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Management Of Copd & Asthma
 

Management Of Copd & Asthma

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  • Asthma is a disease of the large airways characterized by airway remodeling (mucosal metaplasia, increased goblet cell and submucosal gland, a/w fibrosis of the lamina reticularis, myocyte hypertrophy and hyperplasia; increase in capillary number and leakiness COPD is characterized by ciliary abn, mucous gland abn, alveolar dysruption.
  • Flow dominant BD response (FEV1>FVC) because asthma is a disease of the large a/w
  • Tolerance to SABA in asthma may be related to its bronchoprotective effect in asthma rather than its BD which predominates in COPD. SMC have many fold more B receptors a than inflammatory cells
  • Today the spirometer must find its rightful place alongside the BP Cuff and glucometer. You wouldn’t have a patient with insulin dependent diabetes not use a glucometer. And I don’t think any of us want to stop monitoring blood pressures on a routine patient visit. Spirometry at the time of initial assessment provides objective documentation of the severity of airflow obstruction, and may reveal a patient to be a “poor perceiver,” i.e., someone who appears to be insensitive to airway narrowing. It is possible that these patients may have a heightened risk of morbidity or even mortality and need aggressive education and care. With early detection and therapy based on a more accurate assessment of disease severity, outcomes may improve and there is greater patient satisfaction. Spirometry gives you objective measurement of reversibility to a bronchodilator to help confirm your diagnosis of asthma. Helps you differentiate between cardiac and pulmonary abnormalities. Is an excellent tool to help reinforce therapeutic decision to your patients. For the steroid phobic patient - seeing the difference in pulmonary function may be all it takes to improve compliance. Abnormal spirometry may be the final motivator in getting a patient to quit smoking. It can be a significant source of revenue. Not in just better diagnosis and patient satisfaction. Medicaid, Medicare, and many managed health plans allow you to bill up to $40 per test. It is important to check in your area . Over the past 5 years, the HCFA has consistently been increasing the spirometry reimbursement amount and concurrently lowering reimbursement for other diagnostic procedures.
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  • 6 Population-based cohort study of 30,569 subjects from 5 to 44 years of age, followed from 1975-1997. Of 562 deaths, 77 were classified due to asthma and 66 of these were matched to control patients (n=2681) who also had severe asthma. The rate of death from asthma decreased by 21% with each additional canister used during the previous year. The rate of death from asthma among users of inhaled corticosteroids compared with nonusers was reduced by 50% with the use of more than 6 canisters per year.
  • Displayed on this slide is the percent change in morning pre-dose FEV1 during the 12 weeks and at Endpoint for each treatment group in the study on ADVAIR 250. Once again, on the Y-axis is the percent change in FEV1 and the X-axis the study week. Treatment with ADVAIR 250 was associated with a significantly greater change in FEV1 (approximately 23%) compared to the individual agents or placebo. As before, the apparent improvement in the placebo and salmeterol groups during the trial is a result of a survival bias which occurred due to the early withdrawal of patients with worsening asthma from these two treatment groups. The endpoint analysis which includes all patients data demonstrates that these groups did not significantly improve as would be expected when discontinuing moderate doses of inhaled corticosteroids at baseline.
  • Displayed on this slide are the results of the probability of remaining in the trial without being withdrawn due to worsening asthma for the study examining ADVAIR 250. As before the Y-axis represents the probability of remaining in the trial and the X-axis study day. Patients treated with ADVAIR 250 were also significantly less likely to withdraw due to worsening asthma compared to other treatment groups and thus had better control of their asthma. Since the withdrawal criteria were useful in identifying patients on salmeterol whose asthma was worsening, this trial also confirmed the findings from the ADVAIR 100 trial that the use of salmeterol does not prevent the recognition of clinical cues associated with worsening asthma.

Management Of Copd & Asthma Management Of Copd & Asthma Presentation Transcript

  • Management of COPD & Asthma
  • COPD Guidelines
    • “ ...disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.”
