Division of Endocrinology and Metabolism, Albany Medical College, 43 New Scotland Avenue, Albany, NY 12008, USA.
Published: June 2005
AI Article Synopsis
Article Abstract
Glucocorticoid therapy in various forms is extremely common for a wide range of inflammatory, autoimmune, and neoplastic disorders. It is therefore important for the physician to be aware of the possibility of both iatrogenic and factitious Cushing's syndrome. Although most common with oral therapy, it is also important to be alert to the fact that all forms of glucocorticoid delivery have the potential to cause Cushing's syndrome. Withdrawal from chronic glucocorticoid therapy presents significant challenges. These include the possibility of adrenal insufficiency after discontinuation of steroid therapy, recurrence of underlying disease as the glucocorticoid is being withdrawn, and the possibility of steroid withdrawal symptoms. Nonetheless, with patience and persistence, a reasonable approach to withdrawal of glucocorticoid therapy can be achieved.
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.
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.
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.
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.
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.
