Book contents
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- Part XXIII Specific Organisms – Viruses
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- 203 Principles of Antibiotic Therapy
- 204 Antifungal Therapy
- 205 Antiviral Therapy
- 206 Hypersensitivity to Antibiotics
- 207 Antimicrobial Agent Tables
- Index
206 - Hypersensitivity to Antibiotics
from Part XXV - Antimicrobial Therapy – General Considerations
Published online by Cambridge University Press: 05 March 2013
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- Part XXIII Specific Organisms – Viruses
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- 203 Principles of Antibiotic Therapy
- 204 Antifungal Therapy
- 205 Antiviral Therapy
- 206 Hypersensitivity to Antibiotics
- 207 Antimicrobial Agent Tables
- Index
Summary
Adverse drug reactions (ADRs) are usefully separated into type A reactions (predictable from known pharmacologic properties and largely dose related) and type B reactions (unpredictable and restricted to a vulnerable subpopulation). Type B reactions comprise 10% to 15% of all ADRs and include immunologic drug reactions, drug intolerance (eg, tinnitus after single aspirin tablet), and idiosyncratic reactions, some of which are pseudoallergic (eg, aspirininduced reactions).
Immune mechanisms are thought to be involved in 6% to 10% of all ADRs. Allergenic drugs can induce the entire spectrum of immunopathologic reactions, which are clinically indistinguishable from reactions elicited by foreign macromolecules (Table 206.1). Gell and Coombs' type I reactions are caused by drug/antigen-specific immunoglobulin E (IgE) that binds to high-affinity Fc-IgE receptors on mast cells and basophils. Cross-linking these receptors leads to the release of vasoactive mediators such as histamine and cysteinyl leukotrienes. Typical syndromes include urticaria, anaphylaxis, rhinitis, and bronchoconstriction, which can occur immediately in a previously sensitized individual. Type II cytolytic reactions are generally confined to rapidly haptenating drugs such as penicillins and are based on immunoglobulin G (IgG)-mediated cytotoxic mechanisms, resulting mainly in blood cell cytopenias. Type III reactions are immune complex mediated and may involve complement activation and stimulation of Fc-α receptor–activated inflammatory cells. Drug-specific immune complexes result from high-dose, prolonged therapy and may produce drug fever, a classic serum sickness syndrome, and various forms of cutaneous vasculitis.
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- Clinical Infectious Disease , pp. 1445 - 1456Publisher: Cambridge University PressPrint publication year: 2008
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