Role of genetic in stimulating Cushing’s syndrome in women and children
1 Institute of Genetic Engineering and Biotechnology for Postgraduate Studies, University of Baghdad, Baghdad, Iraq.
2 Department of Physiology, College of Medicine, Fallujah University, Al-Ramadi, Iraq.
Review
World Journal of Biology Pharmacy and Health Sciences, 2024, 18(03), 283–286.
Article DOI: 10.30574/wjbphs.2024.18.3.0335
Publication history:
Received on 26 April 2024; revised on 21 June 2024; accepted on 24 June 2024
Abstract:
Pituitary adenomas that secrete corticotropin and form from monoclonal expansion of cortical cells in the anterior pituitary gland are the source of Cushing's disease. These tumors are typically benign. An adrenal tumor, whether benign or malignant, secretes cortisol due to increased endogenous cortisol synthesis, which also results in Cushing's syndrome. Many problems, such as hyperglycemia, aberrant protein catabolism, immunosuppression, anomalies in neurocognition, bone diseases like osteoporosis, and mood disorders like depression, can be brought on by elevated cortisol levels. Therefore, the adrenocorticotropic hormone (ACTH) and genetic molecular pathways causing primary adrenal lesions to secrete excessive amounts of cortisol. Protease 8 (USP8) and USP48 somatic activating genetic variants have been found in roughly 21% to 60% of adenocarcinomas, and 6% to 12% of them, respectively. As a result, the most common Cushing's syndrome can be diagnosed at any age between 5 and 75, although the average diagnosis age is between 30 and 49.
Keywords:
Cushing's syndrome; Exogenous CS; Adrenocorticotropic hormone; Steroid hormone; Corticotropin dependent
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