A Longitudinal Study of Plasma and Urinary Cortisol in Pregnancy and Postpartum
Context:There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol.Design, Subjects, and Measurements:We conducted a prospective lon...
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| Published in | The journal of clinical endocrinology and metabolism Vol. 96; no. 5; pp. 1533 - 1540 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Bethesda, MD
Oxford University Press
01.05.2011
Copyright by The Endocrine Society Endocrine Society |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-972X 1945-7197 1945-7197 |
| DOI | 10.1210/jc.2010-2395 |
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| Abstract | Context:There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol.Design, Subjects, and Measurements:We conducted a prospective longitudinal study on morning plasma cortisol (total and free), corticosteroid-binding globulin (CBG), and 24-h urinary free cortisol (UFC) levels in 20 pregnant women during the first, second, and third trimesters and 2–3 months postpartum compared with 12 subjects on low-dose OCP and 15 nonpregnant subjects not taking the OCP (control group).Results:A progressive rise in total plasma cortisol, CBG, and 24-h UFC was demonstrated during pregnancy, peaking during the third trimester (mean 3-fold rise compared with controls). Plasma free cortisol increased 1.6-fold by the third trimester. In the OCP group, total plasma cortisol and CBG were 2.9- and 2.6-fold elevated, respectively, whereas 24-h UFC and plasma free cortisol were not significantly different from controls. Compared with liquid chromatography-mass spectrometry, a commercial immunoassay underestimated mean total plasma cortisol concentrations by 30% during second and third trimesters and in OCP users and overestimated UFC levels by 30–35% during pregnancy.Conclusions:Our study demonstrated elevations in total plasma cortisol and CBG concentrations during pregnancy and with low-dose OCP use. Pregnancy was also associated with significant increases in plasma free cortisol and UFC, suggesting that the rise in total plasma cortisol is contributed to by up-regulation of the maternal hypothalamic-pituitary-adrenal axis in addition to elevated CBG. |
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| AbstractList | Context:There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol.Design, Subjects, and Measurements:We conducted a prospective longitudinal study on morning plasma cortisol (total and free), corticosteroid-binding globulin (CBG), and 24-h urinary free cortisol (UFC) levels in 20 pregnant women during the first, second, and third trimesters and 2–3 months postpartum compared with 12 subjects on low-dose OCP and 15 nonpregnant subjects not taking the OCP (control group).Results:A progressive rise in total plasma cortisol, CBG, and 24-h UFC was demonstrated during pregnancy, peaking during the third trimester (mean 3-fold rise compared with controls). Plasma free cortisol increased 1.6-fold by the third trimester. In the OCP group, total plasma cortisol and CBG were 2.9- and 2.6-fold elevated, respectively, whereas 24-h UFC and plasma free cortisol were not significantly different from controls. Compared with liquid chromatography-mass spectrometry, a commercial immunoassay underestimated mean total plasma cortisol concentrations by 30% during second and third trimesters and in OCP users and overestimated UFC levels by 30–35% during pregnancy.Conclusions:Our study demonstrated elevations in total plasma cortisol and CBG concentrations during pregnancy and with low-dose OCP use. Pregnancy was also associated with significant increases in plasma free cortisol and UFC, suggesting that the rise in total plasma cortisol is contributed to by up-regulation of the maternal hypothalamic-pituitary-adrenal axis in addition to elevated CBG. CONTEXT:There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol. DESIGN, SUBJECTS, AND MEASUREMENTS:We conducted a prospective longitudinal study on morning plasma cortisol (total and free), corticosteroid-binding globulin (CBG), and 24-h urinary free cortisol (UFC) levels in 20 pregnant women during the first, second, and third trimesters and 2–3 months postpartum compared with 12 subjects on low-dose OCP and 15 nonpregnant subjects not taking the OCP (control group). RESULTS:A progressive rise in total plasma cortisol, CBG, and 24-h UFC was demonstrated during pregnancy, peaking during the third trimester (mean 3-fold rise compared with controls). Plasma free cortisol increased 1.6-fold by the third trimester. In the OCP group, total plasma cortisol and CBG were 2.9- and 2.6-fold elevated, respectively, whereas 24-h UFC and plasma free cortisol were not significantly different from controls. Compared with liquid chromatography-mass spectrometry, a commercial immunoassay underestimated mean total plasma cortisol concentrations by 30% during second and third trimesters and