Background: The clinical signs of hyperadrenocorticism (hypercortisolism) in dogs are known to be caused by chronic overexposure to glucocorticoids. The quantification of cortisol in serum, saliva or urine reflects the cortisol concentration at the time of sample collection, but in suspected hyperadrenocorticism it may be preferable to examine a long-term parameter of cortisol production.
Hypothesis/objectives: There is a need for a noninvasive method to monitor the long-term production of cortisol in dogs. It seems possible that measuring cortisol levels in hair could represent such a method.
Animals: Hair was collected from 12 dogs with hyperadrenocorticism and from 10 healthy control dogs.
Methods: Immunoreactive cortisol, cortisone and corticosterone concentrations were determined by enzyme immunoassay. High-performance liquid chromatography was performed to test the validity of the cortisol assay.
Results: Levels of immunoreactive cortisol, cortisone and corticosterone were significantly higher in dogs with hyperadrenocorticism than in control dogs. The difference was most pronounced for the cortisol level.
Conclusions And Clinical Importance: The determination of cortisol in hair offers the advantage that sampling is easier and less invasive than taking blood, urine, faeces or saliva. Measuring cortisol in hair may represent a valuable tool for the diagnosis of hyperadrenocorticism in dogs.
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http://dx.doi.org/10.1111/vde.12043 | DOI Listing |
World J Gastroenterol
January 2025
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, Henan Province, China.
Background: Liver injury manifesting as hepatic enzyme abnormalities, has been occasionally identified to be a feature of primary or secondary Addison's disease, an uncommon endocrine disease characterized by adrenal insufficiency. There have been no more than 30 reported cases of liver injury explicitly attributed to Addison's disease. Liver injury resulting from adrenal insufficiency due to glucocorticoid withdrawal is exceptionally rarer.
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February 2025
Clinica Medica 3, Department of Medicine-DIMED, University Hospital of Padova, Padova 35128, Italy.
Growth hormone (GH) secretion by the pituitary is regulated by stimulatory and inhibitory pathways such as growth hormone releasing hormone (GHRH) and somatostatin, respectively, being also modulated by different neurotransmitters acting at the hypothalamic/pituitary level. The pineal gland hormone melatonin regulates GH secretion in many mammals, including humans, although its role in modulating GH secretion has been debated. We describe the case of a young woman chronically taking melatonin for sleep disturbances, referring to her general practitioner for flushing that appeared just after starting melatonin intake.
View Article and Find Full Text PDFCompr Psychoneuroendocrinol
February 2025
University of South Florida, College of Nursing, United States.
Background: Individuals undergo significant stress throughout pregnancy and are at high risk for depressive symptoms. Elevated stress and depressive symptoms are associated with inflammatory processes and adverse maternal-infant outcomes. However, the biological processes associated with psychosocial outcomes and the maternal immune system remain unclear.
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The First People's Hospital of Chengdu Shuangliu District /Sichuan University West China Airport Hospital, Department of Clinical Laboratory, Chengdu, Sichuan, China.
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Child Maltreat
January 2025
Mt. Hope Family Center, University of Rochester, Rochester, NY, USA.
Identifying proximal and multigenerational distal risk mechanisms through which adversity exposure may shape neuroendocrine dysregulation among children is critical to advancing effective preventive interventions for adversity-exposed individuals. Utilizing longitudinal data ( = 247), the current study examined maternal and offspring history of childhood maltreatment (CM) as predictors of offspring cortisol/DHEA ratios, and, in exploratory analyses, extended this longitudinally to offspring depressive symptoms in young adulthood. Youth (ages 8-13 years) initially attended a research camp, then were followed up approximately eight years later (ages 18-22 years).
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