Michael Kaliner
George Washington University
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The Journal of Allergy and Clinical Immunology | 2004
Eli O. Meltzer; Daniel L. Hamilos; James A. Hadley; Donald C. Lanza; Bradley F. Marple; Richard A. Nicklas; Claus Bachert; James N. Baraniuk; Fuad M. Baroody; Michael S. Benninger; Itzhak Brook; Badrul A. Chowdhury; Howard M. Druce; Stephen R. Durham; Berrylin J. Ferguson; Jack M. Gwaltney; Michael Kaliner; David W. Kennedy; Valerie J. Lund; Robert M. Naclerio; Ruby Pawankar; Jay F. Piccirillo; Patricia E. W. Rohane; Ronald A. Simon; Raymond G. Slavin; Alkis Togias; Ellen R. Wald; S. James Zinreich
Background There is a need for more research on all forms of rhinosinusitis. Progress in this area has been hampered by a lack of consensus definitions and the limited number of published clinical trials. Objectives To develop consensus definitions for rhinosinusitis and outline strategies useful in clinical trials. Methods Five national societies, The American Academy of Allergy, Asthma and Immunology; The American Academy of Otolaryngic Allergy; The American Academy of Otolaryngology Head and Neck Surgery; The American College of Allergy, Asthma and Immunology; and the American Rhinologic Society formed an expert panel from multiple disciplines. Over two days, the panel developed definitions for rhinosinusitis and outlined strategies for design of clinical trials. Results Committee members agreed to adopt the term “rhinosinusitis” and reached consensus on definitions and strategies for clinical research on acute presumed bacterial rhinosinusitis, chronic rhinosinusitis without polyposis, chronic rhinosinusitis with polyposis, and classic allergic fungal rhinosinusitis. Symptom and objective criteria, measures for monitoring research progress, and use of symptom scoring tools, quality-of-life instruments, radiologic studies, and rhinoscopic assessment were outlined for each condition. Conclusion The recommendations from this conference should improve accuracy of clinical diagnosis and serve as a starting point for design of rhinosinusitis clinical trials.
The Journal of Allergy and Clinical Immunology | 1999
Nancy Fox Ray; James N. Baraniuk; Mae Thamer; Cheryl S. Rinehart; Peter J. Gergen; Michael Kaliner; Shelby Josephs; Yung-Hao Pung
BACKGROUND There have been no recent assessments of the economic burden of sinusitis in the peer-reviewed literature. OBJECTIVE We sought to estimate the 1996 total direct health care expenditures for the treatment of sinusitis. METHODS This study determined (1) direct expenditures of medical and surgical encounters in which sinusitis was the primary diagnosis and (2) attributable expenditures when related airway diseases were the primary diagnosis and sinusitis was a comorbid condition. An expert panel used the Delphi consensus-building technique to determine the proportions for the latter. RESULTS Overall health care expenditures attributable to sinusitis in 1996 were estimated at
The Journal of Allergy and Clinical Immunology | 1997
Michael Kaliner; J. David Osguthorpe; Philip Fireman; Jack B. Anon; John W. Georgitis; Mary L. Davis; Robert M. Naclerio; David W. Kennedy
5.8 billion, of which
Allergy | 2008
Jean Bousquet; N. Khaltaev; Alvaro A. Cruz; Judah A. Denburg; W. J. Fokkens; Alkis Togias; T. Zuberbier; Carlos E. Baena-Cagnani; G. W. Canonica; C. van Weel; Ioana Agache; N. Aït-Khaled; Claus Bachert; Michael S. Blaiss; Sergio Bonini; Louis-Philippe Boulet; P.-J. Bousquet; Paulo Augusto Moreira Camargos; K.-H. Carlsen; Yijing Chen; Adnan Custovic; Ronald Dahl; P. Demoly; H. Douagui; Stephen R. Durham; R. Gerth van Wijk; O. Kalayci; Michael Kaliner; Y.‐Y. Kim; M. L. Kowalski
1.8 billion (30.6%) was for children 12 years or younger. A primary diagnosis of acute or chronic sinusitis accounted for 58.7% of all expenditures (
Journal of Clinical Investigation | 1981
Zvi Marom; James H. Shelhamer; Michael Kaliner
3.5 billion). About 12% each of the costs for asthma and chronic otitis media and eustachian tube disorders were attributed to diagnosis and treatment of comorbid sinusitis. Nearly 90% of all expenditures (
Journal of Clinical Investigation | 1983
Zvi Marom; James H. Shelhamer; Frank Sun; Michael Kaliner
5.1 billion) were associated with ambulatory or emergency department services. CONCLUSION The economic burden of sinusitis in the United States is significant. However, the limitations of this type of evaluation suggest the
The Journal of Allergy and Clinical Immunology | 1984
Thomas B. Casale; Scott Bowman; Michael Kaliner
5.8 billion amount may be an underestimate of the true direct costs.
