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Allergic Infections Others
- IDIOPATHIC - NARES - OCCUPATIONAL - HORMONAL - DRUGS-INDUCED - IRRITANTS - FOODS - EMOTIONAL
V. Lund, International Consensus Report, 1994
- SEASONAL - PERENNIAL
- CHRONIC -Specific -Non-Specific
Allergic rhinitis: epidemiology
• Heterogenous disorder • Affecting 25-30% of the population • Increasing in prevalence
Prevalence of allergic rhinitis
Shiffer et al., 1995
. 1995 .Prevalence of asthma Shiffer et al.
Estonia .Uzbekistan .Singapore .Pakistan .Greece .Philippines | | 0 | Prevalence of allergic rhinitis (%) 10 20 | | 30 | | 40 | | 50 | | .Ohman .Latvia .Belgium .Malta .Romania .Austria .Georgia .Nigeria .Sweden . .Germany .Argentina .Korea .K.Taiwan .Marocco .U.Portugal .Lebanon .Indonesia Indonesia Albania Iran Panama China Ethiopia Russia Spain Hong Kong Costa Rica Mexico Brazil Chile France Canada Poland Malaysia Kenya Japan Kuwait Australia USA Finland Algeria Ireland Uruguay South Africa Peru Paraguay .| | | | | | | | | | | | | | -India India .New Zealand .Madeira (South) .Thailand .Italy .
(SAPALDIA study). 1995 .Prevalence of seasonal allergic rhinitis (Switzerland) 16% 14% 12% 10% 8% 6% 4% 2% 0% 1926 1958 1985 1993 SAR Wütrich et al.
Prevalence of asthma (USA) 6.00% 1.00% 3.00% 1980 1981-83 1984-86 1987-89 1990-92 1993-94 Asthma Mannino et al.00% 2.00% 0.00% 4.00% 5.. 1998 .
Prevalence of allergic disease in 18 year old conscripts 1973-1993 18 16 14 12 10 8 6 4 2 0 1973 1977 1981 1986 1989 1993 Allergic Rhinitis Atopic Eczema Asthma Contact Eczema .
. dust mites. – Sneezing – Itching – Rhinorrhea – Nasal obstruction ..Allergic rhinitis: symptoms • Inflammation induced by IgE-mediated immune response to specific allergens: pollen. moulds .
and > 4 weeks Mild normal sleep & no impairment of daily activities. leisure . sport. abnormal work and school . Š 4 days per week . > 4 days per week .ARIA Classification Intermittent Persistent . or Š 4 weeks . leisure & normal work and school & no troublesome symptoms in untreated patients Moderatesevere one or more items . abnormal sleep . sport. troublesome symptoms . impairment of daily activities.
selective recruitment.Allergic rhinitis: mechanisms • Inflammatory infiltrate made up of different cells: – Chemotaxis. transendothelial migration of cells – Localisation of cells within different compartiments of nasal mucosa – Activation and differentiation of various cell types .
Allergic Rhinitis An inflammatory disorder of the nasal mucosa involving: • Mast cells • Basophils • Eosinophils • T-lymphocytes • Endothelial cells • Epithelial cells • Langerhans cells .
Cellular Numerical Changes in Allergic Rhinitis Basophils Epithelium Eosinophils Mast cells Langerhans Cells Lamina propria Eosinophils .
prostaglandins. mediator leukotrienes) release Tissue recruitment Cytokines (TH2 profile) Endothelial cell activation T cell Eosinophils Basophils B cell IgE Epithelial cells Chemokine expression production .Inflammatory process underlying the expression of allergic rhinitis Allergen mast cells Dendritic cell (immune antigen presenting cell) mediator release symptoms (histamine. tryptase.
T-Lymphocytes • Principal factors for regulation and coordination of immune responses in allergic diseases Th1-lymphocytes Th2-lymphocytes .
CD4+ T-lymphocyte Cytokines TH1 IL-3 GM-CSF TNFα IL-2 IFN-γ Lymphotoxin TH2 IL-3 GM-CSF TNFα IL-4 IL-5 IL-6 IL-10 IL-13 TH0 IL-2 IFN-γ IL-4 IL-5 .
