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Drug Allergy
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Type III hypersensitivity reactions generally can present as Arthus reactions, serum sickness or vasculitis reactions. Immune complex reactions originally were described following administration of heterologous antisera, but they also may be caused by small-molecular-weight drugs, protein medications such as anti-thymocyte globulin and monoclonal antibodies such as infliximab, though can also occur with prolonged use of small molecule medications including beta-lactams. This type of reaction occurs when drug-specific IgG antibodies bind to drug antigens forming antigen-antibody immune complexes. These immune complexes can precipitate in various tissues including joints and blood vessels leading to complement activation and inflammation. Symptoms often include fever, rash, urticaria, lymphadenopathy and arthralgias, usually starting 1 to 3 weeks after exposure to the offending agent. The prognosis for recovery is excellent; however, symptoms may last for several weeks. Treatment usually consists of corticosteroids and H1 antihistamines.
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).
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.
Two unusual cases of lacrimal sac inflammatory polyps with allergic mucin sine fungi
Published in Orbit, 2020
Imran Haq, Hardeep Singh Mudhar, Zanna Currie, Showkat Mirza, Sachin Salvi
Allergic fungal sinusitis (AFS) is a condition that typically presents with a history of nasal polyps, asthma, and allergies. Histology reveals layered mucin with entrapped effete and viable eosinophils in different stages of degranulation, termed allergic mucin. In many cases, although not all, fungal hyphae are present. The immunologic mechanism is thought to be a combined type I and type III immune hypersensitivity response.1,2There are also rare reports describing allergic mucin in the absence of fungi.3 There have been three previous cases of AFS affecting the lacrimal sac, two of which demonstrated fungi.4–6 Here, we present our experience of two cases of lacrimal sac involvement by allergic mucin with unique clinical and histopathological features.