in OCP users and overestimated UFC levels by 30–35% during pregnancy. CONCLUSIONS:Our study demonstrated elevations in total plasma cortisol and CBG concentrations during pregnancy and with low-dose OCP use. Pregnancy was also associated with significant increases in plasma free cortisol and UFC, suggesting that the rise in total plasma cortisol is contributed to by up-regulation of the maternal hypothalamic-pituitary-adrenal axis in addition to elevated CBG. There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol. DESIGN, SUBJECTS, AND MEASUREMENTS: We conducted a prospective longitudinal study on morning plasma cortisol (total and free), corticosteroid-binding globulin (CBG), and 24-h urinary free cortisol (UFC) levels in 20 pregnant women during the first, second, and third trimesters and 2-3 months postpartum compared with 12 subjects on low-dose OCP and 15 nonpregnant subjects not taking the OCP (control group).CONTEXTThere is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol. DESIGN, SUBJECTS, AND MEASUREMENTS: We conducted a prospective longitudinal study on morning plasma cortisol (total and free), corticosteroid-binding globulin (CBG), and 24-h urinary free cortisol (UFC) levels in 20 pregnant women during the first, second, and third trimesters and 2-3 months postpartum compared with 12 subjects on low-dose OCP and 15 nonpregnant subjects not taking the OCP (control group).A progressive rise in total plasma cortisol, CBG, and 24-h UFC was demonstrated during pregnancy, peaking during the third trimester (mean 3-fold rise compared with controls). Plasma free cortisol increased 1.6-fold by the third trimester. In the OCP group, total plasma cortisol and CBG were 2.9- and 2.6-fold elevated, respectively, whereas 24-h UFC and plasma free cortisol were not significantly different from controls. Compared with liquid chromatography-mass spectrometry, a commercial immunoassay underestimated mean total plasma cortisol concentrations by 30% during second and third trimesters and in OCP users and overestimated UFC levels by 30-35% during pregnancy.RESULTSA progressive rise in total plasma cortisol, CBG, and 24-h UFC was demonstrated during pregnancy, peaking during the third trimester (mean 3-fold rise compared with controls). Plasma free cortisol increased 1.6-fold by the third trimester. In the OCP group, total plasma cortisol and CBG were 2.9- and 2.6-fold elevated, respectively, whereas 24-h UFC and plasma free cortisol were not significantly different from controls. Compared with liquid chromatography-mass spectrometry, a commercial immunoassay underestimated mean total plasma cortisol concentrations by 30% during second and third trimesters and in OCP users and overestimated UFC levels by 30-35% during pregnancy.Our study demonstrated elevations in total plasma cortisol and CBG concentrations during pregnancy and with low-dose OCP use. Pregnancy was also associated with significant increases in plasma free cortisol and UFC, suggesting that the rise in total plasma cortisol is contributed to by up-regulation of the maternal hypothalamic-pituitary-adrenal axis in addition to elevated CBG.CONCLUSIONSOur study demonstrated elevations in total plasma cortisol and CBG concentrations during pregnancy and with low-dose OCP use. Pregnancy was also associated with significant increases in plasma free cortisol and UFC, suggesting that the rise in total plasma cortisol is contributed to by up-regulation of the maternal hypothalamic-pituitary-adrenal axis in addition to elevated CBG. There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol. DESIGN, SUBJECTS, AND MEASUREMENTS: We conducted a prospective longitudinal study on morning plasma cortisol (total and free), corticosteroid-binding globulin (CBG), and 24-h urinary free cortisol (UFC) levels in 20 pregnant women during the first, second, and third trimesters and 2-3 months postpartum compared with 12 subjects on low-dose OCP and 15 nonpregnant subjects not taking the OCP (control group). A progressive rise in total plasma cortisol, CBG, and 24-h UFC was demonstrated during pregnancy, peaking during the third trimester (mean 3-fold rise compared with controls). Plasma free cortisol increased 1.6-fold by the third trimester. In the OCP group, total plasma cortisol and CBG were 2.9- and 2.6-fold elevated, respectively, whereas 24-h UFC and plasma free cortisol were not significantly different from controls. Compared with liquid chromatography-mass spectrometry, a commercial immunoassay underestimated mean total plasma cortisol concentrations by 30% during second and third trimesters and in OCP users and overestimated UFC levels by 30-35% during pregnancy. Our study demonstrated elevations in total plasma cortisol and CBG concentrations during pregnancy and with low-dose OCP use. Pregnancy was also associated with significant increases in plasma free cortisol and UFC, suggesting that the rise in total plasma cortisol is contributed to by up-regulation of the maternal hypothalamic-pituitary-adrenal axis in addition to elevated CBG. |
