May 2005 Medical Journal Review

Reviewed by Richard F. Lockey, M.D., Editor-In-Chief

1. THIS IS A NESTED CASE-CONTROL STUDY TO EXAMINE THE ASSOCIATION BETWEEN ASTHMA AND INVASIVE PNEUMOCOCCAL DISEASE. A TOTAL OF 635 PERSONS WITH INVASIVE PNEUMOCOCCAL DISEASE AND 6, 350 CONTROLS WERE IDENTIFIED, OF WHOM 114 (18%) AND 516 (8.1%), RESPECTIVELY, HAD ASTHMA. PERSONS WITH ASTHMA HAD AN INCREADED RISK (DOUBLED) OF INVASIVE PNEUMOCOCCAL DISEASE (ADJUSTED ODDS RATIO, 2.4; 95% CONFIDENCE INTERVAL, 1.9 TO 3.1) AS COMPARED WITH CONTROLS. Editor's comment: This paper suggests that pneumococcal vaccine should be administered to all asthmatics. Talbot TR, et al. N Engl J Med 352; 20: 2082.

2. THIS STUDY SURVEYED 605 HEALTHY, 540 HIGH-RISK, AND 1,388 HOSPITALIZED PATIENTS FOR RESPIRATORY SYNCYTIAL VIRUS (RSV) INFECTION OVER FOUR CONSECUTIVE WINTERS. RSV ACCOUNTED FOR 10.6% OF HOSPITALIZATIONS FOR PNEUMONIA, 11.4% FOR CHRONIC OBSTRUCTIVE PULMONARY DISEASE, 5.4% FOR CONGESTIVE HEART FAILURE, AND 7.2% FOR ASTHMA. IN THE HOSPITAL COHORT, RSV AND INFLUENZA A RESULT IN SIMILAR MORBIDITY AND MORTALITY. Editor's comment: RSV infection is a risk factor (similar to influenza A) for the elderly and high-risk adults. Falsey AR, et al. N Engl J Med 2005; 352: 1749.

3. A CHIMERIC HUMAN-CAT FUSION PROTEIN BLOCKS CAT-INDUCED ALLERGY IN MICE. IT HAS THE POTENTIAL TO PROVIDE A MORE EFFECTIVE AND SAFER ALTERNATIVE FOR ALLERGEN IMMUNOTHERAPY. THE AUTHORS ADMINISTERED A CHIMERIC HUMAN-CAT PROTEIN COMPRISED OF CAT ALLERGEN (Fel d1) LINKED TO PART OF THE CONSTANT (Fcγ) PORTION OF IgG. THIS APPROACH SURPRESSES Fel d1 ALLERGEN-AND IgE-DEPENDENT ACTIVATION OF MAST CELLS AND BASOPHILS, THE KEY EFFECTOR CELLS THAT PRODUCE THE MEDIATORS OF THE ALLERGIC REACTION. Editor's comment: Better, safer, and more effective immunotherapy is on the way. Zhu D, et al. Nature Medicine 2005; 11: 446, Kalesnikoff J, Galli SJ, editorial. Nature Medicine 2005; 11: 381.

4. SURGICAL SAMPLES WERE OBTAINED FROM PATIENTS WITH NON-CYSTIC FIBROSIS NASAL POLYPS (NON-CF-NP), CYSTIC FIBROSIS (CF) WITH NASAL POLYPS (CF-NP) AND CONTROL PATIENTS (CO). mRNA FOR INNATE MARKERS WAS MEASURED BY PCR AND INFLAMMATORY MEDIATORS BY ELISA AND UNICAP. HUMAN β DEFENSINS 2, TOLL-LIKE RECEPTOR 2, MYELOPEROXIDASE, AND IL-8 WERE INCREASED IN CF-NP. MACROPHAGE MANNOSE RECEPTOR, IL-5, EOSINOPHILIC CATIONIC PROTEIN, EOTAXIN, AND IgE WERE INCREASED IN NON-CF-NP. Editor's comment: There are differences in inflammatory mediators and innate markers in polyps of patients with CF vs. non-CF. Claeys S, et al. Clin Exp Allergy 2005; 35: 467.

5. STEM CELL FACTOR (SCF) WAS ASSESSED IN HUMAN NASAL POLYP EPITHELIAL CELLS AS RELATED TO PATIENTS' CLINICAL PHENOTYPES (ASA-INTOLERANT AND ASA-TOLERANT). THE NUMBER OF NASAL POLYPECTOMIES CORRELATED WITH THE EXPRESSION OF STEM CELL FACTOR mRNA, SCF PROTEIN IN HUMAN NASAL POLYP EPITHELIAL CELL (NPEC) SUPERNATANTS AND WITH THE DENSITY OF MAST CELLS IN THE EPITHELIAL AND STROMAL LAYERS OF NASAL POLYPS. Editor's comment: SCF can be directly related to the severity of nasal polyposis. The SCF/ β-actin mRNA ratios were higher as was the SCF protein concentrations in the NPEC supernatants in the ASA-intolerant vs. ASA-tolerant patients. Kowalski ML, et al. Allergy 205; 60: 631.

