2011
DOI: 10.1016/j.ecl.2011.09.001
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Adrenal Disorders in Pregnancy

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Cited by 32 publications
(21 citation statements)
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“…During pregnancy, the incidence of adrenal disorders (particularly adenomas) and CD is 60 and 33% respectively, in contrast to non-pregnant patients, where the incidence is 15% for adrenal adenoma and 70% for CD (1). This preponderance is probably related to the exclusive cortisol production from adrenal adenomas as compared to CD, which exhibits a mixed secretion of cortisol and androgens (15). Lindsay et al (1), upon reviewing 136 pregnancies in 122 women with CS, described the following etiologies: CD (nZ40); adrenal adenoma (nZ56); adrenal carcinoma (nZ12); ectopic ACTH secretion (EAS) (nZ4); Carney's complex (nZ1); and ACTH-independent hyperplasia (nZ4), possibly resulting from aberrant receptor stimulation.…”
Section: Pregnancy With Csmentioning
confidence: 85%
“…During pregnancy, the incidence of adrenal disorders (particularly adenomas) and CD is 60 and 33% respectively, in contrast to non-pregnant patients, where the incidence is 15% for adrenal adenoma and 70% for CD (1). This preponderance is probably related to the exclusive cortisol production from adrenal adenomas as compared to CD, which exhibits a mixed secretion of cortisol and androgens (15). Lindsay et al (1), upon reviewing 136 pregnancies in 122 women with CS, described the following etiologies: CD (nZ40); adrenal adenoma (nZ56); adrenal carcinoma (nZ12); ectopic ACTH secretion (EAS) (nZ4); Carney's complex (nZ1); and ACTH-independent hyperplasia (nZ4), possibly resulting from aberrant receptor stimulation.…”
Section: Pregnancy With Csmentioning
confidence: 85%
“…24 Box 1 HPA axis changes in a normal pregnancy Increase in zona fasciculata in adrenal gland 1,2 Increase in total and free cortisol and UFC Starting about 11 weeks' gestation Free cortisol levels by 1.2-fold, 1.4-fold, and 1.6-fold and 24-hour UFC by 1.7-fold, 2.4-fold, and 3.1-fold in the first, second, and third trimesters respectively 13 Increase in ACTH Beginning in the late first trimester, peaking during labor and delivery 16,17 Increase in CRH Mostly from placental production Detectable then steadily increases in middle of the second trimester, with a sharp increase at the end of gestation 13,15 Increase in CBG 13 Increase in aldosterone Levels increase steadily up to 3-fold to 8-fold then plateau in the third trimester [21][22][23] Increase in plasma renin activity Approximately 4-fold by eighth week; 7-fold at term 23 Increase in deoxycorticosterone. 24,26,27 CRH and ACTH levels return to nonpregnant values within 24 hours of delivery, 18 and, at 2 to 3 months postpartum, plasma free cortisol and UFC levels return to baseline but CBG and total plasma cortisol levels remain increased. 13 …”
Section: Changes To the Hypothalamus-pituitary-adrenal Axis In Pregnancymentioning
confidence: 97%
“…The increase in prostaglandin synthesis and arterial venous shunt of the placental unit cause a decrease in systemic vascular resistance which are thought to initiate an activation of RAAS. 23 Extrarenal production of renin by the ovaries and maternal decidua as well as stimulation of renal renin release directly by estrogen 24,25 likely contribute to the early increase in renin. The direct effect of estrogen and the estrogen-stimulated increase in CBG from the liver contribute to the increase in PRA, promoting increased angiotensin II levels and ultimately, increased aldosterone production from the adrenal glands.…”
Section: Changes To the Hypothalamus-pituitary-adrenal Axis In Pregnancymentioning
confidence: 98%
“…MIBG is not considered to be safe for the fetus because of placental transfer of the isotope resulting in radiation and iodine exposure (17,18).…”
Section: Diagnosismentioning
confidence: 99%