Allergen IFN-γ MHC TCR Th 1 IL-4. IL-5 Th 0 Th 2 APC Interaction APC – T-Lymphocyte .
Th1-lymphocytes • Involved in delayed hypersensitivity immune reactions • Th1 cytokines: – Activation phagocytes – Production of opsonizing and complement-fixing AB by B-Lymphocytes Romagnani. 2000 . JACI.
2000 . JACI. activation and in situ survival of eosinophils – Stimulate production of AB by Blymphocytes – Stimulate growth of mast cells and basophils Romagnani.Th2-lymphocytes • Th2 cytokines: – Differentiation.
mast cell IgE Bousquet et al.. IL-5. JACI.eosinophil IL-4. IL-13 IL-3. GM-CSF GM-CSF macrophage T-cell (Th2) IL-3. IL-4. 2001 . IL-10 B-cell Basophil.
Risk for atopy Th2 •Changes of the commensal flora due to: .Use of cleaner water •Reduced exposure to and/or severity of natural infections due to: . alum as adjuvant) Romagnani. cat pets. pertussis. diphteria.Less crowded accomodation .Antimicrobial treatment (GERM FREE LIKE STATE) Th1 . neoallergens) .Reduced family size .Th2-biasing vaccinations (tetanus.Vaccinations . 2000 .Consumption of semi-steriele foods .Increased exposure to some allergens (mites.
D 4 Kinins Cytokines: IL-4 IL-5 IL-6 GM-CSF TNF α .Mast Cell Activation Allergen Ig E Mediators: Histamine Tryptase Prostaglandin D 2 Leukotriene C4 .
Nasal Allergen Challenge: Lavage Tryptase (U/l) * * * * * * Time (mins) * * Histamine (nmol) Time (mins) .
blood vessels Nerve stimulation eos M Φ lymph Late phase reaction Hyperreactivity Bousquet et al.. Th2 cytokines Other cells Mucous glands. CysLT.Mast cells Histamine. 2001 . pro-inflammatory cytokines Chemotactic mediators. JACI.
Basophils • Absent in normal nasal mucosa • Demonstrated in nasal mucosa and secretions of pt with AR • Histamine-containing cell during latephase reactions • IL-3 = developmental factor .
The Basophil Mediators Histamine LTC4/LTD4 Cytokines IL-4 IL-13 .
decreased apoptosis Vasoactive properties Chemo-attractant Bousquet et al.. 2001 .Eosinophils ECP H2O2 MBP Th2 cytokines CysLT PAF cytotoxic Enhanced inflammation. JACI.
The eosinophil Growth factors TGF-β Mediators LTC4 LTD4 PAF Basic proteins ECP EPX MBP Enzymes Arylsulphatase Histaminase MMP-9 Cytokines/chemokines IL-4 IL-5 RANTES Eotaxin .
Macrophages / Dendritic cells • Mucosal environment (place of allergic reaction): rich in MΦ and DC • Both significantly increased in the nose in AR • MΦ : production of growth factors and cytokines • Langerhans cells: important group of DC in AR • Airway mucosal DC: important role in the primary sensitisation or tolerance to antigens .
mastcells and basophils • Involves series of surface molecules as well as presence of IL-4 and IL-13 cytokines . T-cells.Allergic rhinitis: IgE-production • Allergy: overproduction of IgE in response to common allergens • IgE production: complex interaction between B-cells.
itching.Allergic rhinitis: 2 phases Early phase S/ sneezing. clear rhinorrhea (and nasal congestion): few minutes after exposure Allergen exposure ↑ IgE-coated mast cells ⇒ through epithelium ⇒ recognition antigen ⇒ degranulation .
itching. rhinorrhea: 4 to 8 hours after exposure Cytokines play more important role promotion infiltration of mucosa with: ⇒ ⇒ ⇒ ⇒ ⇒ eosinophils neutrophils basophil T-lymphocytes macrophages . sneezing.Late phase S/ nasal obstruction.
