April 2005 Medical Journal Review

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

1. THE EFFICACY OF INTERMITTENT SHORT-COURSE CORTICOSTEROID (CS) TREATMENT GUIDED BY A SYMPTOM-BASED ACTION PLAN ALONE OR IN ADDITION TO DAILY TREATMENT WITH EITHER INHALED BUDESONIDE OR ORAL ZAFIRLUKAST WAS EVALUATED OVER A ONE-YEAR PERIOD IN A DOUBLE-BLIND TRIAL OF 225 ADULTS. OUTCOMES INCLUDED PEF, FEV₁ BEFORE AND AFTER BRONCHODILATOR, FREQUENCY OF EXACERBATIONS, DEGREE OF ASTHMA CONTROL, SYMPTOM-FREE DAYS, AND QUALITY OF LIFE. THE STUDY CONCLUDES THAT MILD PERSISTENT ASTHMA CAN BE EFFECTIVLY TREATED WITH SHORT, INTERMITTENT COURSES OF INHALED OR ORAL CS TAKEN WHEN SYMPTOMS WORSEN. Editor's comment: This paper challenges the current national and international guidelines which recommend regularly scheduled treatment with inhaled CS for mild persistent asthma. Boushey HA, et al. N Engl J Med 2005; 352: 1519. Editorial by: Fabbri LM, 1589.

2. CHRONIC AUTOIMMUNE URTICARIA IS CAUSED BY COMPLEMENT FIXING IgG ANTIBODY DIRECTED TO THE α-SUBUNIT OF THE IgE RECEPTOR. THIS STUDY DETERMINED THE SUBCLASS DISTRIBUTION OF IgG ANTIRECECEPTOR ANTIBODIES ON THE BASIS OF HISTAMINE RELEASE. PATIENTS WITH AUTOIMMUNE CHRONIC URTICARIA HAVE FUNCTIONAL (IgG3 PRIMARILY, IgG1 FREQUENTLY, AND OCCASIONALLY IgG4) SUBCLASS ANTIBODIES TO THE α-SUBUNIT OF THE IgE RECEPTOR, WHEREAS IgG2 IS TYPICALLY INACTIVE. Editor's comment: This study sheds additional light on the pathogenesis of autoimmune urticaria. Soundararajan S, et al. J Allergy Clin Immunol 2005; 115: 815.

3. THIS STUDY INVESTIGATED THE PRESENCE OF EPITHELIAL RETICULAR BASEMENT MEMBRANE THICKENING AND EOSINOPHILIC INFLAMMATION IN BRONCHIAL BIOPSIES OBTAINED FROM 53 CHILDREN DURING CLINICAL BRONCHOSCOPY FOR SEVERE WHEEZE AND/OR COUGH. THE CHARACTERISTICS OF ASTHMA PRESENT IN OLDER CHILDREN AND ADULTS ARE NOT PRESENT IN SYMPTOMATIC INFANTS WITH REVERSIBLE AIRWAY FLOW OBSTRUCTION, EVEN IN THE PRESENCE ATOPY. Editor's comment: Perhaps children younger than 2 years of age with suspected asthma are not yet susceptible to airway remodeling. Fabbri L, et al. Am J Respir Crit Care Med 2005; 171: 686.

4. INFLAMMATORY CELL PROFILES WERE INVESTIGATED IN BRONCHIAL AND NASAL TISSUES IN PATIENTS WITH NASAL POLYPS ALONE, AND NASAL POYLPS WITH CONCOMITANT ASTHMA. THE RESULTS DEMONSTRATE THAT THE INFILTRATION OF INFLAMMATORY CELLS IN THE UPPER AND LOWER AIRWAYS DO NOT DIFFER APPRECIABLY BETWEEN THESE 2 GROUPS OF PATIENTS. Editor's comment: Inflammatory cells in patients with nasal polyps are similar in the upper and lower airways regardless of whether or not asthma is present. Ediger D, et al. Clin Exp Allergy 2005; 35: 319.

5. STAPHYLOCOCCAL ENTEROTOXIN B (SEB) AND STAHYLOCOCCAL ENTEROTOXIN C1 (SEC1) SPECIFIC IgG ANTIBODY SUBCLASSES WERE ASSESSED IN 89 ADULT ATOPIC DERMATITIS (AD) PATIENTS AND IN 28 HEALTHY AGE-MATCHED CONTROLS. 38% OF THE AD PATIENTS SHOWED A SELECTIVE DEFICIENCY IN IgG2 ANTIBODIES AGAINST SEC1 COMPARED TO 14% IN THE CONTROL GROUP. ITS ABSENCE WAS ASSOCIATED WITH SEVERE DISEASE. NORMAL PRODUCTION LEVELS OF IgG2 WERE FOUND AGAINST PNEUMOCOCCAL CAPSULAR POLYSACCHARIDE AND SEB. A SUBGROUP OF AD PATIENTS HAVE SELECTIVE DEFICIENCY TO PRODUCE ANTI-SEC1 IgG2 ANTIBODIES. Editor's comment: This work should be confirmed and sheds additional light on the pathogenesis of this complex disease. Mrabet-Dahbi S, et al. Clin Exp Allergy 2005; 35: 274.

