Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hypersensitivities01:30

Hypersensitivities

Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
Types of Hypersensitivities
Hypersensitivity reactions are categorized into four types: Type 1, Type 2, Type 3, and Type 4. Each type has a distinct mechanism...
Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
Disorders of Erythrocytes01:27

Disorders of Erythrocytes

Disorders of erythrocytes, or red blood cells (RBCs), include a range of conditions affecting their number, shape, or function.
Erythrocyte disorders can be broadly categorized into two main types: anemic and polycythemic conditions.
A low oxygen-carrying capacity of the blood due to the loss, lower production, or destruction of erythrocytes is termed anemia. Hemorrhagic anemia, for example, occurs when bleeding from an external wound or internal ulcer reduces erythrocyte counts.
On the other...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Early access disparities in innovative therapies across the US, EU, China, and Japan.

Frontiers in medicine·2025
Same author

Clinical value at baseline and follow-up of myeloperoxidase-antibodies in ANCA-associated vasculitis.

Frontiers in immunology·2025
Same author

COVID-19 burden of illness in people who are immunocompromised due to cancer: an expert opinion review.

The oncologist·2025
Same author

Internal medicine at the crossroads of long COVID diagnosis and management.

Frontiers in medicine·2025
Same author

Targeting IFNβ in dermatomyositis.

Lancet (London, England)·2025
Same author

Is COVID-19 Still a Threat? An Expert Opinion Review on the Continued Healthcare Burden in Immunocompromised Individuals.

Advances in therapy·2024

Related Experiment Video

Updated: Jul 11, 2026

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis
03:23

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis

Published on: May 10, 2024

Hypereosinophilic syndromes.

Florence E Roufosse1, Michel Goldman, Elie Cogan

  • 1Institute for Medical Immunology, Université Libre de Bruxelles, Gosselies, Belgium. froufoss@ulb.ac.be

Orphanet Journal of Rare Diseases
|September 13, 2007
PubMed
Summary

Hypereosinophilic syndromes (HES) are rare disorders marked by high eosinophil counts causing organ damage. Diagnosis involves excluding other causes, with targeted therapies improving prognosis.

Area of Science:

  • Hematology
  • Immunology
  • Genetics

Background:

  • Hypereosinophilic syndromes (HES) are rare, heterogeneous disorders characterized by persistent eosinophilia and eosinophil-induced organ damage.
  • Exclusion of other causes of hypereosinophilia, such as allergic, parasitic, and malignant disorders, is critical for diagnosis.
  • HES affects various age groups, with a historical male predominance potentially linked to specific genetic variants.

Purpose of the Study:

  • To outline the diagnostic criteria for Hypereosinophilic Syndromes (HES).
  • To describe the underlying pathogenesis, including genetic mutations and cytokine involvement.
  • To review current therapeutic strategies and their impact on patient prognosis.

Main Methods:

  • Diagnosis relies on identifying persistent marked hypereosinophilia with organ damage.

More Related Videos

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity
10:22

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity

Published on: September 16, 2011

Cultivation of Heligmosomoides Polygyrus: An Immunomodulatory Nematode Parasite and its Secreted Products
12:40

Cultivation of Heligmosomoides Polygyrus: An Immunomodulatory Nematode Parasite and its Secreted Products

Published on: April 6, 2015

Related Experiment Videos

Last Updated: Jul 11, 2026

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis
03:23

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis

Published on: May 10, 2024

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity
10:22

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity

Published on: September 16, 2011

Cultivation of Heligmosomoides Polygyrus: An Immunomodulatory Nematode Parasite and its Secreted Products
12:40

Cultivation of Heligmosomoides Polygyrus: An Immunomodulatory Nematode Parasite and its Secreted Products

Published on: April 6, 2015

  • Exclusion of secondary causes of hypereosinophilia is essential.
  • Pathogenic classification involves cytogenetic and functional analyses to identify specific variants (e.g., FIP1L1-PDGFRA fusion gene).
  • Main Results:

    • Two main pathogenic pathways identified: myeloid cell involvement (FIP1L1-PDGFRA fusion gene) and increased IL-5 production by T cells.
    • Organ damage is variable, frequently affecting skin, heart, lungs, and nervous systems.
    • Specific treatments like imatinib for F/P+ variant and mepolizumab for F/P-negative patients show efficacy.

    Conclusions:

    • HES diagnosis requires rigorous exclusion of other conditions and identification of pathogenic variants.
    • Therapeutic strategies are tailored to disease severity and specific HES subtypes.
    • Advances in understanding pathogenesis and targeted therapies have significantly improved HES patient outcomes.