Skin manifestations in drug allergy (drug eruptions).
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Drug Eruptions↗
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Gene polymorphisms within the immune system that may underlie drug allergy.
Drug allergy encompasses a broad spectrum of different diseases. It occurs in some individuals, whereas it does not occur in many others. This suggests, among others, the involvement of hereditary factors, and thus of gene polymorphisms. Since drug metabolising enzymes as well as the immune system itself may be responsible for drug allergy, gene polymorphisms are relevant in both systems. While already some information exists on gene polymorphisms of drug metabolising enzymes that result in drug allergy, little information is available on gene polymorphisms within the immune system that result in such allergy. This review sets out to provide an avenue for future research aimed at discovering such polymorphisms. To this end, immune mechanisms that underlie drug allergy will be discussed. A pivotal mechanism underlying several types of drug allergy, immediate-type (type I) hypersensitivity, is also a hallmark of asthma, and therefore drug allergy and asthma share a range of candidate genes. Research on asthma has come relatively far in establishing associations of disease with polymorphisms in these genes. Therefore, these polymorphisms and their associations with asthma will be discussed. These studies on asthma provide us with lessons on how to conduct such studies on drug allergy.
Animals↗
[Diagnostic possibilities in drug allergies].
Drug allergies can be subclassified into three subgroups, which differ in their pathophysiology and require different diagnostic steps: (1.) classical drug allergies, which are directed to the drug itself, a reactive compound of the drug, or some contamination of it; (2.) pseudo-allergic reactions, which are caused by non-immune mediated degranulation of mast cells and basophils, and (3.) autoimmune reactions, in which the drug elicits an immune reaction to autologous structures. A very detailed (criminalistic) history has the highest priority for clarification of a suspected drug allergy. In addition, skin tests, serological tests and the lymphocyte transformation test may be useful. It is necessary to differentiate between tests which imitate the drug elicited allergic reaction (i.e. Coombs test in drug induced hemolytic anemia) and tests which only indicate sensitization. The detection of IgG antibodies to drugs bound to various carriers (nitrocellulose, sepharose) is controversial and the meaning of a positive result is unclear. Therefore, this test cannot be recommended for the routine diagnosis of drug allergy. Special emphasis is placed on the value of the lymphocyte transformation test, which is more often positive than other test procedures and may sometimes strengthen the suspicion that a disease may be caused by a drug. Nevertheless, this test requires cautious interpretation as it may be falsely positive as well as falsely negative.
Basophils↗
[Drug allergy].
Drug allergies can cause a great variety of symptoms and can thus imitate various diseases, like in previous times the lues. Drug allergies can be classified into three subgroups, which differ in their pathophysiology and require different diagnostic steps: firstly, classical drug allergies which are directed to the drug itself, a reactive compound of it or some contamination of the drug; secondly, pseudoallergic reactions which are caused by nonimmune mediated degranulation of mast cells and basophils; and thirdly, autoimmune reactions in which the drug elicits an immune reaction to autologous structures. A very detailed (criminalistic) history has the highest priority for the clarification of a suspected drug-allergic reaction; in addition, skin tests, serological tests and the lymphocyte transformation test might be useful. One should differentiate between tests which imitate the drug-elicited allergic reaction (i.e. Coombs test in drug induced hemolytic anemia) and tests which solely indicate a sensitization, these tests should be interpreted accordingly.
Drug Eruptions↗
[Drug allergies].
Drug allergies can be classified into three subgroups which differ in their pathophysiology and require different diagnostic steps: 1. classical drug allergies, which are directed against the drug itself, a reactive metabolite or some contaminant of the drug, 2. pseudoallergic reactions, which are caused by non-immune mediated degranulation of mast cells and basophils, and 3. autoimmune reactions, in which the drug elicits an immune reaction to autologous structures. A very detailed accurate history is of the greatest importance in the clarification of a suspected drug allergic reaction, as well as experience with the drug. In addition, skin tests, serological tests and the lymphocyte transformation test may be useful. One should differentiate between tests which imitate the drug-elicited allergic reaction (i.e., Coombs test in drug-induced hemolytic anemia) and tests which solely indicate a sensitization and the tests must be interpreted accordingly.
Antibody Formation↗
Drug allergy.
Drug allergy is an important complication in the use of agents such as penicillins, cephalosporins, sulphonamides, insulin and streptokinase. The allergenic properties of drugs are a function of molecular size and chemical reactivity. Factors determining an individual's risk of an allergic response are not fully understood but include genetic predisposition, prior exposure, route of administration, drug dosage, age and concomitant disease. The most dangerous but least common form of drug allergy is generalised anaphylaxis. The majority of reactions are non-anaphylactic and involve the skin, with a lesser incidence of haematological, renal, musculoskeletal, cardiorespiratory and other systemic manifestations. The only definitive test for allergy in a patient with a history of previous allergic reaction is rechallenge, a dangerous and seldom indicated procedure. An alternative is skin testing, but this requires an experienced practitioner and has intrinsic risk. In vitro testing may be of value in predicting the risk of rechallenge. Safe use of a suspect drug requires a careful assessment of risk and a cautious approach. Use of an offending drug in a high-risk patient is rarely indicated, but if it is considered essential, initial therapy or desensitisation in an intensive care environment is recommended.
