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Related Concept Videos

Hypersensitivity Reactions: Cytolytic Reactions01:01

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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...
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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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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...
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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...
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Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid...
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Atypical pneumonia, often caused by Mycoplasma pneumoniae, is a form of pulmonary infection that differs from the classical presentation of bacterial pneumonia in both its cause and clinical symptoms. Mycoplasma pneumoniae is a pleomorphic bacterium notable for its lack of a rigid cell wall. This structural characteristic imparts resistance to beta-lactam antibiotics and significantly influences the bacterium’s behavior within the human host.Other pathogens responsible for the disease...
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Related Experiment Video

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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
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[Atypical HUS caused by complement-related abnormalities].

Yoko Yoshida1, Masanori Matsumoto

  • 1Department of Blood Transfusion Medicine, Nara Medical University.

[Rinsho Ketsueki] the Japanese Journal of Clinical Hematology
|March 14, 2015
PubMed
Summary

Atypical hemolytic uremic syndrome (aHUS) is a rare genetic disorder often caused by complement system dysfunction. Early diagnosis and understanding the specific cause are crucial for effective treatment and improved patient outcomes.

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Area of Science:

  • Rare diseases
  • Complement system biology
  • Hematology

Context:

  • Atypical hemolytic uremic syndrome (aHUS) is a rare thrombotic microangiopathy.
  • It presents with hemolytic anemia, thrombocytopenia, and acute kidney injury.
  • Historically differentiated from Shiga-toxin producing E. coli (STEC)-HUS.

Purpose:

  • To review atypical hemolytic uremic syndrome (aHUS) focusing on complement system dysfunction.
  • To highlight diagnostic criteria and therapeutic strategies.
  • To emphasize the importance of early diagnosis and pathogenic mechanism identification.

Summary:

  • Approximately 70% of aHUS cases result from genetic mutations causing uncontrolled complement activation in the alternative pathway.
  • Mutations in complement genes (CFH, CFI, MCP, THBD, C3, CFB) and coagulation genes (DGKE, plasminogen) are implicated.
  • Diagnosis involves clinical triad, normal ADAMTS13 activity, negative STEC-HUS, and genetic complement studies.

Impact:

  • Early diagnosis and identification of underlying mechanisms are vital for improving aHUS patient outcomes.
  • Plasma therapy is a first-line treatment for suspected aHUS.
  • Eculizumab, an anti-C5 monoclonal antibody, is an effective therapeutic option for aHUS.