    • COPD should be considered in any patient with:
      • History of exposure to risk factors (especially cigarette smoke)
      • Cough (sputum)
      • Dyspnea
    • Cough and sputum production may precede development of airflow limitation
  • Leading Causes of Death, US (1998) Causes of Death 1. Heart disease 2. Cancer 3. Cerebrovascular disease (stroke) 4. COPD and allied conditions 5. Accidents 6. Pneumonia and influenza 7. Diabetes 8. Suicide 9. Nephritis 10. Chronic liver disease All other causes of death Number 724,269 538,947 158,060 114,381 94,828 93,307 64,574 29,264 26,295 24,936 469,314 Global Obstructive Lung Disease (GOLD) Initiative website (www.goldcopd.com), accessed April 2, 2001.
  • Percent Increases in Adjusted Death Rates, US, 1965 – 1998 0.0 0.5 1.0 1.5 2.0 2.5 3.0 Coronary Heart Disease Stroke Other CVD COPD All Other Causes - 59% - 64% - 35% + 163% - 7% 1965–1998 1965–1998 1965–1998 1965–1998 1965–1998 Proportion of 1965 Rate Global Obstructive Lung Disease (GOLD) Initiative website (www.goldcopd.com), accessed April 2, 2001.
  • Risk Factors
  • Risk Factors in COPD:
  • COPD: Risk Factors
    • Exposures
      • Smoking (generally ≥90%)
      • Passive smoking
      • Ambient air pollution
      • Occupational dust/chemicals
      • Childhood infections (severe respiratory, viral)
      • Socioeconomic status
    • Host factors
      • Alpha1-antitrypsin deficiency (<1%)
      • Hyperresponsive airways
      • Lung growth
  • Differential Diagnosis Chronic Bronchitis Emphysema Asthma COPD Airflow Obstruction
  • Asthma
    • Definition: Airways hyper-responsiveness, reversible airways obstruction
    • Pathophysiology: Inflammation
  • Emphysema Inelastic collapsible bronchioles Enlarged air sacs due to destruction of alveolar walls (bullae) Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls and without obvious fibrosis Destruction of the alveolar wall damages pulmonary capillaries by tearing, fibrosis, or thrombosis Walls of individual sacs torn (repair not possible)
  • Chronic Bronchitis Presence of chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded Air passage narrowed by plugged and swollen mucous membrane Bronchiole Mucus and pus impede action of respiratory cilia
  •  
  • Asthma Is A Disease Of The Large & COPD The Small Airways Asthma Emphysema Bronchitis Bronchitis trachea bronchi alveoli
  • Disease Pathology Asthma COPD Reversible airflow obstruction + ++ + Airway inflammation + + + + + Mucus hypersecretion + + + + Goblet cell metaplasia + + + Impaired mucus clearance + + + + Epithelial damage ++ — Alveolar destruction — ++ Smooth muscle hypertrophy + + — Basement membrane thickening +++ —
  • Inflammation: COPD vs Asthma
    • Inflammation is an important component in the pathogenesis of asthma and COPD
    • The inflammatory response in asthma and COPD is markedly different, although some cell types are present in both diseases
    • The predominant inflammatory cells in asthma include
      • Eosinophils
      • Mast cells
      • CD4+ T lymphocytes
    • The predominant inflammatory cells in COPD include
      • Neutrophils
      • CD8+ T lymphocytes
      • Macrophages
    • The role of these cells in COPD is not fully understood
  •  