6. USING POSITRON EMISSION TOMOGRAHY THE AUTHORS OBSERVED THAT BRONCHOCONSTRICTED ASTHMATICS DEVELOP REGIONS OF POORLY VENTILATED LUNG. USING A COMPUTATIONAL MODEL, EVEN FOR UNIFORM SMOOTH MUSCLE ACTIVATION OF A SYMMETRIC BRONCHIAL TREE, THE PRESENCE OF MINIMAL HETEROGENEITY BREAKS THE SYMMETRY AND LEADS TO LARGE CLUSTERS OF POORLY VENTILATED LUNG UNITS. THESE FINDINGS HELP EXPLAIN WHY INHALED ASTHMA DRUGS ARE NOT ALWAYS EFFECTIVE FOR TREATMENT. Editor's comment: Inhalation of a drug to treat asthma may promote delivery to regions least in need of medication. Delivery to the vascular system may be necessary in some severe cases. Venegas JG, et al. Nature 2005; 434: 777.

7. THIS PAPER DEMONSTRATES THAT MOST MOUSE AND HUMAN NATURAL KILLER T (NKT) CELLS RECOGNIZE GLYCOSPHINGOLIPIDS FROM SPHINGOMONAS, GRAM-NEGATIVE BACTERIA, THAT DO NOT CONTAIN LIPOPOLYSACCHARIDE. DATA SUGGEST THAT NKT CELLS ARE T LYMPHOCYTES THAT PROVIDE AN INNATE-TYPE IMMUNE RESPONSE TO CERTAIN MICROORGANISMS THROUGH RECOGNITION BY THEIR ANTIGEN RECEPTOR. Editor's comment: There is more and more evidence that the innate immune system is important in providing protection against pathogens. Kinjo Y, et al. Nature 2005; 434: 520.

8. EXCELLENT REVIEW ARTICLE ON CHRONIC OBSTRUCTIVE PULMONARY DISEASE: A DISORDER OF THE CARDIOVASCULAR AND RESPIRATORY SYSTEMS. Editor's comment: Excellent reading about the pathogenesis and consequences of this chronic respiratory ailment. Farmer SG, Rennard SI, Voelkel N (eds), Proc Am Thorac Soc 2005; 2: 7.

9. EXCELLENT REVIEW ARTICLE ABOUT THE MECHANISMS OF RESPIRATORY VIRUS-INDUCED ASTHMA EXACERBATIONS. DISCUSSES THE PREVALENCE OF RESPIRATORY VIRAL INFECTIONS IN ASTHMA EXACERBATIONS, THE SEVERITY OF SUCH EXACERBATIONS, AS WELL AS THE SYNERGISM BETWEEN VIRAL INFECTIONS AND ATOPY. THERE IS PROBABLY ALSO SYNERGISM BETWEEN VIRAL INFECTIONS AND AIR POLUTANTS. Editor's comment: Must reading for physicians to understand the importance of viral respiratory tract infections in asthma. Contoli M, et al. Clin Exp Allergy 2005; 35:137.

10. "RAPID REVIEW" ARTICLE ON OPTIMISED GLUCOCORTICOID (GC) THERAPY, SIDE EFFECTS AND ADVANCES WHICH MAY LEAD TO INNOVATIVE GC OR GC-RECEPTOR LIGANDS WITH AN IMPROVED THERAPEUTIC RATIO. NITROSTEROIDS (CONVENTIONAL GC DERIVATIVE LINKED WITH NITRIC OXIDE), E.G., NO-PREDNISOLONE, IS TEN-FOLD MORE POTENT THAN PREDNISOLONE AND HAS FEWER SIDE EFFECTS. LIKEWISE, SELECTIVE GC- RECEPTOR AGONISTS (SEGRAs) ARE ANTI-INFLAMMATORY BUT CAUSE FEWER ADVERSE EFFECTS. Editor's comment: New and better GC on the way? Buttgereit F, et al. Lancet 2005; 365: 801.

THE SECOND "RAPID REVIEW" IS ABOUT 45% OF ADULT PATIENTS WITH ASTHMA WHO REMAIN SYMPTOMATIC OR WHO HAVE DIFFICULT-TO-CONTROL ASTHMA DESPITE MULTIPLE THERAPIES. IT OUTLINES REASONS WHY SUCH PATIENTS EXIST (CO-EXISTING CONDITIONS, POOR ADHERANCE, PSYCHOLOGICAL FACTORS AND THERAPY-RESISTANT ASTHMA) AND REFERS TO THE ENCOURAGING REPORTS ON OMALIZUMAB FOR TREATMENT OF SEVERE ALLERGIC ASTHMA. Editor's comment: Severe asthma is just that and is difficult to treat. Heaney L, et al. Lancet 2005; 365: 974.

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