Cytokines and Tissue Eosinophilia Epithelial cells GM-CSF IL-3 IL-5 GM-CSF IL-5 GM-CSF Stimulate progenitor cells and enhance maturation Inhibit apoptosis T-lymphocytes Weak chemotactic activity Blood vessel Mast cells Prime eosinophils .
Endothelial cell interactions in allergic inflammation Endothelial cells FLOW Selectins (P+E) Rolling margination Chemokine exposure Ligand expression ICAM-1 + VCAM-1 Firm adherence Diapedesis .
Tissue cell recruitment Post capillary venule Separation of interendothelial pores Exudation of fluid Emigration of leucocytes .
Cell mediators and symptoms of rhinitis Sneezing Histamine Endothelin Itching Rhinorrhoea Histamine Leukotrienes Endothelin MEDIATORS Histamine Endothelin Histamine Leukotrienes B4/C4/D4 Prostaglandins D2/E2/I2 Kinins Blockage .
Development of Allergic Rhinitis Immune activation Structural cell activation Tissue cell recruitment and activation Symptom development Mast cells Langerhan’s cells T-lymphocytes B-lymphocytes Endothelial cells Epithelial cells Mast cells Eosinophils Basophils Neural and vascular interactions .
geen borstvoeding.) • Etnische afkomst (Aziaten in Engeland) • Aantal broers en zussen.Wat is de etiologie van de toename in prevalentie? • Genetische en familiale factoren • Risicofactoren in het vroege leven (prematuriteit. rangorde van het kind • Buiten..en binnenpollutie • Roken • Sociale klasse ...
Infection theory Infections in early childhood may prevent allergic sensitisation .
2000 .02 Percentage of Children with Frequent Wheezing 20 One or no sibling and no day care Two or more sibling or day care N = 1246 children P=0. 2000 Ball TM et al.02 P=0..Allergy and siblings. day-care 30 P=0..04 10 7 | | | | | | | | | | | | | | 1 2 3 4 5 6 7 8 YEAR 9 10 11 12 13 14 Ball TM et al.
.00 1.50-0.27 < 0.10 NS 1.00 95% CI Pvalue Farm 1098 13.08 0.92-1.490.4 1. Crude 95% CI P-value Adjuste OR d OR Rural 1248 20.9 0.26 NS Kilpeläinen M et al.61 0.63 0.77 0.001 0.79< 0.95-1. 2000 .Allergy and farm environment Total Preval.001 Urban 7307 22.8 1.
1997 3 .08 p=1 No of older siblings Matricardi PM et al.Allergy and Hepatitis A 25 Percentage of subjects with atopy Seronegative Seropositive 20 15 10 5 0 0 1 2 p<0.05 p=0.001 p<0..
Anecdotal reports of children who developed respiratory allergies temporally associated with URTI • 1988: Holt et al. Animal models show that RSV can enhance allergen sensitisation .Early viral infections may increase allergy • 1979: Frick et al.
Early viral infections may increase allergy • Similar findings: – Chlamydia pneumoniae – Mycoplasma pneumoniae – Parainfluenzae virus .
3 mm) • >> Dermatophagoïdes pteronyssinus. vochtige plekjes) • Per gram stof: 2000 -15000 mijten • Matras zorgt voor ideale temperatuur en vochtigheidsgraad . Dermatophagoïdes farinae • Leven van huidschilfers en microscopische schimmels • Uitwerpselen zijn sterk allergeen • Leven voornamelijk in beddengoed (donkere. warme.• Huisstofmijtallergie: • Uiterst kleine spinnen (0.
Clin Exp Allergy 1997 4. Am J Respir Crit Care Med. 2000 .Co-existence allergic rhinitis and asthma AR Astma % Astma % AR 38 % ¹.Plashke. J Allergy Clin Immunol 1997 2. J Allergy Clin Immunol 1997 3.Corren.5 AR (atopici) Asthma Rhinitis (non-atopici) Asthma 1.Kapsali.³ 78 % ¹.Scadding.7 OR= 3. 93-99 % ² OR= 5.