Drug Hypersensitivity↗
[Drug allergy].
Drug reactions can be differentiated into immediate and delayed types. Immediate type reactions are life threatening or manifest themselves as urticaria /angioedema, asthma or anaphylaxis. They may be mediated by specific IgE antibodies or more frequently by non-immunological mechanisms (so-called "pseudoallergies"). Delayed type reactions are the most frequent immunological reactions. They appear mostly as maculo-papulous exanthema. Rarely they may become life threatening and lead to fever and involvement of visceral organs. In life threatening reactions further exposure to the causative drug should be strictly avoided. If the diagnosis of a drug allergy and of the causative drug is insecure, further allergological investigations are justified.
Drug Hypersensitivity↗
[Drug allergy].
Drug allergies represent about 10% of all adverse drug reactions. According to the Gell and Coombs classification, they are based on immunological mechanisms, with sensitization during the first contact, and later a clinical and (or) biological reaction after the second contact. Metabolism of drugs, often genetically determined, results in reactive metabolites which conjugate with endogenous proteins to become immunogenic. Anaphylaxis induced by myorelaxant drugs and beta-lactams, and delayed type drug eruptions are discussed as examples. All acute drug reactions are not, however, anaphylactic. Many exanthematous reactions occurring during antibiotic treatment are in fact caused by a virus.
Anesthetics↗
Metabolic activation in drug allergies.
Drug allergies are a major problem in the clinic and during drug development. At the present time, it is not possible to predict the potential of a new chemical entity to produce an allergic reaction (hypersensitivity) in patients in preclinical development. Such adverse reactions, because of their idiosyncratic nature, only become apparent once the drug has been licensed. Our present chemical understanding of drug hypersensitivity is based on the hapten hypothesis, in which covalent binding of the drug (metabolite) plays a central role in drug immunogenicity and antigenicity. If this theory is correct, then it should be possible to develop in vitro systems to assess the potential of drugs to bind to critical proteins, either directly or indirectly after metabolic activation to protein-reactive metabolites (bioactivation) and initiate hypersensitivity. The purpose of this review is to assess critically the evidence to support the hapten mechanism, and also to consider alternative mechanisms by which drugs cause idiosyncratic toxicity.
Animals↗
[Study of the cell cycle using flow cytometry in drug allergy].
Drug allergy has been studied by flow cytometry with the technique of cellular cycle, of which the principle is based on cellular activity. There were four groups of patients in the study: The first reference groups (A:20 patients) gave evaluation of phase S + G2-M without antigenic stimulation of monodisperse lymphocyte cultures. This was 4%. The second group (B:15 patients) presented a phase S + G2-M of 14.1% with PHA compared with the reference response significant at 2.5%. The third group (C) was composed of 5 wasp venom allergic subjects with cellular activity phase of 17.3% and 5 nonallergic subjects with an almost identical response of around 15%. The fourth group was 5 subjects who were allergic to drugs with clinical history that strongly indicated an allergy. The response to stimulation in these subjects was much greater for each of the drugs than that of a reference subject who was taking the same drug without problem. Wasp venom seems to behave like PHA, as a mitogen. In contrast, the subjects who were objectively and clinically sensitive to drugs, had an overall greater response to them than those shown by references. It is important to have a control for each drug used.
Adolescent↗
[Drug allergy].
Drug allergies (DA) are mainly observed by general practitioners. The immediate management of reactions as well as further investigations include to know what are placebo negative reactions, linked to autonomic system hyper-reactivity. The chronology of drug intakes and related symptoms has to be specified. In case of reactions, any drug must be stopped. Subsequent worsening of symptoms requires hospitalization. Biology is not useful, the dosage of tryptase excepted in the case of anaphylactoid shock. Allergological investigations should be conducted in the next three months. Safe guiding principles for future treatments are detailed.
Anaphylaxis↗
8. Drug allergy.
Drug reactions can be considered as being either predictable or unpredictable. A predictable reaction would be the result of the pharmacologic action of the medication. An unpredictable reaction might be idiosyncratic, might be drug intolerance, or might have or imply an immunologic basis, such as being IgE mediated. Immediate reactions that are not IgE mediated can be considered as pseudoallergic (non-IgE-mediated mast cell activation). This review will discuss allergic and immunologic reactions to immunomodulators, penicillins and cephalosporins, sulfonamides, aspirin, and nonselective nonsteroidal anti-inflammatory drugs and consider the serious drug-related conditions of Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The field of drug "allergy" has expanded to include adverse reactions associated with immunosuppressive medications, anticytokine therapies, and mAbs. The cytokine release reaction that occurs with anti-CD20 antibody infusions in patients with leukemia and white blood cell counts of greater than 50 x 10(9)/L is associated with high concentrations of TNF, IL-6, and IL-8. Because of the findings of fever, dyspnea, rigors, and hypotension, this reaction resembles the Jarisch-Herxheimer reaction that occurs 60 to 90 minutes after penicillin administration in patients with secondary syphilis. Furthermore, the care of the patient with penicillin allergy has been made more difficult in the absence of the major determinant, penicilloyl-polylysine, in that from 34% to 84% of patients who have positive skin test reactions to penicillin have exclusively positive reactions to the major determinant. SJS and TEN typically are caused by medications within 1 to 8 weeks of initiation of therapy. Evidence for death of the keratinocytes through (1) drug-specific cytotoxicity with the perforin-granzyme B-mediated killing and (2) activation of Fas on keratinocytes have provided explanations for the sloughing of skin. Unfortunately, intravenous immunoglobulin therapy for SJS and TEN has been disappointing.
