Sympathomimetic drug allergy: cross-reactivity study by patch test.

INTRODUCTION: Sympathomimetic (alpha-adrenergic) drugs are mainly used because of their vasoconstrictor properties, for nasal congestion, or as mydriatics. Although sympathomimetic drugs are used often, allergic reactions are rare, especially when the drugs are administered systemically. Cross-reactivity may exist among catecholamine derivatives, although reported data on this are contradictory. In this study, we investigate if there is cross-reactivity in patch tests among these drugs. MATERIAL AND METHODS: Patch tests with 10% phenylephrine and 10% pseudoephedrine in petrolatum, and 10% and 20% ephedrine, 10% phenylpropanolamine, 5% fepradinol, 1% methoxamine, and 10% oxymetazoline, all administered in dimethyl sulfoxide (DMSO), were carried out in 14 patients with a history of allergy to any of these drugs. DMSO was used as the negative control. RESULTS: All patients except one (patient number five) showed positive patch-test reactions to at least two different drugs. Nine patients (64.3%) were cross-sensitized to three or more different drugs, and 57.1% of patients were sensitized to four or more sympathomimetic drugs. Patients who experienced generalized rashes caused by orally administered pseudoephedrine had a stronger response and more cross-reactivity with other sympathomimetic drugs in patch tests than those who experienced local contact dermatitis. CONCLUSIONS: We conclude that there is cross-reactivity among the different sympathomimetic drugs tested, especially if the drug is administered systemically.

Eyedrop-induced allergy: clinical evaluation and diagnostic protocol.

BACKGROUND: In the last few years, adverse reactions to mydriatic eyedrops have been investigated. However, is not still available a standardized protocol, capable of identify the pathogenetic mechanism. In the light of these findings we have evaluated the reliability of a protocol with well established concentration of specific allergens. METHODS: The diagnostic method includes the application of patch test series Gruppo Italiano Ricerca Dermatiti da Contatto e Ambientali (GIRDCA), medicaments, corticosteroids, local anesthetics, main eyedrops' excipients, pure active principles and extemporaneous preparations with mydriatic eyewashes. At the same time, skin prick test with a solution of atropine sulfate at 1 per thousand and an intradermal test with injection of atropine at 0.01 per thousand were carried out. RESULTS: After patch tests were removed, we detected seven positiveness to the phenylephrine, two to the benzalkonium chloride, one to thiomersal, one to the ethylendiamine and one to the atropine sulfate 1 per thousand. With intradermal tests we obtained three positiveness in patients who reported adverse reactions to atropine. CONCLUSIONS: Our results show that phenylephrine is frequently responsible for allergic conjunctivitis (53.8%). In the case of atropine, even though the limited number of patients suggests to perform more extensive studies, it emerges that our diagnostic protocol is safe and might be able to screen allergic reactions in the field of ophthalmopathies.

Interleukin-1 beta rapidly inhibits aortic endothelium-dependent relaxation by a DNA transcription-dependent mechanism.

OBJECTIVES: This study examined the effects of interleukin-1 beta on isometric tension development and relaxation in isolated rat aortic rings in response to the alpha-1 adrenergic agonist phenylephrine, the endothelium-dependent vasodilator acetylcholine, and the endothelium-independent vasodilator sodium nitroprusside. DESIGN: Randomized, controlled, paired design. SETTING: Animal laboratory within a university department of physiology. SUBJECTS Paired aortic thoracic aortic rings from specific pathogen-free Sprague-Dawley rats. INTERVENTIONS: Series I examined the potential for interleukin-1 beta to cause early arterial endothelial dysfunction. Paired aortic rings were incubated for 2 hrs with interleukin-1 beta or vehicle. Series II examined the potential for inhibition of DNA transcription to attenuate interleukin-1 beta-mediated endothelial dysfunction. Paired rings received either dactinomycin or vehicle before interleukin-1 beta incubation. Series III quantified the degree to which inhibition of DNA transcription inhibited early interleukin-1 beta-mediated endothelial dysfunction. Paired rings received either dactinomycin pretreatment followed by interleukin-1 beta incubation, or pretreatment and incubation with inert vehicles. Series IV assessed the effects of interleukin-1 beta on responsiveness to an exogenous nitric oxide donor, sodium nitroprusside, in the presence of the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester. MEASUREMENTS AND MAIN RESULTS: Incubation with interleukin-1 beta for 2 hrs had no effect on contractile response but attenuated endothelium-dependent relaxation significantly relative to control. Dactinomycin pretreatment inhibited early interleukin-1 beta-mediated endothelial dysfunction. The combination of interleukin-1 beta and dactinomycin produced effects on endothelium-dependent relaxation that were not different from that seen in rings not exposed to interleukin-1 beta. Interleukin-1 beta attenuated responsiveness to sodium nitroprusside relative to control. CONCLUSIONS: Interleukin-1 beta causes an early impairment of endothelium-dependent vasorelaxation with an onset that precedes its effects on systemic contractility. This impairment occurs via a mechanism that is wholly or predominantly dependent on DNA transcription. The altered vasorelaxation induced by interleukin-1 beta is at least partly mediated by a reduction in nitric oxide responsiveness.