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Related Concept Videos

Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
Cushing Syndrome I: Introduction01:26

Cushing Syndrome I: Introduction

Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
Adrenal Gland Disorders01:27

Adrenal Gland Disorders

Adrenal gland disorders manifest when the production of adrenal hormones deviates from the norm, resulting in either excessive or insufficient concentrations.
Adrenal insufficiency, characterized by insufficient cortisol and aldosterone production, leads to conditions like Addison's disease. This disorder, affecting the adrenal cortex, exhibits symptoms such as skin bronzing, dehydration, low blood pressure, fatigue, and weight loss. Congenital adrenal hyperplasia, a genetic ailment causing...
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Hypothalamic-Pituitary Axis

The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
Hormones of the Adrenal Glands01:31

Hormones of the Adrenal Glands

Adrenal hormones play a pivotal role in maintaining the body's electrolyte balance and orchestrating responses to stress, showcasing the intricate functions of the adrenal cortex and medulla.
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Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats
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Bone involvement in exogenous hypercortisolism.

L Sinigaglia1, D Mazzocchi, M Varenna

  • 1Department of Rheumatology, Gaetano Pini Institute, University of Milan, 20122 Milan, Italy. sinigagl@gpini.it

Journal of Endocrinological Investigation
|May 14, 2008
PubMed
Summary
This summary is machine-generated.

Corticosteroids cause significant bone loss, leading to glucocorticoid-induced osteoporosis. This condition is a frequent cause of secondary osteoporosis, impacting many patients on long-term corticosteroid therapy.

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Area of Science:

  • Endocrinology
  • Bone Metabolism
  • Pharmacology

Background:

  • Corticosteroids are widely used for various medical conditions.
  • Long-term corticosteroid use is associated with substantial bone loss.
  • Glucocorticoid-induced osteoporosis is a major clinical concern.

Purpose of the Study:

  • To review the epidemiology of glucocorticoid-induced osteoporosis.
  • To elucidate the pathogenesis of corticosteroid-induced bone loss.

Main Methods:

  • Literature review of epidemiological data.
  • Analysis of mechanisms underlying glucocorticoid effects on bone.

Main Results:

  • Glucocorticoid-induced osteoporosis is the most common cause of secondary osteoporosis.
  • Nearly 50% of patients on chronic corticosteroids experience osteoporotic fractures.
  • Specific pathways of bone metabolism are disrupted by glucocorticoids.

Conclusions:

  • Understanding the epidemiology and pathogenesis is crucial for managing corticosteroid-induced osteoporosis.
  • Further research may lead to targeted prevention and treatment strategies.