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Hypersensitivity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
A type III hypersensitivity (Figure 58.3) is an immune-complex-mediated reaction resulting in the deposition of antigen–antibody complexes in host tissues, leading to complement activation, neutrophil infiltration and tissue damage. There are two forms of reaction: (i) complexes formed in the circulation and then deposited in the tissues, causing systemic effects (e.g. serum sickness) and (ii) complexes formed within the tissues resulting in localized effects (e.g. Arthus phenomenon). Normally, immune complexes deposited in small amounts in tissues are easily removed by the reticuloendothelial system, but in type III hypersensitivity, these immune complexes are either too abundant or too small to be cleared effectively.
The immune system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Conditions in which type III hypersensitivity reactions occur include severe infections, systemic lupus erythematosus (an autoimmune condition in which antigen-antibody complexes form against collagen in the body), and serum sickness (a condition in which antibodies form against foreign substances in the blood such as drugs, venoms and foreign blood antigens).
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Type III hypersensitivity reaction occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and activation of leukocytes. Such reactions result in immune complex diseases. Antibody (IgG) binds to soluble antigen, forming a circulating immune complex. Examples include systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).
Understanding Retinal Vasculitis Associated with Brolucizumab: Complex Pathophysiology or Occam’s Razor?
Published in Ocular Immunology and Inflammation, 2022
Ashish Sharma, Nilesh Kumar, Nikulaa Parachuri, Sonali Singh, Francesco Bandello, Carl D. Regillo, David Boyer, Quan Dong Nguyen
It is possible that small size may allow higher molar concentration and incite a strong local immune reaction leading to inflammation. We have highlighted the role of type III hypersensitivity reaction (HSR) in the past.15 The majority of vasculitic diseases involve the deposition of antigen-antibody complex, which is Type III HSR. These deposits have been shown in the capillary bed and vessel walls and can lead to occlusive vasculitis. Arthus reaction, a subtype of Type III HSR has been reported in patients on systemic monoclonal antibody (mAb), including systemic anti-VEGF therapies. Such reactions are assumed to be due to high antigen load, which leads to a subsequent increase of antibodies.16,17 Arthus reaction is more frequent in patients with auto-immune conditions. The higher molar concentration of brolucizumab (11 and 22 times greater than aflibercept and ranibizumab, respectively), if antigenic, may produce a higher rate of antibody formation. Type III HSR is due to the formation of biologic/ADA immune complexes in the circulation. When these complexes are in the correct stoichiometric ratio, they are deposited in tissues and cause inflammation and tissue damage. The requirement of the correct ratio to have tissue deposition might explain why vasculitis is seen in some individual rather than in clusters as each individual having differing amounts of ADAs leading to different stoichiometric ratios.18
An unusually “complex” glomerulonephritis
Published in Baylor University Medical Center Proceedings, 2022
Gabriela Martinez-Zayas, Daniel Savino, Sumit Kumar, Kathryn H. Dao
Hypersensitivity reactions are inappropriate immune responses to an antigen and are classified into four types, I to IV.1 Type III hypersensitivity reactions or immune-complex (IC) reactions occur when excess antigen-antibody complexes cannot be cleared and precipitate in tissues.2,3 If deposited in the renal glomeruli, immune complexes can cause glomerulonephritis (GN). Common associations with IC-GN include infections (e.g., HIV), autoimmune diseases (e.g., systemic lupus erythematous), and vaccines (e.g., pneumococcal).2,3 Vaccines enhance host defenses through immune activation against antigen, with some inducing IC formation important in B, T, and antigen-presenting cell activation.4 Amid the pandemic, SARS-CoV-2 infection has been reported to cause IC diseases including GN,5,6 and COVID-19 vaccines may induce de novo autoimmunity or flare underlying immune-mediated inflammatory diseases.7–9 Here, we present an unusual case of IC-GN presenting shortly after COVID-19 vaccination in a patient with granulomatosis with polyangiitis (GPA) and HIV infection.
Scorpion envenomation: a deadly illness requiring an effective therapy
Published in Toxin Reviews, 2021
Faez Amokrane Nait Mohamed, Fatima Laraba-Djebari
Adverse antivenom reactions appearing after hours or even days, called “late adverse reactions” were first reported by Pirquet and Schick in 1905. They found that many days after injection of large quantities of antivenoms, some patients showed rashes and fever and also kidney damage with proteinuria and lymphadenopathy (Pirquet 1905). Type-III hypersensitivity is mediated by immune complexes antigen-antibody. As a consequence of failing to clear antivenom, the patient’s immune system induces local inflammation by producing antibodies that attach to the antivenom, resulting in the formation of immune complexes (Morais and Massaldi 2009, Morais 2018).