Bronchial involvement in allergic rhinitis
• Approximately 40% of patients with rhinitis present with clinical asthma • Many patients with rhinitis present with increased non-specific BHR • Endobronchial allergen challenge in rhinitis patients leads to bronchial symptoms
Braman SS et al. Chest 1987
Allergic rhinitis precedes asthma The allergic march
Populatie n = 7225
Outcome Asthma at 7 years Asthma at 5-9 years Asthma at 7 years Asthma life 23 years folluw-up
Odds ratio 7,1 2,9 3,9 3
n = 770
n = 8585
Allergic rhinitis as a risk factor for the development of asthma
Incidence of asthma over a 23 year period
Diagnosis at start of study Allergic rhinitis No allergic rhinitis Total at risk* 162 528 New asthma cases 17 19 New asthma % 10.5 3.6
*No present or past history of asthma at the time of original evaluation
p<0.002 comparing the incidence of asthma in the two subject groups
Settipane G et al. Allergy Proc 1994
M Lukin 1992 . Kokkonen. J.10-year prognosis for childhood allergic rhinits (aged 3-17 y) % 70 60 50 40 30 20 10 0 SAR n = 110 PAR n = 44 symptom-free perennial AR asthma seasonal AR T ype AR at the beginning of the study O Linna.
Basisprincipes van de diagnose en behandeling van allergische rhinitis .
DIAGNOSIS OF AR SYMPTOMS • Nasal itching • Sneezing • Rhinorrhea • Nasal congestion • Conjunctivitis MEDICAL HISTORY .
EXAMINATION OF THE NOSE • anatomical structure of the nose • colour of nasal mucosa • amount and aspect of mucus anterior rhinoscopy nasal endoscopy .
ALLERGY DIAGNOSIS SKIN MASTCELL Skin test BLOODVESSEL Y Serum specific IgE Histamine release Basophil activation Nasal challenge BASOPHIL MASTCELL NASAL MUCOSA .
SKIN TEST Skin testing methods • Scratch test: – Poor reproducibility – Possible systemic reaction • Prick test: – Diagnosis of immediate type allergy – High degree of correlation between symptoms and provocative challenge .
SKIN TEST Skin testing methods • Prick test: – Standarised methods (trained investigator) – 2 cm apart • Intradermal skintest (weak allergen solution) – Less sensitive – False positive reactions – Correlate less well with symptoms – Less safe (β -blocker) .
Allergy skin prick testing • Skin prick test / positive result .
FACTORS AFFECTING SKIN TESTING • Quality of allergen extract • Age •Drugs .
CLINICAL VALUE OF SKIN TESTS A positive skin test alone does not confirm a definite clinical reactivity to an allergen !
Serum total IgE ↑< allergic / parasitic diseases + other conditions barely predictive for allergy screening in rhinitis Serum specific IgE High predictability in diagnosis of immediate type allergy
– Less in clinical practice
important in diagnosis of occupational allergic rhinitis
NASAL CHALLENGE NASAL CHALLENGE WITH ALLERGEN Indications: • Allergen provocations: – Discrepancy between history of AR and tests or between tests – Diagnosis of occupational AR – Before immunotherapy – As research tool .
histamine. . – Not for clinical practice – Used in research ...NASAL CHALLENGE • Lysin-aspirin: nasal provocation = substitute for oral provocation in aspirin-intolerance • To test non-specific hyperreactivity – Cold air.
NASAL CHALLENGE •Assessment of nasal response: symptom score + objective measures: – Counting sneezes / attacks of sneezes – Measuring volume / weight of nasal secretions – ∆ of nasal patency / airflow / airflow resistence .
To exclude chronic sinusitis .In pt who do not respond to treatment .To eliminate other conditions .In pt with unilateral sinusitis – MRI: rarely (fungal sinusitis) .To eliminate complications of sinusitis .OTHER ENT DIAGNOSTIC TOOLS • Imaging – Sinus radiographs: not for AR – CT scan: after specialist advice: .
