Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many patients complain about hyperreactivity of the skin or mucosal membranes, whereby rather harmless "triggers" lead to exaggerated reactions like running nose, bronchospasm, urticaria, etc. Most of these hyperreactivities have an underlying inflammation. It is important not to focus only on the triggers, but to look for the agent causing the inflammation and to avoid/treat it: elimination of the cause also eliminates the hyperreactivity. Four examples are presented where this cause--trigger model of hyperreactivity is illustrated (exercise induced asthma, pollen associated food allergy, flare-up reactions in drug allergy and hyperreactivity in chronic urticaria).
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PMID:[Intolerance as consequence of hyperreactivity]. 1934 Jul 69

Immune reactions to drugs can cause a variety of diseases involving the skin, liver, kidney, lungs, and other organs. Beside immediate, IgE-mediated reactions of varying degrees (urticaria to anaphylactic shock), many drug hypersensitivity reactions appear delayed, namely hours to days after starting drug treatment, showing a variety of clinical manifestations from solely skin involvement to fulminant systemic diseases which may be fatal. Immunohistochemical and functional studies of drug-specific T cells in patients with delayed reactions confirmed a predominant role for T cells in the onset and maintenance of immune-mediated delayed drug hypersensitivity reactions (type IV reactions). In these reactions, drug-specific CD4+ and CD8+ T cells are stimulated by drugs through their T cell receptors (TCR). Drugs can stimulate T cells in two ways: they can act as haptens and bind covalently to larger protein structures (hapten-carrier model), inducing a specific immune response. In addition, they may accidentally bind in a labile, noncovalent way to a particular TCR of the whole TCR repertoire and possibly also major histocompatibility complex (MHC)-molecules - similar to their pharmacologic action. This seems to be sufficient to reactivate certain, probably in vivo preactivated T cells, if an additional interaction of the drug-stimulated TCR with MHC molecules occurs. The mechanism was named pharmacological interaction of a drug with (immune) receptor and thus termed the p-i concept. This new concept may explain the frequent skin symptoms in drug hypersensitivity to oral or parenteral drugs. Furthermore, the various clinical manifestations of T cell-mediated drug hypersensitivity may be explained by distinct T cell functions leading to different clinical phenotypes. These data allowed a subclassification of the delayed hypersensitivity reactions (type IV) into T cell reactions which, by releasing certain cytokines and chemokines, preferentially activate and recruit monocytes (type IVa), eosinophils (type IVb), or neutrophils (type IVd).
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PMID:Drug hypersensitivity reactions involving skin. 2002 Feb 58

Drug hypersensitivity reactions (HSRs) are the adverse effects of drugs which, when taken at doses generally tolerated by normal subjects, clinically resemble allergy. Immediate-reaction of drug HSRs are those that occur less than 1 hour after the last drug intake, usually in the form of urticaria, angioedema, rhinitis, conjunctivitis, bronchospasm, and anaphylaxis or anaphylactic shock. Acute urticarial and angioedema reactions are common clinical problems frequently encountered by internists and general practitioners. They are not specific to drug allergic reaction, and can be caused by various pathogenic mechanisms. Despite the benign course of urticaria and angioedema, a mucocutaneous swelling of the upper respiratory tract could be life-threatening by itself or a feature of anaphylaxis. This article reviews acute symptoms of drug HSR-related urticaria, angioedema, anaphylaxis, and anaphylactic shock, and how clinicians should approach these problems.
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PMID:Acute symptoms of drug hypersensitivity (urticaria, angioedema, anaphylaxis, anaphylactic shock). 2060 58

Drugs may elicit a considerable variety of clinical signs, often affecting the skin and the mucous membranes. The most common are maculopapular exanthemas and urticaria, more rarely pustules, bullae vasculitic lesions, and lichenoid lesions may also be observed. Apart from the morphology, the chronology of the occurrence and the evolution of single skin lesions and exanthema are also paramount in the clinical diagnosis of cutaneous drug hypersensitivity. Often, the skin represents the only organ manifestation; however, it may be the herald for a systemic involvement of internal organs, such as in severe drug-induced hypersensitivity syndromes or anaphylaxis.
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PMID:Delayed cutaneous manifestations of drug hypersensitivity. 2060 59

Angio-oedema and urticaria can be symptoms of both allergic (IgE-mediated) and non-allergic drug hypersensitivity reactions. Non-allergic drug reactions, that may have a similar clinical presentation as allergic drug reactions, are not caused by an IgE-mediated immune mechanism. Because of unfamiliarity with non-allergic drug reactions and the unclear time course between drug use and reactions, the relationship with the responsible drug is often not recognized, leading to unnecessary patient risks. In the present article three patients with angio-oedema and urticaria as side effects of frequently used drugs (ACE-inhibitors, NSAIDs and betalactams) are presented and discussed. Patient A was a 69-year-old man with ACE-inhibitor induced angio-oedema. Patient B was a 40-year-old woman with urticaria and angio-oedema after ingestion of a NSAID caused by a non-allergic drug reaction. Patient C was a 54-year-old woman who developed an anaphylactic shock because of a type I allergy to betalactams.
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PMID:[Angio-oedema and urticaria as side effects of frequently used drugs]. 2071 7