  • Inflammatory Cell Levels in Ex-Smokers With COPD (>1 Year of Smoking Cessation) Rutgers et al. Thorax. 2000;55:12-18. Values are expressed as percentages of the total number of nonsquamous cells. The role of these cells in COPD is not fully understood. Sputum Neutrophils (%) Sputum Lymphocytes and Eosinophils (%) Neutrophils P =0.0001 Patients with COPD Healthy controls Lymphocytes P =0.0161 Eosinophils P =0.0083 100 90 80 70 60 50 40 30 20 10 0 10 8 6 4 2 0
  •  
  • Asthma Sensitizing agent COPD Noxious agent Asthmatic airway inflammation CD4+ T-lymphocytes Eosinophils COPD airway inflammation CD8+ T-lymphocytes Macrophages Neutrophils Airflow limitation Completely reversible Completely irreversible
  • Physiologic Differences
    • Asthma
    • Normal DLCO
    • Normal lung volume
    • Normal elastic recoil
    • Flow dominant BD response
    • COPD
    • Abnormal DLCO
    • Hyperinflation
    • Decreased elastic recoil
    • Volume dominant BD response
    Sciurba FC, CHEST 2004;117S-124S
  • Response to Bronchodilators
    • ASTHMA
      • SABA
        • Tolerance
        • Dosed PRN
      • LABA
        • Monotherapy assoc. with increased frequency of exacerbations
        • Little tolerance
      • Anticholinergic
        • Efficacious in acute attack
    • COPD
      • SABA
        • No tolerance
        • Regularly dosed
      • LABA
        • Monotherapy assoc. with decreased frequency of exacerbations
        • Little tolerance
      • Anticholinergic
        • Efficacious in stable disease
    Donohue JF, CHEST 2004;125S-137S
  • Similarities
    • Bronchial hyper-reactivity
    • Bronchodilator response
    • Peripheral blood eosinophilia
    • Elevated IgE
    • Eosinophils in the BAL and airways
  • Lung Health Study Methacholine Bronchial Responsiveness
    • Dose Cumulative Percent
    • (mg) Men Women
    • 1 4 9
    • 5 26 48
    • 10 46 74
    • 25 63 87
    Tashkin et al AJRCCM 1996; 153:1802-11
  • Relationship Between Initial Histamine Threshold and Annual Rate of Decline in FEV 1 16 127 ± 59 < 2 50 77 ± 42 2-3 15 47 ± 22 > 4 Patients (n) Decline in FEV1 (ml/yr) Log Histamine Threshold Postma, Am Rev Respir Dis 1986: 134:276-280
  • Level Of BHR And Mortality From COPD During 30 Years of Follow Up RR (95% CI) COPD mortality Threshold histamine dose n (n=60 ) > 32 mg/ml 998 1 32 mg/ml 391 3.83 (0.97 - 15.10) 16 mg/ml 286 4.40* (1.16 - 16.67) 8 mg/ml 191 4.78* (1.27 - 18.00) 4 mg/ml 103 6.69* (1.71 - 26.13) 1 mg/ml 39 15.8* (3.72 - 67.13) * p  0.05 Hospers, et al. Lancet 2000; 356:1313-1317
  • Changes in Responder Classification After Albuterol and Ipatroprium Bromide
  • Bronchodilator Response: COPD vs. Asthma Higgins BG, Eur Resp J; 1991 p415
  • Assessment/Diagnosis
  • Why Do We Need Spirometry?
    • Objective Vital Sign for the Lungs (“ Poor Perceiver” )
    • More Accurate Assessment of Severity
      • Early recognition of disease
      • Improves choice of therapy
      • Leads to greater patient satisfaction
    • Determine Reversibility ( Asthma ) Vs. fixed obstruction (COPD) or Restriction
    • Differential Diagnosis (Pulmonary & Cardiac Abnormalities)
    • Identify and Quantify Defects in Lung Function
    • Reinforces therapeutic decisions to patients
    • Potential Source of Revenue
    Adapted from Crapo RA.: Current Concepts - Pulmonary-Function Testing. N Engl J Med 2001; Vol 331:61-67 and (http://www.nlhep.org/resources/PreventEmphysemaNow.html -page 1 ) Prevent Emphysema Now! by: Thomas L. Petty, M.D. and Dennis E. Doherty, M.D.