CONCLUSION The diagnosis of allergic rhinitis is based on several milestones: – Symptoms of AR – Medical history – Examination of the nose – SPT – IgE – Nasal challenge .
diphenydramine. promethazine.Treatment of allergic disease: First generation oral antihistamines • Chlorpheniramine. tripolidine • Use limited by sedative and anticholinergic effects .
non-competitive H1-receptor blockade • additive anti-allergic activities • no interference of activity by foods • known therapeutic dose Pharmacokinetics: • rapid onset and 24 hour duration of action • once daily administration • no tachyphylaxis .Treatment of allergic disease: properties required of ideal second/third generation antihistamines Pharmacological: • potent.
Treatment of allergic disease: properties required of ideal second/third generation antihistamines Lack of unwanted effects •no sedation •no anticholinergic effect •no weight gain •no cardiac toxicity .
azelastine. ebastine. (des)loratadine. (astemizole*). ketotifen. fexofenadine. mizolastine • Greatly reduced unwanted effects • First line treatment for intermittent or mild persistent AR * Withdrawn from some markets because of rare cardiotoxic effects when taken in association with azolic antifungal agents and macrolide antibiotics .Treatment of allergic disease: Second generation oral antihistamines Acrivastine. (terfenadine*). levocetirizine. epinastin. (levo)cetirizine.
Treatment of allergic rhinitis: Topical antihistamines Azelastine and levocabastine • • • • Rapid onset of action (15 minutes) Twice daily administration Recommended for organ-limited disease May be used ‘on-demand’ in addition to a continuous medication • Good safety profile .
Treatment of allergic disease: Topical corticosteroids • • • • • • • Beclomethasone dipropionate Budesonide Flunisolide Fluocortinbutyl Fluticasone propionate Mometasone furoate Triamcinolone acetonide .
1 • Potent anti-inflammatory agents • Effective in treatment of all nasal symptoms including blockage • Once or twice daily administration • Superior to antihistamines for all nasal symptoms • First line pharmacotherapy for moderatesevere persistent allergic rhinitis .Treatment of allergic rhinitis: Topical corticosteroids .
perforation of the nasal septum has been reported • One study reports decrease in growth in children taking Beclomethasone dipropionate .Treatment of allergic rhinitis: Topical corticosteroids .2 Safety • Occasional unwanted effects • Rarely affect HPA axis (some exceptions) • Anecdotally.
Treatment of allergic rhinitis: Systemic corticosteroids • Short courses of oral corticosteroids (< 3 weeks) can be prescribed for severe refractory symptoms • Can be repeated every 3 months • May be used with caution in children and in pregnancy. if no alternative available • Intramuscular injection of corticosteroid suspensions should be avoided .
De Schryver WHO position paper. 1998 .Specific immunotherapy (SIT) • Interference with basic pathophysiological mechanisms of allergic disease • Effective treatment for seasonal and perennial allergic rhinoconjunctivitis and asthma • Prevention of the development of new sensitisations and asthma in patients with allergic rhinitis L.
Mechanisms of immunotherapy Th1 IFNγ IL-4 IgE IgG Allergen APC Th2 IL-5 Eosinophils Immune deviation: Anergy of TH2/TH0 cells ? Increase in Th0/Th1 cells ? L. JACI 1998 . De Schryver Durham and Till.
Mechanisms of immunotherapy • Decrease in inflammatory mediators during both early. De Schryver .and late-phase responses • Reduction of mast cell numbers with a consequent reduction in immediate allergic sensitivity • Decrease in eosinophil counts and eosinophil cationic protein concentrations in bronchoalveolar lavage fluid Durham and Till. JACI 1998 L.
BMJ 1999 Ia evidence for meta-analysis of randomised controlled trials Ib evidence from at least one randomised controlled trial IIa evidence from at least one controlled study without IIb evidence from at least one other type of randomisation quasi-experimental study III evidence from non-experimental descriptive studies.Statement of evidence: Category of evidence Shekelle et al. such as comparative studies. correlation studies and case-control studies IV evidence from expert committee reports or opinions or clinical experience of respected authorities. or both .
Statement of evidence: Strength of evidence Shekelle et al. BMJ 1999 A directly based on category I evidence B directly based on category II evidence or extrapolated recommendation from category I evidence C directly based on category III evidence or extrapolated recommendation from category I or II evidence D directly based on category IV evidence .