| Author | Jung, Caroline Ho, Jui T. Inder, Warrick J. Rogers, Anne Lewis, John G. Czajko, Raymond J. Torpy, David J. Doogue, Matt |
| AuthorAffiliation | Department of Endocrinology (C.J., W.J.I.), St. Vincentʼs Hospital, Melbourne, Melbourne, Victoria 3065, Australia; University of Melbourne, (C.J., W.J.I.), Melbourne, Victoria 3010, Australia; Endocrine and Metabolic Unit (J.T.H., D.J.T.), Royal Adelaide Hospital, Hanson Institute (D.J.T.), Adelaide, South Australia 5000, Australia; University of Adelaide (D.J.T.), Adelaide, South Australia 5005, Australia; Flinders University (A.R., M.D.), Flinders Medical Centre (M.D.), South Australia 5042, Australia; Canterbury Health Laboratories (J.G.L.), Christchurch, New Zealand; and Department of Biochemistry (R.J.C.), Royal Melbourne Hospital, Victoria 3050, Australia |
| AuthorAffiliation_xml | – name: Department of Endocrinology (C.J., W.J.I.), St. Vincentʼs Hospital, Melbourne, Melbourne, Victoria 3065, Australia; University of Melbourne, (C.J., W.J.I.), Melbourne, Victoria 3010, Australia; Endocrine and Metabolic Unit (J.T.H., D.J.T.), Royal Adelaide Hospital, Hanson Institute (D.J.T.), Adelaide, South Australia 5000, Australia; University of Adelaide (D.J.T.), Adelaide, South Australia 5005, Australia; Flinders University (A.R., M.D.), Flinders Medical Centre (M.D.), South Australia 5042, Australia; Canterbury Health Laboratories (J.G.L.), Christchurch, New Zealand; and Department of Biochemistry (R.J.C.), Royal Melbourne Hospital, Victoria 3050, Australia |
| Author_xml | – sequence: 1 givenname: Caroline surname: Jung fullname: Jung, Caroline email: caroline.jung@svhm.org.au organization: 1Department of Endocrinology (C.J., W.J.I.), St. Vincent's Hospital, Melbourne, Melbourne, Victoria 3065, Australia – sequence: 2 givenname: Jui T. surname: Ho fullname: Ho, Jui T. organization: 3Endocrine and Metabolic Unit (J.T.H., D.J.T.), Adelaide, South Australia 5000, Australia – sequence: 3 givenname: David J. surname: Torpy fullname: Torpy, David J. organization: 3Endocrine and Metabolic Unit (J.T.H., D.J.T.), Adelaide, South Australia 5000, Australia – sequence: 4 givenname: Anne surname: Rogers fullname: Rogers, Anne organization: 6Flinders University (A.R., M.D.), South Australia 5042, Australia – sequence: 5 givenname: Matt surname: Doogue fullname: Doogue, Matt organization: 6Flinders University (A.R., M.D.), South Australia 5042, Australia – sequence: 6 givenname: John G. surname: Lewis fullname: Lewis, John G. organization: 8Canterbury Health Laboratories (J.G.L.), Christchurch, New Zealand – sequence: 7 givenname: Raymond J. surname: Czajko fullname: Czajko, Raymond J. organization: 9Department of Biochemistry (R.J.C.), Royal Melbourne Hospital, Victoria 3050, Australia – sequence: 8 givenname: Warrick J. surname: Inder fullname: Inder, Warrick J. organization: 1Department of Endocrinology (C.J., W.J.I.), St. Vincent's Hospital, Melbourne, Melbourne, Victoria 3065, Australia |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24133756$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21367926$$D View this record in MEDLINE/PubMed |
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| Keywords | Human Urine Corticosteroid Obesity Nutrition Steroid hormone Nutrition disorder Antiinflammatory agent Metabolic diseases Cortisol Hydrocortisone Puerperium Glucocorticoid Blood plasma Pregnancy Follow up study Adrenal hormone Female Woman Endocrinology Nutritional status |
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| Snippet | Context:There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist... CONTEXT:There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist... There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to... |
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| SubjectTerms | Adult Biological and medical sciences Body Mass Index Chromatography, High Pressure Liquid Contraceptives, Oral, Hormonal - adverse effects Cortisol Cortisone - blood Endocrinopathies Feeding. Feeding behavior Female Fundamental and applied biological sciences. Psychology Globulins Hormones Humans Hydrocortisone - blood Hydrocortisone - urine Hypothalamic-pituitary-adrenal axis Hypothalamo-Hypophyseal System - physiology Hypothalamus Immunoassay Liquid chromatography Longitudinal Studies Mass spectroscopy Medical sciences Oral contraceptives Pituitary Pituitary-Adrenal System - physiology Plasma Postpartum Postpartum period Postpartum Period - blood Postpartum Period - urine Pregnancy Pregnancy Trimester, Third - blood Prospective Studies Tandem Mass Spectrometry Transcortin - metabolism Vertebrates: anatomy and physiology, studies on body, several organs or systems Vertebrates: endocrinology |
| Title | A Longitudinal Study of Plasma and Urinary Cortisol in Pregnancy and Postpartum |
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