Anti-Inflammatory Agents, Non-Steroidal↗
[Identifying and understanding drug allergies].
Drug hypersensitivity reactions frequently occur in hospitalized and out-patients. Clinical presentations are numerous and heterogeneous, from a mild urticaria to a dramatic anaphylactic shock and an extensive bullous skin disease. Allergic reactions are unpredictable reactions, related to immunologic mechanisms. Some reactions mimic allergic reactions but no drug specific antibody or T cell proliferation can be demonstrated. A true diagnosis is rarely set up and the tools for it are lacking. In this review, we will focus on the available epidemiological data concerning these reactions, including data on incidence and mortality and on the most recent advances in the pathophysiology and allergy diagnosis of drug hypersensitivity reactions.
Anaphylaxis↗
[Pharmacologic and biologic basis of drug allergies].
Drugs are able to activate the immune system, which may generate hypersensitivity states in individuals. This article first deals with the critical processes that are involved in drug sensitizations: what are the specific features of drugs as immunogens; how are drugs recognized as non-self by activated immune cells; what is the spontaneous outcome of an immune response to drugs in individuals; does a genetic predisposition regulate the immune response to drug antigens; how much are biotransformation processes involved in the immunogenicity of drugs? The second part is mostly devoted to the biological investigation of drug sensitizations: what are we looking for and why; are all the available methods equally suitable for routine diagnosis; what are the major methological problems that we have to deal with in investigating patients who have presented with symptoms which are clinically suspected to be of immuno-allergic origin?
Animals↗
[Drug allergy].
Drug hypersensitivity results from interactions between a pharmacologic agent and the human immune system. However, some reactions involve additional, poorly-understood, non-immunological mechanisms. The clinical picture is usually very similar to that of real allergic reactions and the therapeutic possibilities are also the same. The clinical symptoms (aspecific symptoms, special diseases, fixed drug eruption, and drug-induced internal symptoms), and the therapeutic and diagnostic possibilities are reported.
Drug Eruptions↗
[Level of histamine in supernatants from the basophil activation test: applications to hymenoptera allergy and drug allergy--preliminary study].
Histamine Release technic consists in calculating histamine liberated by blood cells in touch with an allergen. To this day, this method is only used in Hymenoptera venom allergy diagnosis. The principle of this study is to measure histamine released by activated basophils in surnageons of Basophil Activation Test (BAT) for different allergens: Hymenoptera venoms: Bee, White Faced Hornet, Vespula Wasp. Drugs: Cefaperos, Clamoxyl, Alfatil, Rapifen, Diprivan, Nesdonal, Mivacron. A threshold of positivity (amplification factor in comparison with the control) is determined for these two classes of allergens: 45 for Hymenoptera venoms and 9 for drugs. These results, compared to the other diagnosis technics (Histamine Release, Basophil Activation Test, Prick Tests) discloses very high correlation rates in each case. This method seems to be a reliable method for Hymenoptera venom allergy diagnosis and for drugs allergy diagnosis too. However, this study is based on a few number of patients, so a significant statistic conclusion can't be expressed but it opens an interesting way of research.
Basophil Degranulation Test↗
[Behavior of the physician in suspicion of drug allergy and in positive drug allergy].
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Drug Hypersensitivity↗
[A case of latex allergy suspected drug allergy].
A 30-year-old female with paroxysmal supraventricular tachycardia (PSVT) underwent catheter ablation. About 30 minutes later, urticaria and dyspnea occurred suddenly. Blood pressure decreased to 62/41 mmHg, and she fell into the state of anaphylactic shock. She recovered within one hour following treatment. We initially suspected the onset of anaphylaxis was caused by either the local anesthetic or the intravenous antibiotic administered. Following thorough investigation (skin tests and challenge tests), we concluded that the anaphylaxis was not drug induced. Subsequently, we suspected latex allergy. Skin prick test showed a positive reaction to rubber gloves. The specific test for IgE antibody against latex was positive at 10.8 UA/ml. From these results, anaphylactic shock caused by latex (probably medical gloves) was diagnosed. Doctors should take preventive measures against latex allergy not only in operating rooms but also during minor treatments. It is possible that latex allergy is responsible for some cases of anaphylaxis of unknown origin.
Adult↗