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Endogenous Cushing's syndrome results from excess glucocorticoid secretion, which leads to a myriad of clinical manifestations, comorbidities, and increased mortality despite treatment. Molecular mechanisms and genetic alterations associated with different causes of Cushing's syndrome have been described in the last decade. Imaging modalities and biochemical testing have evolved; however, both the diagnosis and management of Cushing's syndrome remain challenging. Surgery is the preferred treatment for all causes, but medical therapy has markedly advanced, with new drug options becoming available. Nevertheless, several comorbidities remain even after patient remission, which can affect quality of life. Accurate and timely diagnosis and treatment are essential for mitigating chronic complications of excess glucocorticoids and improving patient quality of life. In this Seminar, we aim to update several important aspects of diagnosis, complications, and treatment of endogenous Cushing's syndrome of all causes.
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http://dx.doi.org/10.1016/S0140-6736(23)01961-X | DOI Listing |
Clin Endocrinol (Oxf)
December 2024
Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Objective: Many review articles have explored data regarding the coexistence of specific types of pituitary adenomas (PAs) and polycystic ovary syndrome (PCOS), particularly focusing on the potential pathogenesis of this intersection and overlapping features. However, a comprehensive evaluation encompassing the full spectrum of PAs and their association with PCOS remains lacking. This review aims to provide a broad assessment of the interactions between these entities, emphasizing pathophysiological mechanisms, clinical presentations, diagnostic challenges and therapeutic implications.
View Article and Find Full Text PDFJ Clin Endocrinol Metab
December 2024
Medizinische Klinik und Poliklinik IV, Innenstadt Klinikum der Universität München, München, Germany.
Introduction: Patients with Cushing's syndrome (CS) suffer from metabolic and cardio-vascular comorbidities caused by hypercortisolism. The human gut microbiome responds to different pathological conditions. Aim of our study was to analyze the impact of chronic endogenous cortisol excess on the gut microbiome.
View Article and Find Full Text PDFJ Steroid Biochem Mol Biol
December 2024
Department of Pathology, University of Michigan, Ann Arbor, MI, United States; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, United States; Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, United States.
Cushing syndrome represents a multitude of signs and symptoms associated with long-term and excessive exposure to glucocorticoids. Solitary cortisol-producing adenomas (CPAs) account for most cases of ACTH-independent Cushing syndrome (CS). Technological advances in next-generation sequencing have significantly increased our understanding about the genetic landscape of CPAs.
View Article and Find Full Text PDFBone
December 2024
Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin 300052, China. Electronic address:
Background: Differences in bone metabolism between patients with adrenal Cushing's syndrome (ACS) and Cushing's disease (CD) have been noted, but the impact of steroid hormones on bone metabolism remains underexplored. The purpose of this study is to explore the differences in bone metabolism between the two subtypes of Cushing's syndrome and the correlation between hormones synthesized by the adrenal reticulum and bone metabolism.
Method: This retrospective study included 75 premenopausal women, consisting of 33 patients with CD and 42 patients with ACS.
Hypertens Res
December 2024
Department of Internal Medicine, National Cheng-Kung University Hospital, Tainan, Taiwan.
The synergistic interplay between cortisol and aldosterone is critical for maintaining homeostasis, particularly in blood pressure regulation, fluid balance, and stress response. Cortisol, a glucocorticoid, and aldosterone, a mineralocorticoid, often act in tandem to regulate sodium retention and blood volume. Dysregulation of these hormones, as seen in hyperaldosteronism or Cushing's syndrome, contributes to hypertension and metabolic imbalances.
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