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5. Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*

Author

Bousquet, J., primary, Khaltaev, N., additional, Cruz, A. A., additional, Denburg, J., additional, Fokkens, W. J., additional, Togias, A., additional, Zuberbier, T., additional, Baena-Cagnani, C. E., additional, Canonica, G. W., additional, Van Weel, C., additional, Agache, I., additional, Aït-Khaled, N., additional, Bachert, C., additional, Blaiss, M. S., additional, Bonini, S., additional, Boulet, L.-P., additional, Bousquet, P.-J., additional, Camargos, P., additional, Carlsen, K.-H., additional, Chen, Y., additional, Custovic, A., additional, Dahl, R., additional, Demoly, P., additional, Douagui, H., additional, Durham, S. R., additional, Van Wijk, R. Gerth, additional, Kalayci, O., additional, Kaliner, M. A., additional, Kim, Y.-Y., additional, Kowalski, M. L., additional, Kuna, P., additional, Le, L. T. T., additional, Lemiere, C., additional, Li, J., additional, Lockey, R. F., additional, Mavale-Manuel, S., additional, Meltzer, E. O., additional, Mohammad, Y., additional, Mullol, J., additional, Naclerio, R., additional, O’Hehir, R. E., additional, Ohta, K., additional, Ouedraogo, S., additional, Palkonen, S., additional, Papadopoulos, N., additional, Passalacqua, G., additional, Pawankar, R., additional, Popov, T. A., additional, Rabe, K. F., additional, Rosado-Pinto, J., additional, Scadding, G. K., additional, Simons, F. E. R., additional, Toskala, E., additional, Valovirta, E., additional, Van Cauwenberge, P., additional, Wang, D.-Y., additional, Wickman, M., additional, Yawn, B. P., additional, Yorgancioglu, A., additional, Yusuf, O. M., additional, Zar, H., additional, Annesi-Maesano, I., additional, Bateman, E. D., additional, Kheder, A. Ben, additional, Boakye, D. A., additional, Bouchard, J., additional, Burney, P., additional, Busse, W. W., additional, Chan-Yeung, M., additional, Chavannes, N. H., additional, Chuchalin, A., additional, Dolen, W. K., additional, Emuzyte, R., additional, Grouse, L., additional, Humbert, M., additional, Jackson, C., additional, Johnston, S. L., additional, Keith, P. K., additional, Kemp, J. P., additional, Klossek, J.-M., additional, Larenas-Linnemann, D., additional, Lipworth, B., additional, Malo, J.-L., additional, Marshall, G. D., additional, Naspitz, C., additional, Nekam, K., additional, Niggemann, B., additional, Nizankowska-Mogilnicka, E., additional, Okamoto, Y., additional, Orru, M. P., additional, Potter, P., additional, Price, D., additional, Stoloff, S. W., additional, Vandenplas, O., additional, Viegi, G., additional, and Williams, D., additional

Published
2008
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37. Effect of upper respiratory tract infection on AIR inhaled insulin pharmacokinetics and glucodynamics in healthy subjects.

Author

Gern JE, Stone CK, Nakano M, Muchmore DB, de la Peña A, Park S, Suri A, Tibaldi F, Soon D, and Busse WW

Subjects
Administration, Oral, Adult, Area Under Curve, Forced Expiratory Volume, Glucose Clamp Technique, Humans, Hypoglycemic Agents administration & dosage, Hypoglycemic Agents adverse effects, Insulin administration & dosage, Insulin adverse effects, Picornaviridae Infections physiopathology, Respiratory Tract Infections physiopathology, Respiratory Tract Infections virology, Spirometry, Vital Capacity, Blood Glucose drug effects, Hypoglycemic Agents pharmacokinetics, Insulin pharmacokinetics, Picornaviridae Infections metabolism, Respiratory Tract Infections metabolism
Abstract

The suitability of employing AIR Inhaled Insulin (AIR Insulin; AIR is a registered trademark of Alkermes) during acute upper respiratory tract infection (URI) has not been determined. Twenty-one healthy, non-diabetic subjects were enrolled in a single-sequence, two-period, euglycemic clamp study. Subjects received a single 12 U-equivalent dose of AIR Insulin before rhinovirus (RV16) inoculation and during symptomatic infection. Spirometry was used to evaluate pulmonary safety. AIR Insulin exposure (the area under the immunoreactive insulin (IRI) concentration vs time curve from time zero until the IRI concentrations returned to the predose baseline value (AUC(0-t'))) and glucodynamic response (total amount of glucose infused (G(tot))) were comparable before and during RV infection (AUC(0-t') 46,300 vs 52,600 pmol min/l, P=0.21; G(tot) 61,800 vs 68,700 mg, P=0.42, respectively). Variability of pharmacokinetic and pharmacodynamic parameters did not change during URI; either did the number or intensity of adverse events. No significant change in forced expiratory volume or forced vital capacity was observed following AIR Insulin administration or during URI. The AIR Insulin system provides similar pharmacokinetic and glucodynamic responses under conditions of an experimentally induced RV infection and is regarded as suitable for use in diabetic patients during URIs.

Published
2008
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38. The role of the common cold in asthma.

Author

Busse WW

Subjects
Asthma complications, Common Cold complications, Humans, Respiratory Tract Infections complications, Respiratory Tract Infections physiopathology, Respiratory Tract Infections virology, Rhinovirus isolation & purification, Asthma physiopathology, Common Cold physiopathology
Abstract

It has long been known that patients with viral respiratory infections develop temporary asthma-like symptoms or see a worsening of their existing asthmatic symptoms or develop full-blown asthma during the infection. It should not be surprising, in view of this observation, that these same viruses have been found to initiate the same inflammatory processes as seen and characterized in the asthmatic patient. This has clear implications for therapy of asthmatic patients.

Published
1999

39. The role of respiratory viruses in asthma.

Author

Busse WW, Gern JE, and Dick EC

Subjects
Asthma immunology, Inflammation, Picornaviridae Infections immunology, Respiratory Tract Infections immunology, Asthma virology, Picornaviridae Infections complications, Respiratory Tract Infections virology, Rhinovirus immunology
Abstract

Respiratory infections are common causes of increased asthma for patients of all ages. Current evidence indicates that viral, and not bacterial, infections are the most important respiratory illnesses which increase the severity of asthma. Of the respiratory viral infections associated with increased asthma, rhinoviruses, i.e. the cause of common colds, have proven to be the virus most often found in association with increased asthma severity. Although the association between rhinovirus infections and asthma is most dramatically illustrated in children, asthma patients of all ages can be affected and the attacks of asthma can be severe. Studies to establish the mechanisms by which rhinoviruses enhance asthma severity have begun to focus on how this virus promotes allergic inflammation. We have found that experimental rhinovirus infections enhance airway responsiveness and, perhaps most importantly, the likelihood that a late allergic reaction will occur to an antigen challenge. Furthermore, using bronchoscopy and segmental antigen challenge, we have found that rhinovirus infections promote mast cell release of histamine and the recruitment of eosinophils to the airways. These data support the concept that rhinovirus infections act to promote allergic inflammation and by this mechanism increase both the likelihood of asthma occurring and the severity of wheezing.

Published
1997
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