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Related Concept Videos

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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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...
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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...
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Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
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Hypothalamic-Pituitary Axis

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Related Experiment Video

Updated: Jul 5, 2026

A Novel Method: Super-selective Adrenal Venous Sampling
06:08

A Novel Method: Super-selective Adrenal Venous Sampling

Published on: September 15, 2017

Secondary hypoadrenalism.

Giuseppe Reimondo1, Silvia Bovio, Barbara Allasino

  • 1Dipartimento di Scienze Cliniche e Biologiche, Medicina Interna I, Università di Torino, ASO San Luigi, Orbassano 10043, Italy.

Pituitary
|April 18, 2008
PubMed
Summary
This summary is machine-generated.

Secondary adrenal insufficiency (SAI) is common due to glucocorticoid use. Identifying subtle HPA axis dysfunction is crucial for preventing adrenal crises, but optimal diagnostic tests remain debated.

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Area of Science:

  • Endocrinology
  • Internal Medicine

Background:

  • Secondary adrenal insufficiency (SAI) arises from hypothalamic/pituitary damage or prolonged supraphysiological glucocorticoid use.
  • Its prevalence exceeds primary adrenal insufficiency due to widespread glucocorticoid use.
  • SAI can range from overt crises to subtle HPA axis dysfunctions, posing risks during stress.

Purpose of the Study:

  • To review the diagnostic challenges and controversies in identifying secondary adrenal insufficiency.
  • To evaluate the effectiveness of various diagnostic tests for the hypothalamic-pituitary-adrenal (HPA) axis in SAI.
  • To highlight the need for optimal diagnostic strategies to prevent life-threatening adrenal events.

Main Methods:

  • Review of existing literature on diagnostic tests for SAI.
  • Discussion of the insulin tolerance test (ITT) as a gold standard.
  • Analysis of alternatives like the standard cosyntropin stimulation test (SST) and low-dose SST.

Main Results:

  • The ITT tests the whole HPA axis but has limitations.
  • SSTs, including low-dose versions, are proposed alternatives as the adrenal gland in SAI has a blunted response to ACTH.
  • Standard ACTH doses may enhance adrenal blood flow and cortisol response; loss of early cortisol response to ACTH is a sensitive marker.
  • SSTs may yield normal results in mild or recent-onset SAI, meaning a negative test does not exclude SAI.

Conclusions:

  • Optimal diagnostic tests and sequences for SAI are still debated.
  • Current tests, including SSTs, may not reliably detect SAI in all cases, particularly milder forms.
  • Further comparative studies are essential to establish the optimal diagnostic strategy for SAI.