  • COPD Risk and Smoking Cessation FEV 1 (% of value at age 25) Age (years) Adapted from Fletcher C et al. Br Med J . 1977;1:1645–1648. 0 25 50 75 100 25 50 75 Death Disability Never smoked or not susceptible to smoke Smoked regularly and susceptible to effects of smoke Stopped smoking at 45 (mild COPD) Stopped smoking at 65 (severe COPD)
  • Laboratory Testing
    • Spirometry (pre- and post-bronchodilator
    • Chest radiography
    • Lung volumes
    • Carbon monoxide diffusing capacity
    • Arterial blood gases
  • GOLD Guidelines for COPD
    • Diagnosis
    • Chronic cough/sputum
    • PFTs within normal limits
    • No symptoms
    • Treatment
    • Avoid risk factors (smoking cessation)
    Stage 0: At Risk
  • GOLD Guidelines for COPD
    • Diagnosis
    • FEV 1 >80% predicted
    • FEV 1 /FVC <70%
    • With/without symptoms
    • Treatment
    • Avoid risk factors
    • Short-acting bronchodilator PRN
    Stage I: Mild
  • GOLD Guidelines for COPD
    • Diagnosis
    • 50%  FEV 1 <80% predicted
    • FEV 1 /FVC <70%
    • With/without symptoms
    • Treatment
    • Avoid risk factors
    • Regular therapy with  1 bronchodilators
    • Inhaled corticosteroids if significant symptoms and lung function response
    • Rehabilitation
    Stage II: Moderate
  • GOLD Guidelines for COPD
    • Diagnosis
    • 30%  FEV 1 < 50% predicted
    • FEV 1 /FVC < 70%
    • With/without symptoms
    • Treatment
    • Avoid risk factors
    • Regular therapy with  1 bronchodilators
    • Rehabilitation
    • Inhaled corticosteroids if significant symptoms and lung function response or if repeated exacerbations
    Stage III:Severe
  • GOLD Guidelines for COPD
    • Diagnosis
    • FEV 1 < 30% predicted
    • FEV 1 /FVC < 70%
    • Respiratory failure
    • Right-side-of-the-heart failure
    • Treatment
    • Avoid risk factors
    • Regular therapy with  1 bronchodilators
    • Inhaled corticosteroids if significant symptoms and lung function response or repeated exacerbations
    • Rehabilitation
    • Treatment of complications
    • Long-term O 2 therapy for hypoxic respiratory failure
    • Evaluate for surgical treatment
    Stage IV: Very Severe
  •  1 –Antitrypsin Deficiency
    • Hereditary disorder
      • Reduced protection vs. neutrophil elastase
      • Destruction of lung parenchyma
    • Increased risk of emphysema and liver disease
    • IV infusions of human  1 –antitrypsin (augmentation therapy)
      • Only currently approved therapy
      • Once-weekly (60 mg/kg)
    • 2% of COPD population
  • Augmentation Therapy: Impact on Mortality 0 6 12 18 24 30 36 42 48 54 60 Never (n = 162) Partially (n = 285) Always (n = 316) Time (months) FEV 1 < 50% Predicted Alpha-1-Antitrypsin Deficiency Registry Study Group. Am J Respir Crit Care Med . 1998;158:49–59. 50 40 30 20 10 0
    • Treatment
    • Effect on
    • Treatment Randomized Exacerbations
    • Study (mcg/day) Patients Placebo ICS vs Placebo
    • ISOLDE FP 1000 751 – 59 – 50  TE 25% ( P = .026)
    • Paggiaro FP 1000 281 – 40 + 110 ME/SE 60% vs 86% ( P  .001)
    • Copenhagen LS BUD 800 290 – 42 – 42  TE 4% (NS)
    • EUROSCOP BUD 800 912 – 69 – 57 Not Available
    • Lung Health II TAA 1200 1,100 – 47 – 44  TE †
    ICS: Effect on FEV 1 and Exacerbations Mean  FEV 1 (mL/year) * *Paggiaro Mean  FEV 1 was mL per 6 months. † P values not reported. BUD = budesonide; FP = fluticasone propionate; TAA = triamcinolone acetonide. TE = total exacerbations; SE = severe exacerbations; ME = moderate exacerbations.
