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Related Concept Videos

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...
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...
Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic Syndrome II : Assessment and Medical Management

IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document any history...
Amebiasis01:28

Amebiasis

Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.Etiology and TransmissionThe infective...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
Endocarditis II: Clinical Features of Infective Endocarditis01:25

Endocarditis II: Clinical Features of Infective Endocarditis

Endocarditis can present various clinical features depending on the causative organism and the patient's underlying health conditions. Initially, the clinical features of infective endocarditis develop gradually, presenting with nonspecific symptoms that can be easily mistaken for other illnesses.General SymptomsEarly symptoms of infective endocarditis are fever, chills, weakness, malaise, fatigue, and weight loss. These symptoms reflect the systemic nature of the infection and the body's...

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Granulocyte-dependent Autoantibody-induced Skin Blistering
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Behçet's syndrome.

Sebahattin Yurdakul1, Hasan Yazici

  • 1Department of Medicine, Division of Rheumatology, Cerrahpasa Medical Faculty, University of Istanbul, Istanbul, Turkey. profsyurdakul@yahoo.com

Best Practice & Research. Clinical Rheumatology
|November 26, 2008
PubMed
Summary

Genetic background appears crucial in Behçet's syndrome (BS) pathogenesis, with distinct clinical clusters suggesting multiple disease mechanisms. Current classification with autoinflammatory disorders is questioned due to differing characteristics.

Area of Science:

  • Rheumatology
  • Immunology
  • Genetics

Background:

  • Epidemiological studies indicate genetic factors are paramount in Behçet's syndrome (BS) development.
  • BS exhibits distinct clinical clusters, including thrombosis, mucocutaneous symptoms, and potential associations with inflammatory bowel disease.
  • The heterogeneity suggests multiple underlying disease mechanisms.

Purpose of the Study:

  • To explore the role of genetic background versus environmental factors in Behçet's syndrome pathogenesis.
  • To investigate the potential for distinct disease mechanisms within Behçet's syndrome based on clinical presentation clusters.
  • To evaluate the current classification of Behçet's syndrome within autoinflammatory disorders.

Main Methods:

  • Review of recent epidemiological work on Behçet's syndrome.

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  • Analysis of clinical presentation clusters and associated conditions.
  • Comparison of Behçet's syndrome characteristics with established autoinflammatory disorders.

    • Main Results:

    • Genetic background appears to outweigh environmental factors in Behçet's syndrome pathogenesis.
    • Identified distinct clusters of disease expression: 1) thrombosis (superficial vein, deep vein, dural sinus) and 2) mucocutaneous/musculoskeletal (acne, arthritis, enthesitis).
    • Association with anti-Saccharomyces cerevisiae antibodies and inflammatory bowel disease suggests another potential cluster.

    Conclusions:

    • The presence of distinct clinical clusters supports the hypothesis of multiple underlying disease mechanisms in Behçet's syndrome.
    • The classification of Behçet's syndrome with autoinflammatory disorders is questionable, as BS lacks typical features like recurrent fevers and defined genetic loci.
    • Current European League Against Rheumatism guidelines are useful for managing certain organ systems but lack controlled studies for vascular, neurological, and gastrointestinal involvement.