E. Di Leo

Kounis Syndrome induced by intravenous administration of piperacillin/tazobactam: a case report.

Kounis Syndrome (KS) is the concurrence of an acute coronary event with conditions associated with a massive mast–cell degranulation, usuallyduringanaphylactic or ananaphylactoid reaction [1]. KS seems to bepromoted by inflammatorymediators, as histamine, chemokines and leukotrienes released by cardiacmast cells [2], able to induce a coronary vasospasm [1,2]. KS was firstly described in 1991 by Kounis and Zavras as allergic angina progressing to “allergic myocardial infarction”[3]. KS can be induced by Hymenoptera stings, food allergy and of course various drugs as well as contrast media, intravenous anaesthetics, NSAIDs and, of course, antibiotics [1]. Betalactams are the commonest cause of drug induced KS and amoxicillin is the most frequently culprit betalactam molecule [4]. We described a KS in a 62-year old man following tazobactam/ piperacillin infusion. An obese non atopic 62 years old man was admitted to the 4° Pneumologic Division of Hospital A. Galateo (Lecce) for an acute pneumonia coming from the First Aid Center of the Civil Hospital Vito Fazzi. The patient claimed cough, malaise and slight chest constriction with no fever or dyspnea. The chest X-ray confirmed presence of a pneumonic process on the basal right lung. Laboratory tests showed a slight neutrophilic leucocytosis (WBC.: 12.200/mm) with a mild hyperglicemia (1.24). Pulse oxymetry was satisfactory (97%) and the electrocardiography (ECG) showed a normal frequency with sinus rhythm. Blood pressure was good (80/130 mm Hg). Thoracic objec-

Treatment of acquired cold urticaria with rupatadine.

fluids was maximally increased. BPremained stable; pulse rate normalizedafter 15 min. A local reaction(30 · 35 mm wheal, 70 · 80 mm flare)developed at the venom injection site in20 min; residual flushing and the cuta-neous reaction were still present beyondone hour. Tryptase showed mild increasecompared to the levels prior to reducingomalizumab (Fig. 1, Phase II).Thereafter, anti-IgEdosewas increasedto 300 mg and patient remained com-pletely free of any adverse effect. Themorning of course No. 13th venom skintests were performed and were positiveagain (10 · 13 mmW, 20 · 47F, at 1 lg/ml) for the first time since Omalizumabtreatment had been initiated; tryptase –measured on that morning – showedcontinuous mild increase (Fig. 1).Subsequently, for financial and conve-nience reasons, a gradual increase in thecourse interval was attempted; uponreaching 35 days (17th course) patientdeveloped facial flushing (no subjectivesensation) 20 min post-VimRx; flarewithout wheal, was noted at the venominjection site. The combined treatmentschedule was again changed to 30-dayintervals and has been continueduneventfully thereafter (courses No.24–26) on an outpatient basis. ID venom-Skin tests performed during the latestsession were negative up to the concen-tration of 1 lg/ml. Tryptase, drawn2 weeks later, dropped to 18.3 mcg(Fig. 1, Phase II).In conclusion, the present case-studyon the protective effect of omalizumabin systemic mastocytosis undergoingVImRx, suggests that the beneficial effectappears to require higher than the rec-ommended omalizumab dose and strictly30-day administration intervals; theoccurrence of mild cutaneous and car-diovascular signs, the immediate localreaction at the venom injection site andthe conversion to skin test positivity,observed upon either omalizumabs dosereduction or increased treatment-interval,suggest that no immunologic changeshave occurred because of VImRx.It appears logical to speculate that theexcellent response noted during Phase Iof this study is exclusively due to oma-lizumabs mast cell stabilizing and prob-ably other actions (5, 6); the changesnoted in serum tryptase are in agreement.Obviously, this concept questions thelogic of continuing VImRx. However, novalid conclusions can be drawn from asingle case and the present findings needto be confirmed; because of the lowsystemic mastocytosis with venomanaphylaxis prevalence, a multicenter-study would be appropriate.No financial or other relations with themanufacturing company of either drugused in this case study.

Long-term selective IgE-mediated hypersensitivity to hydrocortisone sodium succinate.

Patients’ data protection. Confidentiality of data. The authors declare that they have followed the protocols of their work centre on the publication of patient data and 3. Benucci M, Manfredi M, Demoly P, Campi P. Injection site rea tions to TNFblocking agents with positive skin tests. Allerg 2008;63:138--9. 4. Brennan PJ, Rodriguez Bouza T, Hsu FI, Sloane DE, Castells M Hypersensitivity reactions to mAbs: 105 desensitizations in 2 patients, from evaluation to treatment. J Allergy Clin Immuno 2009;124:1259--66. 5. Rodriguez Jimenez B, Dominquez-Ortega J. Successful ada mumab desensitization after generalized urticaria and rhiniti J Investig Allergol Clin Immunol. 2009;19:246--7. 6. Zeltser R, Valle L, Tanck C, Holyst MM, Ritchlin C, Gaspari A Clinical, histological, and immunophenotypic characteristics injection site reactions associated with etanercept: a recom binant tumor necrosis factor alpha-receptor: Fc fusion protei Arch Dermatol. 2001;137:893--9. 7. Winfield H, Lain E, Horn T, Hoskyn J. Eosinophilic cellulites lik fin