Annals of Internal Medicine | 1982
Michael Kaliner; James H. Shelhamer; Pamela B. Davis; Laurie J. Smith; J. Craig Venter
Sinusitis, an inflammatory disease of the sinus, is one of the most commonly reported diseases in the United States, affecting an estimated 14% of the population. The prevalence of sinusitis is rising. Between 1990 and 1992, persons with sinusitis reported approximately 73 million restricted activity days--an increase from the 50 million restricted activity days reported between 1986 and 1988. Because critical questions remain unanswered about its cause, pathophysiology, and optimal treatment, sinusitis continues to generate significant health care costs and affects the quality of life of a large segment of the U.S. population. To identify critical directions for research on sinus disease, the American Academy of Allergy, Asthma and Immunology and the American Academy of Otolaryngology-Head and Neck Surgery Foundation, Inc., convened a meeting in January 1996 in collaboration with the National Institutes of Allergy and Infectious Disease. This document summarizes the proceedings of that meeting and presents what is intended to be the background for future investigation of the many unanswered questions related to sinusitis.
Journal of Clinical Investigation | 1989
G D Raphael; E V Jeney; James N. Baraniuk; I Kim; S D Meredith; Michael Kaliner
J. Bousquet, N. Khaltaev, A. A. Cruz, J. Denburg, W. J. Fokkens, A. Togias, T. Zuberbier, C. E. Baena-Cagnani, G. W. Canonica, C. van Weel, I. Agache, N. A t-Khaled, C. Bachert, M. S. Blaiss, S. Bonini, L.-P. Boulet, P.-J. Bousquet, P. Camargos, K.-H. Carlsen, Y. Chen, A. Custovic, R. Dahl, P. Demoly, H. Douagui, S. R. Durham, R. Gerth van Wijk, O. Kalayci, M. A. Kaliner, Y.-Y. Kim, M. L. Kowalski, P. Kuna, L. T. T. Le, C. Lemiere, J. Li, R. F. Lockey, S. Mavale-Manuel , E. O. Meltzer, Y. Mohammad, J. Mullol, R. Naclerio, R. E. O Hehir, K. Ohta, S. Ouedraogo, S. Palkonen, N. Papadopoulos, G. Passalacqua, R. Pawankar, T. A. Popov, K. F. Rabe, J. Rosado-Pinto, G. K. Scadding, F. E. R. Simons, E. Toskala, E. Valovirta, P. van Cauwenberge, D.-Y. Wang, M. Wickman, B. P. Yawn, A. Yorgancioglu, O. M. Yusuf, H. Zar Review Group: I. Annesi-Maesano, E. D. Bateman, A. Ben Kheder, D. A. Boakye, J. Bouchard, P. Burney, W. W. Busse, M. Chan-Yeung, N. H. Chavannes, A. Chuchalin, W. K. Dolen, R. Emuzyte, L. Grouse, M. Humbert, C. Jackson, S. L. Johnston, P. K. Keith, J. P. Kemp, J.-M. Klossek, D. Larenas-Linnemann, B. Lipworth, J.-L. Malo, G. D. Marshall, C. Naspitz, K. Nekam, B. Niggemann, E. Nizankowska-Mogilnicka, Y. Okamoto, M. P. Orru, P. Potter, D. Price, S. W. Stoloff, O. Vandenplas, G. Viegi, D. Williams
The Journal of Allergy and Clinical Immunology | 1993
Bernard Mosimann; Martha V. White; Robert J. Hohman; Michael S. Goldrich; Helen C. Kaulbach; Michael Kaliner
Human lung explants maintained in culture for 7 d incorporate [(3)H]glucosamine into mucous glycoproteins. Ethanol-precipitable, glucosamine-labeled mucous secretion was measured, and the effects of different pharmacologic agents upon this secretion were investigated. Anaphylaxed human lung generates prostaglandin (PG) synthesis and increased mucous release. Arachidonic acid (AA), PGA(2), PGD(2), and PGF(2alpha) significantly increased mucous glycoprotein release, whereas PGE(2) significantly reduced release. Evidence which suggests that lipoxygenase products of AA augment mucous release includes the following: (a) Nonsteroidal anti-inflammatory drugs (NSAID: acetylsalicylic acid and indomethacin) increase mucous release while preventing prostaglandin formation. (b) The increase in mucous release induced by AA or NSAID is additive once the agents are combined. (c) Several nonspecific lipoxygenase inhibitors (eicosa-5,8,11,14-tetraynoic acid; vitamin E; nordihydroguaiaretic acid; and alpha-naphthol) inhibit mucous release. Three additional lines of evidence directly indicate that monohydroxyeicosatetraenoic acid (HETE) causes increased mucous release: (a) the addition of a mixture of synthetic HETE (24-600 nM) increases mucous release; (b) pure 12-HETE (1-100 nM) also increases mucous release; (c) mucous release is increased synergistically by the combination of HETE and NSIAD. These data taken together demonstrate that HETE are capable of increasing mucous release and that conditions which may influence HETE production alter mucous release. Thus, although not directly demonstrating HETE production by human airways, the data strongly suggest that lipoxygenase products of AA in airways may profoundly influence mucous release; and it seems possible that lipoxygenase inhibitors may have a role in treating bronchorrhea.