Suspected allergic reactions to drugs and biological substances (anti-infectious drugs and antipyretics, non opioid analgesics and nonsteroidal anti-inflammatory drugs especially) are reported in 5 to 12% of children. Most frequent reactions are morbilliform/maculopapular rashes, urticaria and angioedema. Other cutaneous and respiratory reactions, and severe allergic and non-allergic anaphylactic reactions are rare. The results of studies based on allergological tests and/or microbiological/serological tests strongly suggest that, except for a few types of reactions (anaphylactic and/or immediate reactions, potentially harmful toxidermias) and for very specific drugs (i.e. latex and myorelaxants), most reactions to commonly used drugs and biological substances in children do not result from drug hypersensitivity, but are rather a consequence of the infectious and/or inflammatory diseases for which the drugs have been prescribed. Non-immediate reactions may also result from complex interactions between drugs, immune system and "danger signals" provided or induced by infectious and/or inflammatory diseases. Diagnosis is based above all on a detailed analysis of clinical history, skin tests (if validated), and challenge tests (if indicated). At present, the diagnostic and predictive values of in vitro tests exploring immediate (specific IgE determination, histamine and leukotriene release tests, basophil activation test) and non-immediate type (lymphocyte activation tests, and cytokine assays in the supernatant of activated blood mononuclear cells) of drug hypersensitivity are not validated.
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PMID:[Diagnosis of allergic and non-allergic hypersensitivity reactions to commonly used drugs and biological substances in children: diagnostic algorithm]. 2139 72

During the anthrax outbreak and threat in Trenton (2001), our allergy practice experienced increased visits from approximately 50 of our regular patients with symptoms they believed resulted from anthrax exposure. In all cases, their symptoms were caused by a combination of an exacerbation of their underlying allergic disease and anxiety because of possible exposure to anthrax. Our objective is to present an orderly approach to the allergist's outpatients presenting with possible exposure to a bioterrorist's agent. The 10 precepts of approach to the management of a biological casualty (index of suspicion, protect yourself, patient assessment, decontaminate, diagnose, treat, infection control, alert authorities, assist in investigation, and maintain proficiency) and the epidemiological characteristics of a biological attack are discussed. In table form, we compared the signs and symptoms of the most common outpatient consultations to an allergist's office practice (chronic rhinitis, asthma, food allergy, venom allergy, atopic dermatitis, drug allergy, chronic urticaria, acute urticaria, immunodeficiency, and anaphylaxis) with those of likely bioterrorism threats. Descriptions of smallpox, plague, tularemia, anthrax, viral hemorrhagic fevers, Q fever, brucellosis, Venezuelan equine encephalitis, glanders, and melioidosis are presented. Patients may readily mistake their allergic symptoms with those of infection with a bioterrorist's agent. At the same time, the allergist may be faced with one of his own chronic patients presenting with symptoms resembling their allergic disease but actually caused by one of the aforementioned pathogens.
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PMID:Biological terrorism and the allergist's office practice. 2178 3

A female in her early 50s presented with a long-standing history of episodic urticaria and angioedema. She also reported urticarial reactions after ingestion of aspirin, prednisone and multiple antibiotics. These medications were all taken during upper respiratory tract infections. An elimination diet followed by a series of open challenges to food chemicals demonstrated an urticarial eruption following the ingestion of mints, which contain high levels of salicylates. A double-blinded placebo-controlled challenge to salicylate confirmed her sensitivity and explained her reaction to aspirin. The patient informed her treating physician of her copious ingestion of mints during upper respiratory tract infections. Drug hypersensitivity to antibiotics and prednisone was excluded on the basis of negative radioallergosorbent tests (RASTs) and/or absent skin-test responses and/or tolerance to oral challenges. This patient had a salicylate intolerance that caused her episodic urticaria and angioedema, and also masqueraded as a drug allergy due to the concurrent ingestion of mints.
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PMID:Salicylate intolerance: a masquerader of multiple adverse drug reactions. 2191 70

Adverse drug reactions (ADR) occur in nearly 10% of hospitalized children and in about 1.5% of ambulatory pediatric patients. The skin is the most frequently affected target organ in drug hypersensitivity (DH) reactions, which account for 20% of all ADR. Due to its pathophysiological heterogeneity and the ensuing morphological diversity, DH often represents a clinical and therapeutic challenge. Urticarial and maculopapular eruptions are usually restricted to the skin and rarely require systemic treatment or hospital admission once the culprit drug has been withdrawn. However, extracutaneous affections should be ruled out promptly in individuals with polymorphous rashes accompanied by fever and lymphadenopathy as well as in patients with bullous skin lesions. Children affected by severe drug reactions usually require in-hospital surveillance and interdisciplinary supportive therapy.
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PMID:[Cutaneous adverse drug reactions in childhood and adolescence]. 2229 Feb 76

Relevant interest has been focused on rapid desensitization for drug hypersensitivity and on its use for reactions to monoclonal antibodies. Natalizumab is a highly effective therapy for multiple sclerosis but its use can be limited by hypersensitivity reactions. Herein we present a case of a 36-year-old male patient with multiple sclerosis who started natalizumab therapy due to rapid neurological deterioration. During the second infusion he developed a reaction involving urticaria, erythema and angioedema. Natalizumab sensitization was demonstrated by a positive result on the intradermal test. The anti-natalizumab IgG neutralizing antibody assay was negative. Lacking any alternative, equally effective treatment, he underwent a rapid intravenous desensitization protocol. Desensitization was successfully repeated eleven times and the patient's neurological conditions improved and remained stable after one year. This case demonstrates that rapid desensitization is a safe and effective procedure in the treatment of natalizumab hypersensitivity.
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PMID:Successful desensitization to natalizumab in a skin test--positive patient: a case report. 2251 29


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