Glottic angioedema, ciprofloxacin, and ACE inhibitors.

Sir, We read with interest the well documented case of ciprofloxacin-induced anaphylactic reaction reported by Vidal et al.' There is no doubt that ciprofloxacin was the cause of the primary reaction occurring after 30 to 60 minutes, and the positive intradermal test supports an antibody-mediated reaction. It would have been of interest, however, to know how this reaction was treated and if the later laryngeal oedema occurred despite treatment. This may indicate that captopril may have played a pathogenic role for the oedema which may be resistant to common anti-allergic therapy. In addition, captopril may have aggravated the anaphylactic reaction. We have observed a 50-year-old insulin-dependent diabetic male who suffered from recurrent soft tissue infections and osteitis of the foot for which he was repeatedly treated with ciprofloxacin and clindamycin or amoxi-cillin. To relieve pain he took mefenamic acid on demand. In February 1993 enalapril 2 x 10 mg daily was started. From there on he suffered from angioedema of the face and the oral cavity whenever he took mefenamic acid or when he was treated with ciprofloxacin or amoxicillin. He was declared allergic to all these drugs, while therapy with enalapril was continued. In May 1994 he was referred for an allergologic investigation. Enalapril-induced angioedema was suspected and this drug was immediately stopped. C3, C4 and Cl-inhibitor levels were normal. Skin tests with the penicillin determinants PPL and MDM, as well with amoxicillin (up to 50 mg/ml) and ciprofloxacin (0.2 mg/ml) were negative. Lymphocyte proliferation tests were negative with ciprofloxacin and amox-icillin. Specific IgEs to amoxicillin, penicillin G and V were not detectable (<0.35 kU/l). Oral provocation tests with mefenamic acid (cumulative doses 300 and 750 mg, respectively) and amoxicillin (dose 1 g) were negative. In addition several infections have since been treated with ciprofloxacin and clindamycin without adverse event. Since enalapril was stopped 18 months ago he has had no further episodes of angioedema. With an incidence of 0.1% to 0.2%, angioedema is a rare, potentially life-threatening adverse effect of angiotensin-converting enzyme (ACE) inhibitors. It involves most often face, oral cavity or the upper respiratory tract.2 Typically, it occurs within the first weeks of ACE inhibitor therapy,2 3 however, latencies of several months4 or even years3'5 have been reported. ACE inhibitors have also been reported to be the cause of anaphylac-toid reactions in individuals treated with wasp venom immunotherapy6 or when combined with allopurinol7 and in patients undergoing …