6. THESE AUTHORS FOUND A RELATIONSHIP BETWEEN THE ABILITY TO ERADICATE S. aureus WITH AN ORAL ANTIHISTAMINE AND A TOPICAL GLUCOCORTICOSTEROID AND SELECTED CLINICAL AND IMMUNOLOGICAL FEATURES IN SUBJECTS WITH ATOPIC DERMATITIS (AD). PATIENTS WITH PERSISTENT S. aureus AFTER TREATMENT PRESENTED WITH HIGHER SERUM IgE LEVELS AND LOWER LYMPHOCYTE PROLIFERATION RESPONSES TO STAPHYLOCOCCAL ENTEROTOXIN B, PHYTOHAEMAGLUTTININ AND ANTI-CD3. THE AUTHORS SPECULATE THAT THESE ABNORMALITIES AND IMMUNOLOGIC PARAMETERS ACCOUNT FOR THE LACK OF RESPONSE TO SUCH TREATMENT. Editor's comment: Just as with every other disease, there are biological differences among patients with AD. Guzik TJ, et al. Clin Exp Allergy 2005; 35: 448.

7. THERE ARE FIVE EDITORIALS CONCERNING OBESITY AND ASTHMA IN THE MAY ISSUSE OF J ALLERGY CLIN IMMUNOL 115(5), 2005. ARTICLES ARE: 1, ADIPOSE TISSUE, ADIPOKINES, AND INFLAMMATION, Fantuzzi G, p-911; 2, DOES OBESITY WEIGH HEAVILY ON THE HEALTH OF THE HUMAN AIRWAY?, Sood A, p-921; 3, OBESITY, SMOOTH MUSCLE, AND AIRWAY HYPERRESPONSIVENESS, Shore SA, Fredberg JJ, p-925; 4, PHYSICAL ACTIVITY AND EXERCISE IN ASTHMA: RELEVANCE TO ETIOLOGY AND TREATMENT, Lucas SR, Platts-Mills TAE, p-928; 5, THE ASTHMA AND OBESITY EPIDEMICS: THE ROLE PLAYED BY THE BUILT ENVIRONMENT-A PUBLIC HEALTH PERSPECTIVE, Brisbon N, et al. p-1024. OBESITY MAY PLAY A ROLE IN THE INCREASED INCIDENCE OF ASTHMA. Editor's comment: These articles are interesting reading and give rationale for another reason why the incidence of asthma is increasing.

8. EXCELLENT REVIEW ARTICLE ON HISTAMINE AND ITS ROLE IN ALLERGIC INFLAMMATION AND IMMUNE MODULATION. Editor's comment: It outlines the importance of this molecule in allergic diseases. Jutel M, et al. Int Arch Allergy Immuno l 2005; 137: 82.

9. THE JOURNAL ALLERGY PUBLISHED AN EXECUTIVE SUMMARY OF THE EAACI'S POSITION PAPER ON RHINOSINUSITIS AND NASAL POLYPS. THE FULL MANUSCRIPT IS ON THE EAACI'S WEB-SITE, WWW.EAACI.ORG AND IN THE JOURNAL RHINOLOGY (SUPPL 18, MARCH 2005). Editor's comment: This is an excellent manuscript about a subject which attracts considerable attention. Fokkens W, et al. Allergy 2005: 60: 583.

10. REVIEW ARTICLE. ANTI-IMMUNOGLOBULIN E TREATMENT WITH OMALIZUMAB REDUCES BOTH NASAL AND BRONCHIAL EOSINOPHILS, BRONCHIAL MAST CELLS, AND T AND B CELLS. IT ALSO DOWN-REGULATES IgE RECEPTORS ON CIRCULATING (PRECURSOR) DENDRITIC CELLS, SUGGESTING THAT BLOCKING IgE MAY INHIBIT THE MORE CHRONIC ASPECTS OF ALLERGIC INFLAMMATION INVOLVING T CELL ACTIVATION. SYSTEMIC OMALIZUMAB IMPROVES ASTHMA SYMPTOMS, QUALITY OF LIFE, AND EXACERBATIONS IN MODERATE TO SEVERE ASTHMA. Editor's comment: This paper suggests that Anti-IgE is an effective treatment for moderate-to-severe allergic asthma and intermittent (seasonal) or persistent (perennial) allergic rhinitis. Holgate ST, et al. Clin Exp Allergy 2005; 35: 408.

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