Strength of evidence for treatment of rhinitis ARIA Intervention SAR PAR oral anti-H1 A AAA intranasal anti-H1A A A A intranasal CS A A A A cromonesA A A A anti-leucotriens A subcutaneous SIT A A A A sublingual/nasal SIT A A A allergen avoidanceD D D D adult children adult children .
ARIA sneezingrhinorrhea nasal nasal eye obstruction itch symptoms H1-antihistamines oral +++ +++ 0 to + +++ ++ intranasal ++ +++ + ++ 0 intraocular0 0 0 0 +++ Corticosteroids +++ +++ ++ ++ + Cromones intranasal + + + + 0 intraocular0 0 0 0 ++ Decongestants intranasal 0 0 ++ 0 0 oral 0 0 + 0 0 Anti-cholinergics 0 +++ 0 0 0 Anti-leukotriens 0 + ++ 0 ++ .Medications of allergic rhinitis .
van Cauwenberge (Belgium) C. Howarth (UK) V. Ghent University Hospital.H. Durham (UK) W. Malling (Demark) N.R. Fokkens (Netherlands) P. Wang (Singapore) Department of Otorhinolaryngology. Canonica (Italy) S. Passalacqua (Italy) J. B-9000 Ghent. Scadding (UK) D. Bousquet (France) G. Mygind (Denmark) D.W. Bachert (Belgium) G. De Pintelaan 185.J.Allergy 2000: 55:116-134 Printed in UK.-Y.-J.K. Passali (Italy) G. Lund (UK) H. Belgium . All rights reserved Copyright © Munksgaard 200 ALLERGY ISSN 0105-4538 Position paper Consensus statement* on the treatment of allergic rhinitis P.
Stepwise approach .
control control Oral or Nasal Antihistamines Inadeq.Seasonal allergic rhinitis Need for therapy ? Mild disease or occasional symptoms Moderate disease or long duration Severe disease Oral or Nasal Antihistamines (Cromones) Nasal Corticosteroids Nasal Inadeq. control For eye symptoms : topical antihistamines or cromones Add further symptomatic treatment Short-course Oral Steroids Consider Immunotherapy . + Corticosteroids Inadeq.
+ Antihistamines control Corticosteroids control Antihistamines Inadeq. control Further examinations . Corticosteroids Nasal Oral or Nasal Inadeq.Perennial allergic rhinitis in adults Avoidance Need for therapy ? Environment control Mild disease or occasional symptoms Moderate disease or long duration Severe symptoms Nasal Inadeq.
Perennial allergic rhinitis in adults RESISTANT CASES Nasal blockage Resistant rhinorrhea Short Course of Topical Decongestants/ Oral Decongestants/ Oral Steroids If resistant Nasal Ipratropium bromide Immunotherapy Surgical turbinate reduction .
Perennial alllergic rhinitis in young children Avoidance Need for therapy ? Environmental control Oral or Nasal Antihistamines (Cromones) Nasal Corticosteroids in adequate dose Add Antihistamines Consider Immunotherapy .
Lund Multicentre. parallel group Comparing two therapeutic strategies (recommended and free choice) in seasonal allergic rhinitis (SAR) patients Study period May 1998 – September 1998 600 adult outpatients in 328 GP centres in Belgium. multinational.Rhinitis guidelines validation study Jean Bousquet Paul van Cauwenberge Valerie J. randomised. France and UK Three weeks duration . open label.
Study plan A Investigators randomised to: B Treat patients according to guidelines Treat patients according to usual practice 225 patients with SAR screened and enrolled 244 patients with SAR screened and enrolled Patients treated for 3 weeks Recorded: – Reflective symptoms twice daily – Medicine utilisation daily – RQLQ and SF-36 at day 7 and day 20 – Global evaluation at day 21 .
Allocation of treatments according to baseline symptoms Conjunctivitis Rhinitis symptoms symptoms Mild rhinitis Mod/severe rhinitis None/mild Oral anti-H1 Oral anti-H1 and conjunctivitis topical nasal steroid Mod/severe Oral anti-H1 Oral anti-H1 and conjunctivitis and topical topical nasal steroid ocular and topical cromone ocular cromone Oral anti-H1 = ebastine Topical nasal steroid = triamcinolone acetonide Topical ocular cromone = nedocromil .
