Authors Jan L. Brozek, MD, PhD – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada Jean Bousquet, MD, PhD – Service des Maladies Respiratoires, Hopital Arnaud de Villeneuve, Montpellier, France, INSERM, CESP U1018, Respiratory and Environmental Epidemiology Team, France, and WHO Collaborating Center for Rhinitis and Asthma Carlos E. Baena-Cagnani, MD – Faculty of Medicine, Catholic University of Cordoba, Cordoba, Argentina Sergio Bonini, MD – Institute of Neurobiology and Molecular Medicine – CNR, Rome, Italy and Department of Medicine, Second University of Naples, Naples, Italy G. Walter Canonica, MD – Allergy & Respiratory Diseases, DIMI, Department of Internal Medicine, University of Genoa, Genoa, Italy Thomas B. Casale, MD – Division of Allergy and Immunology, Department of Medicine, Creighton University, Omaha, Nebraska, USA Roy Gerth van Wijk, MD, PhD – Section of Allergology, Department of Internal Medicine, Erasmus Medical Centre, Rotterdam, the Netherlands Ken Ohta, MD, PhD – Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan Torsten Zuberbier, MD – Department of Dermatology and Allergy, Charite Universitatsmedizin Berlin, Berlin, Germany Holger J. Schunemann, MD, PhD, MSc – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada

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Allergic Rhinitis and Its Impact on Asthma

These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology; the American College of Allergy, Asthma and Immunology; and the Joint Council of Allergy, Asthma and Immunology. The American Academy of Allergy, Asthma & Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing "The diagnosis and Management of Rhinitis: An Updated Practice Parameter." This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion.

The diagnosis and management of rhinitis: An updated practice parameter

Objective: To determine whether intranasal corticosteroids are superior to oral H 1 receptor antagonists (antihistamines) in the treatment of allergic rhinitis. Design: Meta-analysis of randomised controlled trials comparing intranasal corticosteroids with oral antihistamines. Setting: Randomised controlled trials conducted worldwide and published between 1966 and 1997. Subjects: 2267 subjects with allergic rhinitis in 16 randomised controlled trials. Main outcome measures: Nasal blockage, nasal discharge, sneezing, nasal itch, postnasal drip, nasal discomfort, total nasal symptoms, nasal resistance, and eye symptoms and global ratings. Outcomes measured on different scales were combined to determine pooled odds ratios (categorical outcomes) or standardised mean differences (continuous outcomes). Assessment of heterogeneity between studies, and subgroup analyses of eye symptoms, were undertaken. Results: Intranasal corticosteroids produced significantly greater relief than oral antihistamines of nasal blockage (standardised mean difference −0.63, 95% confidence interval −0.73 to −0.53), nasal discharge (−0.5, −0.6 to −0.4), sneezing (−0.49, −0.59 to −0.39), nasal itch (−0.38, −0.49 to −0.21), postnasal drip (−0.24, −0.42 to −0.06), and total nasal symptoms (−0.42, −0.53 to −0.32), and global ratings gave an odds ratio for deterioration of symptoms of 0.26 (0.08 to 0.8). There were no significant differences between treatments for nasal discomfort, nasal resistance, or eye symptoms. The effects on sneezing, total nasal symptoms, and eye symptoms were significantly heterogeneous between studies. Other combined outcomes were homogeneous between studies. Subgroup analysis of the outcome of eye symptoms suggested that the duration of assessment (averaged mean score over the study period versus mean score at end of study period) might have accounted for the heterogeneity. Conclusion: The results of this systematic review, together with data on safety and cost effectiveness, support the use of intranasal corticosteroids over oral antihistamines as first line treatment for allergic rhinitis.

https://www.bmj.com/content/bmj/317/7173/1624.full.pdf

Intranasal corticosteroids versus oral H1 receptor antagonists in allergic rhinitis: systematic review of randomised controlled trials

