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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 II hypersensitivity drug reactions are uncommon. Initially a drug binds to and acts as a hapten, stimulating IgG or IgM production to that foreign hapten-protein complex. Subsequent binding of the drug to preformed IgG or IgM causes cell destruction by macrophage- or complement-mediated lysis. These reactions usually occur with high-dose and prolonged treatment courses. Immune-induced thrombocytopenia may occur following treatment with heparin, quinidine, propylthiouracil, gold salts, beta-lactams sulfonamides, vancomycin and other drugs. Membrane damage occurs due to drug–antibody complexes, which are adsorbed onto cell membranes. Type II reactions are usually associated with a positive direct and indirect Coombs test.
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
Type II hypersensitivity (Figure 58.2) is an antibody-mediated ‘cytotoxic’ reaction involving IgG or IgM antibodies binding to a cell surface antigen, resulting in: Complement activation through the classical pathway, causing cell lysis, mast cell activation and neutrophil recruitment.Mobilization and activation of neutrophils, eosinophils, monocytes and killer cells with antibody-dependent, cell-mediated cytotoxicity. Neutrophils recruited bind IgG and release their granules. Lymphocytes bind IgG and induce apoptosis.
Overview of hypersensitivity
Published in Gabriel Virella, Medical Immunology, 2019
This second type of hypersensitivity involves, in its most common forms, complement-fixing antibodies (IgM or IgG) directed against cellular or tissue antigens. The clinical expression of type II hypersensitivity reaction depends largely on the distribution of the antigens recognized by the responsible antibodies.
Acute rheumatic fever and erythema marginatum in an adult patient
Published in Baylor University Medical Center Proceedings, 2022
Sonali Batta, Hannah Pederson, Karen B. Brust, Katherine H. Fiala
ARF is an inflammatory sequelae arising 2 to 3 weeks after group A beta-hemolytic streptococcal (GAS) pharyngitis.1 ARF manifests as a type II hypersensitivity reaction between streptococcal and host antigens.2 Diagnosis requires a combination of two major or one major and two minor Jones criteria.2 Major criteria include polyarthritis/polyarthralgia, carditis, chorea, subcutaneous nodules, and erythema marginatum.2 Minor criteria include fever, mono-arthralgia, elevated erythrocyte sedimentation rate (>30 mm in the first hour), elevated acute-phase reactants (CRP > 3.0 mg/dL), and prolonged PR interval.2 Evidence of prior GAS infection is also needed. Antistreptococcal antibodies are highly sensitive for this compared to throat culture, which is positive in only 25% of patients over 10 days after diagnosis.2,3
Hypophysitis related to immune checkpoint inhibitors: An intriguing adverse event with many faces
Published in Expert Opinion on Biological Therapy, 2021
Maria V Deligiorgi, Charis Liapi, Dimitrios T Trafalis
The only, to date, available autopsy series reported by Cartrugelli et al suggests that the ir hypophysitis results from integration of inflammatory and autoimmune mechanisms triggered by binding of anti-CTLA-4 to CTLA-4 ectopically expressed on pituitary cells. This study suggested three pillars of the anti-CTLA-4-induced destruction of pituitary: (i) expression of CTLA-4 on pituitary endocrine cells mainly on gonadotropin-secreting and TSH-secreting cells; (ii) inflammatory type II hypersensitivity reactions triggered by immune complexes consisting of the CTLA-4 antibody administered therapeutically and the pituitary CTLA-4 antigen, which in turn destructs the pituitary cells and recruit macrophages and other inflammatory cells, responsible for phagocytosis and enhanced antigen presentation; (iii) autoimmune type IV hypersensitivity reactions involving tissue damage via production of cytokines, activation of B lymphocytes and phagocytes, and direct granzyme/perforin-mediated cytotoxicity. The inflammatory type II hypersensitivity reactions were recognized as early events followed by the autoimmune type IV hypersensitivity reactions [26].
Efficacy of autologous whole blood or serum therapy for chronic spontaneous urticaria: a systematic review and meta-analysis
Published in Journal of Dermatological Treatment, 2019
Hua-Ching Chang, Chih-Wei Sung, Ming-Hsiu Lin
Release of histamine by mast cells and basophils is considered the final event in the pathophysiology of all types of urticaria, and autoimmunity is considered one of the most common initial causes of CSU (3). Two mechanisms of the pathogenesis of autoreactivity in CSU have been identified. The first mechanism, a type I hypersensitivity reaction, represents autoallergy in which autoantigens crosslink immunoglobulin E (IgE) autoantibodies (AAbs) on mast cells and basophils. The second mechanism is a type II hypersensitivity reaction in the presence of IgG AAbs against the α subunit of the high-affinity IgE receptor (FcεRIα), low-affinity IgE receptor (FcεRII), or IgE. Both autoimmunity-based mechanisms finally induce the release of vasoactive mediators, including histamine, from mast cells and basophils (3,4). In addition, the autologous serum skin test (ASST) through intradermal injection of a patient’s own serum is considered a screening test for autoimmune CSU (4).