03 (0.05 (0.48 (0.07) 1.02 (0.07) 7.42 (0.45 (0.61 (0.08) 4.10)* -0.07) 0.10)* -2.67 (0.) 2.54 (0.12)* -0.28) -0.48 (0.02 (0.09)* -0.93 (0.38)* *p < 0.07) 1.07) 0.Mean symptom score over the treatment period Strategy A LS mean + SE (n = 207) Stuffiness Rhinorrhea Sneezing Itching Eye symptoms Total score 1.63 (0. between LS LS mean + SE Mean group A/B (n = 224) (SE of diff.09) 1.06) 1.28) Strategy B Diff.55 (0.60 (0.32 (0.73 (0.39 (0.08) 1.001 .06) 1.09)* -0.
282) 6 4 2 0 *** Strategy A Strategy B .Total symptom scores (SE) over 21 days Group A: Treatment according to guidelines Group B: Treatment according to free choice Least square means (SE) 10 7.93 (0.48 (0.276) 8 4.
5 *** 1.001 Group A vs Group B .Individual symptom scores over 24 hours – days 1–7 Group A: Treatment according to guidelines Group B: Treatment according to free choice Least square means 2.5 Rhinorrhoea Stuffiness Sneezing Itching Eye symptoms ***p<0.5 *** *** *** *** 0.
38 (0.73 (0.12)* -0.64 (0.07) 1.61 (0.07) -0.09) 0.10) 1.10) 0.02 (0.55 (0.13)* -0.78 (0.50 (0.61 (0.07)* -0.14 (0.) 1.14)* -0.12)* -0.71 (0.10)* -0.RQLQ: Mean change from baseline Strategy A LS mean + SE Activities Sleep Non hay fever S/ Practical Problems Nasal symptoms Eye symptoms Emotion Total score 0.04 (0.10) 0.78 (0.54 (0.09) 1.82 (0.13)* -0.08) 0.43 (0.11) 0. between LS LS mean + SE Mean group A/B (n = 189) (SE of diff.27 (0.09) 0.10) 1.09) 1.001 .53 (0.69 (0.10)* *p < 0.08) 0.09) 1.07) Strategy B Diff.63 (0.45 (0.07 (0.19 (0.36 (0.07) 1.
s s s ns ot io p s Ac tiv iti e pt om pt om bl em Sl ee sy Em pr o er m m To ta l m *** *** *** *** *** *** *** *** fe v al sy al Pr ac tic ha y on - N as N Ey e ***p<0.001 Group A vs Group B sy .6 1.8 0.4 0 p.RQLQ (disease specific QOL scale) day 21 Group A: Treatment according to guidelines Group B: Treatment according to free choice Least square means 1.2 0.
5 1 Greatly worsened 0.5 0.5 0 Not recorded 19 23 7 11 Statistically significant differences between groups A & B: For patient’s opinion (p=0.026) .5 1.Patient and investigator opinion Opinion Patient Investigator A B AB %% %% Greatly improved 55 38 69 54 Somewhat improved 18 30 20 33 No change 79 6 7 Somewhat worsened 0.5 0.5 0.016) For investigator’s opinion (p=0.
systemic antihistamine TE .topical eye cromone NC .nasal corticosteroid SA SA + TE SA + NC SA + NC + TE NC Other combinations .Study medication usage – moderate/severe rhinitis and moderate/severe conjunctivitis No of patients (%) 80 60 40 20 0 Strategy A (n=134) Strategy B (n=150) SA .
Results from guidelines study • Treating seasonal allergic rhinitis based on the International Rhinitis Guidelines has proved beneficial in terms of both symptom scores and QOL compared with a nonguided therapeutic strategy • When a non-guided strategy is used. often the medication chosen is inappropriate or not sufficiently efficacious .
Recommendations 1.Patients with persistent rhinitis should be evaluated for asthma 2.Patients with persistent asthma should be evaluated for rhinitis 3.A strategy should combine the treatment of upper and lower airways in terms of efficacy and safety .
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