Unlabelled: Whereas trauma-associated arousal has been linked fairly consistently with elevations in both glucocorticoids and catecholamines, neuroendocrine correlates of hyperarousal in the context of posttraumatic stress disorder (PTSD) have been more variable. Further, neuroendocrine predictors of the development of PTSD following trauma have been related to prior exposure, and data from several laboratories suggests that hyperarousal may develop in a neuroendocrine milieu of relatively diminished basal glucocorticoid secretion.
Methods: In this article we examined 24-h cortisol and norepinephrine excretion in 42 treatment-seeking survivors of the 9/11 World Trade Center (WTC) attacks, 32 of whom met criteria for PTSD, and 15 of whom met criteria for major depression, at the time of evaluation; 14 of the 15 subjects meeting criteria for major depression also suffered from PTSD.
Results: PTSD subjects' 24-h cortisol excretion (46.3 +/- 20.0 microL/dL) was lower than that of the non-PTSD cohort (72.2 +/- 22.4 microL/dL; t = 3.18, df = 37, P = 0.003), and 24-h urinary cortisol was negatively correlated with the experience of the WTC attacks as a Criterion-A event (r = -0.427, P = 0.007), and with self-rated avoidance (r = -0.466, P = 0.003) and total score (r = -0.398, P = 0.012) on the PTSD Symptom Scale (PSS). In contrast, 24-h norepinephrine excretion was not associated with the development of PTSD or with PTSD-related symptoms, but was negatively correlated with days since 9/11 at the time of evaluation (r = -0.393, P = 0.015).
Discussion: The latter finding suggests a relationship of norepinephrine to a dimension of stress-related arousal not captured by the symptom-rating scales chosen for this study to reflect symptoms related to PTSD and other neuropsychiatric disorders, but instead, of one to that of the sudden multidimensional life disruption suffered by the WTC survivors that applied for treatment. These data also confirm, in a naturalistic sample, the previously observed negative association of urinary cortisol excretion with development of PTSD in the aftermath of severe trauma exposure.
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http://dx.doi.org/10.1196/annals.1364.055 | DOI Listing |
Compr Psychoneuroendocrinol
February 2025
Department of Kinesiology, University of North Carolina at Greensboro, Greensboro, Mailing address: P.O. Box 26170 Greensboro, NC, 27402-6170, USA.
Background: Previous studies have identified links between fluid intake, hydration related hormones and cortisol measured at one timepoint but have not considered how hydration may influence cortisol dynamics throughout the day. This study assessed associations between hydration status (copeptin, urinary osmolality, urine volume) and habitual fluid intake with cortisol dynamics.
Methods: The day before (DB) a 6-h laboratory visit, 29 male participants (age, 23±4y; BMI, 25.
Rev Cardiovasc Med
January 2025
The First School of Clinical Medicine, Southern Medical University, 510000 Guangzhou, Guangdong, China.
Background: Given the close relationship between excessive cortisol secretion and obesity, as well as their intimate associations with cardiometabolic sequelae, this study aimed to evaluate whether elevated cortisol levels and obesity are independently and potentially interactively related to hypertension-mediated organ damage (HMOD) in patients with untreated hypertension.
Methods: A total of 936 untreated hypertensive patients were recruited. Body mass index (BMI), 24-hour urinary free cortisol (24 h UFC), and HMOD indicators, including left ventricular hypertrophy (LVH), carotid intima-media thickness (CIMT), and albuminuria, were assessed.
Endocrine
January 2025
Department of Endocrinology and Metabolic Diseases, Manisa Celal Bayar University Hospital, Manisa, Turkey.
Purpose: Our study evaluated skeletal muscle mass, function and quality among mild autonomous cortisol secretion (MACS) patients and non-functioning adrenal incidentaloma (NFAI) patients in comparison with the control group without adrenal mass.
Methods: 63 NFAI (49 female, 14 male) and 31 MACS (24 female, 7 male) patients were included in the study. As the control group, 44 patients (31 women, 13 men) who were known to have no radiological adrenal pathology on computed tomography or magnetic resonance imaging performed for other reasons were selected.
Vet Sci
January 2025
Department of Clinics, Faculty of Veterinary Medicine, "Ion Ionescu de la Brad" Iasi University of Life Sciences, 700490 Iasi, Romania.
A 3-year-old spayed male mixed-breed Labrador presented to the Emergency and Critical Care Unit with lethargy, loss of appetite, vomiting, a recent history of presyncopal episodes, and severe exercise intolerance. On admission, the patient had bradycardia, low blood pressure, and mild abdominal pain. Serum biochemistry information revealed severe hyperkalemia, hyponatremia, hypoglycemia, and mildly increased liver and kidney parameters.
View Article and Find Full Text PDFNat Rev Dis Primers
January 2025
Endocrine Division, Department of Medicine, Centre hospitalier de l'Université de Montréal (CHUM), Montreal, Québec, Canada.
Cushing syndrome (CS) is a constellation of signs and symptoms caused by excessive exposure to exogenous or endogenous glucocorticoid hormones. Endogenous CS is caused by increased cortisol production by one or both adrenal glands (adrenal CS) or by elevated adrenocorticotropic hormone (ACTH) secretion from a pituitary tumour (Cushing disease (CD)) or non-pituitary tumour (ectopic ACTH secretion), which stimulates excessive cortisol production. CS is associated with severe multisystem morbidity, including impaired cardiovascular and metabolic function, infections and neuropsychiatric disorders, which notably reduce quality of life.
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