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Related Concept Videos

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...
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...
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...

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Related Experiment Video

Updated: May 10, 2026

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids
08:02

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

Glucocorticoid hypersensitivity syndrome--a case report.

R Krysiak1, B Okopien

  • 1Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, Katowice, Poland. r.krysiak@interia.pl

The West Indian Medical Journal
|June 14, 2013
PubMed
Summary

Glucocorticoid hypersensitivity syndrome, a rare condition, was identified in a patient presenting with hypertension and obesity. Early diagnosis and treatment with ketoconazole and cabergoline showed clinical improvement.

Related Experiment Videos

Last Updated: May 10, 2026

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids
08:02

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

Area of Science:

  • Endocrinology
  • Internal Medicine

Background:

  • Glucocorticoid hypersensitivity syndrome is a rare endocrine disorder.
  • It is characterized by an exaggerated response to glucocorticoids, leading to clinical manifestations mimicking Cushing's syndrome.

Observation:

  • A unique case of glucocorticoid hypersensitivity syndrome is presented in a 24-year-old female with arterial hypertension and obesity.
  • The patient exhibited low levels of adrenocorticotropic hormone (ACTH) and cortisol, with a blunted response to corticotrophin-releasing hormone and Synacthen.
  • An overnight low-dose dexamethasone suppression test revealed a significant decrease in morning cortisol levels.

Findings:

  • The diagnostic criteria for glucocorticoid hypersensitivity were met.
  • Treatment with ketoconazole and cabergoline resulted in partial clinical improvement.

Implications:

  • This case highlights the importance of considering glucocorticoid hypersensitivity in the differential diagnosis of suspected Cushing's syndrome.
  • Increased clinical awareness is crucial for timely diagnosis and management of this rare condition.