(±)[125Iodo]cyanopindolol (ICYP) is a radioligand which binds with an extraordinarily high affinity and specificity to β-adrenoceptors. In contrast to (±)[125Iodo]-hydroxybenzylpindolol (IHYP), the new ligand has neither affinity to α- nor to 5-HT-receptors. The dissociation constants of ICYP for β-adrenoceptors in various tissues range from 27 to 40 pM, thereby exceeding the affinity of IHYP by a factor of ∼ 3. ICYP does not discriminate between β1− and β2−. Therefore, the densities of the two receptor subtypes can be determined from competition curves of ICYP by drugs previously found to show in vitro selectivity for β1−adrenoceptors. The guinea pig left ventricle contains only β1− adrenoceptors, whereas in the lung tissue, the ratio of β1− to β2−adrenoceptors is 1 to 4. The calculated affinities of five β1− selective antagonists for β1−adrenoceptors were nearly identical in the ventricle and the lung. Kinetic studies of ICYP binding to guinea pig lung membranes indicated that the dissociation reaction consists of two components, a fast process (t
1/2=9 min) and a slower process (t
1/2=8.8 h). A mathematical treatment revealed two possibilities of interpretation: 1. Two forms of the receptor exist which are interconvertible. 2. The (+)- and (−)-enantiomers of ICYP dissociate with different rate constants. The low dissociation constant of ICYP in combination with its high specific radioactivity (2175 Ci mmole−1) allows binding studies to be carried out with small protein and ligand concentrations, e.g. 3 μg protein per assay in guinea pig lung membranes.

(+/-)[125Iodo] cyanopindolol, a new ligand for beta-adrenoceptors: identification and quantitation of subclasses of beta-adrenoceptors in guinea pig.

Autonomic neural influences on the dysrhythmias resulting from myocardial infarction.

Studies in both animals and man have shown that metoprolol is a β1-selective adrenergic receptor antagonist devoid of betamimetic activity. The cardiac stimulant effect of isoprenaline is markedly inhibited by metoprolol in doses that only slightly influence the vasodilator and bronchodilator effects of isoprenaline. Metoprolol markedly inhibits the cardiac response to exogenous or neuronally released noradrenaline. This action is probably the main determinant of the acute general hemodynamic effects of the compound. Metoprolol differs from propranolol in being a very weak inhibitor of the peripheral vasodilator effect of adrenaline. The two blockers may therefore produce differential hemodynamic effects in situations in which endogenous adrenaline contributes to cardiovascular control.



Metoprolol has a preventive antihypertensive action in rats with genetically determined hypertension. This effect is associated with an impaired vasoconstrictor fibre control, the mechanism of which is discussed.



The results of the toxicological and general pharmacological studies indicate that metoprolol is a highly specific β-blocker.



The pharmacokinetic studies indicate that metoprolol is completely absorbed after oral administration. The first pass elimination in man is about 55% and independent of dose in the therapeutic dose range. Metoprolol is eliminated from human blood plasma with a half-life of 3–4 hours. The main metabolites have been isolated and characterized pharmacologically. Unchanged metoprolol appears to be responsible for the β-blocking action.



The pharmacological characterization of metoprolol gave results that warranted reformulation of the β1—β2-receptor classification of Lands et al. (1967). This modified adrenergic β-receptor concept is described and its implications are discussed.

A survey of the pharmacological properties of metoprolol in animals and man.

Pharmacological Properties of H 56/28—a ß-Adrenergic Receptor Antagonist

Cardiac effects of beta-adrenergic receptor antagonists.

A randomized double blind placebo controlled cross-over study comparing budesonide 400 micrograms and budesonide 800 micrograms daily in 59 patients is presented. Nasal obstruction was the predominant symptom and was subjectively and objectively improved by both doses of budesonide (P less than 0.001). No significant difference was found between the two treatments. Both patient subgroups with non-allergic, non-eosinophilic rhinitis and perennial allergic rhinitis benefitted from therapy. Basal and stimulated plasma cortisol levels remained unchanged with either dose of budesonide, and no increase in adverse effects occurred with higher dose therapy.

A double blind comparison of intranasal budesonide 400 micrograms and 800 micrograms in perennial rhinitis.

A N D ~ N , N.-E. & MAGNUSSON, T. (1967). Acta physiol. scand., 69, 87-94. BERTLER, A., CARLSSON, A. & ROSENGREN, E. (1958). Ibid., 44, 273-292. CARLSSON, A. & LINDQVIST, M. (1962). HAGGENDAL, J. (1963). Ibid., 59, 242-254. GREEN, H. & ERICKSON, R. W. (1964). Int. J. Neuropharmac., 3, 315-320. KAHLSON, G., ROSENGREN, E. & THUNBERG, R. (1963). J. Physiol., Lond., 169, 467-486. SADAVONGVIVAD, C. (1970). C. V. ATACK

Inhibitory effect of propranolol on the vasoconstrictor response to sympathetic nerve stimulation.

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