Contact allergy to benzocaine in a condom

L. Muratore, G. Calogiuri, C. Foti, E. Nettis, E. Di Leo and A. Vacca Allergy and Clinical Immunology Center, Civil Hospital Vito Fazzi, 73100 Lecce, 4th Department, Hospital for Pulmonary Disease A. Galateo, 73016 San Cesario di Lecce, Lecce, Department of Internal Medicine, Immunology and Infectious Disease, Unit of Allergy and Clinical Immunology and Department of Dermatology and Venereology, University of Bari, 70124 Bari, Italy

Acquired Angioedema with C1 Inhibitor Deficiency Associated with Anticardiolipin Antibodies

Acquired angioedema (AAE) with C1 inhibitor deficiency is often associated to B cell lymphoproliferative disorders or autoimmune diseases. We report a case of AAE associated with IgM anti-cardiolipin antibodies, with frequent edematous attacks, that disappeared completely after a slight immunosuppression and danazol therapy.

Immediate rhinoconjunctivitis induced by metamizole: an allergic reaction?

1. Rietkötter J, Körber A, Grabbe S, Dissemond J. Eradication of methicillin-resistant Staphylococcus aureus in a chronic wound by a new polyhexanide hydrogel. J Eur Acad Dermatol Venereol 2007;21: 1416–1417. 2. Olivieri J, Eigenmann PA, Hauser C. Severe anaphylaxis to a new disinfectant: polyhexanide, a chlorhexidine polymer. Schweiz Med Wochenschr 1998;128: 1508–1511. 3. Ferrarini A, Baggi M, Flückiger R, Bianchetti MG. Intraoperative anaphylaxis to a chlorhexidine polymer in childhood. Paediatr Anaesth 2006;16:705. (abstract). 4. Krautheim AB, Jermann TH, Bircher AJ. Chlorhexidine anaphylaxis: case report and review of the literature. Contact Dermatitis 2004;50:113–116. 5. Pham NH, Weiner JM, Reisner GS, Baldo BA. Anaphylaxis to chlorhexidine. Case report. Implication of immunoglobulin E antibodies and identification of an allergenic determinant. Clin Exp Allergy 2000;30:1001–1007. 6. Garvey LH, Krøigaard M, Poulsen LK, Skov PS, Mosbech H, Venemalm L et al. IgE-mediated allergy to chlorhexidine. J Allergy Clin Immunol 2007;120:409–415.

Diagnosis of latex allergy: the importance of hev B 11.

We present the cases of 5 patients with a positive clinical history of cutaneous symptoms due to contact with latex products. A latex allergological assessment was made through skin prick tests (SPTs) both with commercial latex extracts and extemporaneous glove extracts, and serum-specific IgE to latex and glove-use tests. In addition, serum-specific IgE to recombinant allergens for Hevea brasiliensis was dosed. Molecular diagnostics in association with the glove-use test and, to a lesser extent, the SPTs with glove eluate are useful diagnostic tests to confirm the diagnosis of latex allergy in patients with mucocutaneous symptoms.

Fixed drug eruption due to sodium fluorescein

We describe a case of fixed drug eruption due to sodium fluorescein diagnosed by a positive patch test. Sodium fluorescein is a dye used in angiography for investigation of many ocular diseases. The use of it is considered generally safe, but adverse reactions to this contrast media are described in the literature (1), including immunoglobulin Emediated events following intravenous administration (2).

Focus on the agents most frequently responsible for perioperative anaphylaxis

Adverse reactions (ARs) to drugs administered during general anesthesia may be very severe and life-threatening, with a mortality rate ranging from 3 to 9%. The adverse reactions to drugs may be IgE and non-IgE-mediated. Neuromuscular blocking agents (NMBA) represent the first cause of perioperative reactions during general anesthesia followed by latex, antibiotics, hypnotic agents, opioids, colloids, dyes and antiseptics (chlorhexidine). All these substances (i.e. NMBA, anesthetics, antibiotics, latex devices) may cause severe systemic non-IgE-mediated reactions or fatal anaphylactic events even in the absence of any evident risk factor in the patient’s anamnesis. For this reason, in order to minimize perioperative anaphylactic reactions, it is important to have rapid, specific, sensitive in vitro diagnostic tests able to confirm the clinical diagnosis of acute anaphylaxis.

Tomato atopy patch test in adult atopic dermatitis: diagnostic value and comparison among different methods

Tomato atopy patch test in adult atopic dermatitis.