2–4 These reactions are characterized by a silent sensitization, with a transient mast-cell unresponsiveness to the initial administration of the drug. 1 IgE-mediated ones occur within 6 hours after the last drug administration (ie, immediate reactions), though typically occur within one hour of the first dose of a new treatment course. Penicillins and cephalosporins are frequently responsible for hypersensitivity reactions (HSRs). Therefore, pre-treatment skin tests with the related β-lactams are suggested before administering them via graded challenges to β-lactam-allergic patients who need alternative β-lactams.Ĭhemical structures of carbapenems and aztreonam. Particular patterns of allergy-test positivity observed in some studies that assessed cross-reactivity among β-lactams seem to indicate that prior exposures may be responsible for coexisting sensitivities. On the other hand, in a few prospective studies of penicillin-allergic individuals, less than 1% of cases show a cross-reactivity between penicillins and both aztreonam and carbapenems. For example, in aminopenicillin-allergic subjects, cross-reactivity with aminocephalosporins could possibly be over 30%. Identities or similarities of β-lactam side-chain structures are mainly responsible for cross-reactivity among these antibiotics. Several studies demonstrated that cross-reactivity connected with the β-lactam ring, causing positive responses to allergy tests with all β-lactams, is infrequent in subjects with an IgE-mediated allergy and anecdotal in those with a T-cell-mediated allergy. This review is mainly about published studies assessing the cross-reactivity among β-lactams in penicillin- or cephalosporin-allergic subjects by carrying out diagnostic tests with alternative β-lactams and, if appropriate, graded challenges. All rights reserved.Β-Lactams which include penicillins, cephalosporins, carbapenems, and monobactams are the most common antibiotic classes reported to cause allergic reactions to drugs. Anticipation and prevention require notifying the patient that DI-AIN is an idiosyncratic, hypersensitivity reaction that recurs on re-exposure, and the drug should be avoided.Īcute Kidney Injury Drug Hypersensitivity Reaction Drug-Induced Interstitial Nephritis.Ĭopyright © 2016 National Kidney Foundation, Inc. Corticosteroids are used in the treatment of DI-AIN because of their potent anti-inflammatory effects on T cells and eosinophils. The essence of management of DI-AIN lies with the four sequential steps: anticipation, diagnosis, treatment, and prevention. Differing structure-activity relationships accounts for effect, hypersensitivity, and cross-reactivity among and between classes. The core structure of each drug or its metabolite is an antigenic determinant, and the host interaction is termed the structure-activity relationship. If the offending drug is not identified and discontinued in a timely manner, irreversible fibrosis and chronic kidney disease will occur. Incriminated antigenic mechanisms include response to a conjugation product of the drug or its metabolite with a host protein (eg, beta-lactam or sulfonamide antibiotic) or the direct binding of the drug to a particular host allele to elicit a hypersensitivity response (eg, certain anti-epileptic drugs). The dendritic cells activate T cells, and the subsequent effector phase of the immune response is mediated by various cytokines. DI-AIN begins with antigen processing and presentation to local dendritic cells. DI-AIN must be differentiated from drug-induced nephrotoxic acute tubular necrosis because of their differing pathophysiology and treatment. More than 250 different drugs from various classes have been incriminated as causative agents of DI-AIN, the third most common cause of acute kidney injury in the hospital. The kidneys are susceptible to DHR because: (1) the high renal blood flow whereby antigens are filtered, secreted, or concentrated, and (2) it is a major site of excretion for drugs and drug metabolites. DHRs account for fewer than 15% of reported adverse drug reactions. Drug-induced acute interstitial nephritis (DI-AIN) is a drug hypersensitivity reaction (DHR) that manifests 7 to 10 days after exposure to the culprit drug.
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