and biochemical characteristics of FH-I normalized during gestation and worsened postpartum. These observations were associated with changes in progesterone concentration, thereby supporting our previous study demonstrating that progesterone inhibits the activity of both native and chimeric aldosterone synthase enzymes in vitro. 2. Our results identify a novel role for progesterone that could protect women against developing hypertension during pregnancy.
Nothing to Disclose: CC, PT, CAC, AV, CV, CAF, JFD, CFL, CAC, AM, MA, HG, CAL, CEF