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General anesthetics and contrast media can cause anaphylactic as well as anaphylactoid reactions. These events are of great concern to radiologists and anesthesiologists because of their relatively high prevalence, possible threat to life, and medical-legal consequences. Points discussed in this review are the critical evaluation of risk factors affecting prevention strategies, the need to be aware of pathogenic mechanisms relevant to prevention strategies, the use of alternative products if a culprit agent is known, the recognition of early signs of a reaction, the need to keep records of reactions on a patient's medical chart, the planning of prophylactic therapy, recommended actions after a reaction to an anesthetic or contrast medium, and the suggested establishment of allergy-anesthesiology centers to improve cooperation, and medical-legal issues. As any drug or contrast medium administered during general anesthesia or a diagnostic procedure can induce a potentially life-threatening or fatal event even in the absence of any evident risk factor in the patient's medical history or clinical status, we usually premedicate susceptible individuals at least to attenuate the severity of an unpredictable reaction, although we cannot rely on the efficacy of premedication to completely prevent a severe event. These recommendations, which are based on the literature and on the experience of our working group, aim to provide useful information for physicians and other specialists who operate in the absence of an allergy consultant.

The furA-katG region of Mycobacterium tuberculosis, encoding a Fur-like protein and the catalase-peroxidase, is highly conserved among mycobacteria. Both genes are induced upon oxidative stress. In this work we analyzed the M. tuberculosis furA promoter region. DNA fragments were cloned upstream of the luciferase reporter gene, and promoter activity in Mycobacterium smegmatis was measured in both the presence and absence of oxidative stress. The shortest fragment containing an inducible promoter extends 45 bp upstream of furA. In this region, -35 and -10 promoter consensus sequences can be identified, as well as a 23-bp AT-rich sequence that is conserved in the nonpathogenic but closely related M. smegmatis. M. tuberculosis FurA was purified and found to bind upstream of furA by gel shift analysis. A ca. 30-bp DNA sequence, centered on the AT-rich region, was essential for FurA binding and protected by FurA in footprinting analysis. Peroxide treatment of FurA abolished DNA binding. Three different AT-rich sequences mutagenized by site-directed mutagenesis were constructed. In each mutant, both M. tuberculosis FurA binding in vitro and pfurA regulation upon oxidative-stress in M. smegmatis were abolished. Thus, pfurA is an oxidative stress-responsive promoter controlled by the FurA protein.