  • Complications of COPD
    • Hypoxemia
    • Cor pulmonale
    • Hypercapnia
    • Dyspnea
  • Hypoxemia
    • Adversely affects cellular metabolism; may lead to
      • Hypoxia
      • Pulmonary hypertension
      • Cor pulmonale
    • Nonspecific signs/symptoms
      • Accurate identification requires arterial blood gas measurements
    • Nocturnal symptoms present in 25%– 45% of patients with severe COPD
    • Oxygen supplementation mainstay treatment
  •  
  • Hypercapnia
    • Usually well tolerated in COPD patients
    • Treatment goals
      • Improve airflow
      • Reduce breathing effort
      • Improve abnormalities affecting respiratory muscle function
    • Noninvasive ventilation suggested therapy
      • Long-term data conflicting
  • Cor Pulmonale
    • Primary cause – hypoxemia
    • Poor prognosis
    • Oxygen therapy and treating underlying disease are key
    • Pulmonary vasodilators offer no clear benefits; may worsen hypoxemia
    • Diuretics may improve ventricular function
      • Closely monitor for side effects
    • Digoxin contraindicated unless left-sided congestive heart failure present
  • Long-Term Oxygen Therapy: Guidelines Indications Absolute Pa O 2 ≤55 mm Hg or Sa O 2 ≤88% In patients with cor pulmonale Pa O 2 55–59 mm Hg or Sa O 2 ≥89% ECG evidence of P pulmonale, hematocrit >55%, and CHD Specific Indications Nocturnal hypoxemia Sleep apnea with nocturnal desaturation not corrected by constant positive airway pressure or bilevel positive airway pressure No hypoxemia at rest, but desaturation during exercise or sleep (PaO 2 <55 mm Hg) Treatment Goals Pa O 2 ≥60 mm Hg or Sa O 2 ≥90%; Appropriately adjusted O 2 dose during sleep and exercise Same as above Appropriately adjusted O 2 dose during sleep Appropriately adjusted O 2 dose during sleep Same as above
  • Effects of Tiotropium Day 1 and Day 92 0.85 0.90 0.95 1.00 1.05 1.10 1.15 1.20 1.25 1.30 1.35 -1 -0.5 0 0.5 1 1.5 2 2.5 3 Day 1 Day 92 Tiotropium (N = 276) Placebo (N = 188) FEV 1 (L) Hours following drug administration Casaburi R, et al. Chest . 2000;118:1294–1302.
  • Salmeterol/Fluticasone Combination Change From Baseline Pre-Dose FEV 1 Time (weeks) * P <0.05 vs. placebo; † P <0.05 vs. SAL; ‡ P <0.05 vs. FP Data on file, GlaxoSmithKline. FEV 1 (mL) *†‡ *†‡ * * * PBO SAL50/FP250 350 300 250 200 150 100 50 0 -50 0 2 4 6 8 12 16 20 24 EP SAL50 FP250 FP500 SAL50/FP500
  • Serial FEV 1 Day 1 Baseline FEV 1 FSC- 1.31L IP/ALB- 1.26L 0 50 100 150 200 250 300 1 2 3 4 5 6 Time (hrs) Change in FEV 1 (mL) 1 2 3 4 5 6 Time (hrs) Change in FEV 1 (mL) FSC IP/ALB 1 2 3 4 5 6 Day 1 Week 8 † † * * * † † FSC vs. IP/ALB: p<0.001 * IP/ALB vs FSC p  0.002 -50 0 50 100 150 200 250 300
  • Predose FEV 1 FSC IP/ALB Endpoint * p <0.001 vs. IP/ALB * 0 * * Week 8 Week 1 * Week 4
  • Acute Exacerbations of COPD (AECOPD)
    • Common during winter months
    • Symptoms
      • Breathlessness
      • Wheeze
      • Cough
      • Increased sputum production
    • Causes
      • Viral infection (e.g., rhinovirus)
      • Environmental causes (including smoking)
      • Allergy
      • Bacterial infection
  • Most Commonly Isolated Bacterial Pathogens
    • Haemophilus parainfluenzae
    • H influenzae
    • Streptococcus pneumoniae
    • Moraxella catarrhalis
    • Pseudomonas aeruginosa
    • Other gram-negative bacilli
    • Alpha-hemolytic streptococci
  • AECOPD Proposed Classification of Patients Adapted from Wilson R. Chest . 1995;108:53S–57S. Baseline Clinical Status I. Acute tracheo- bronchitis Criteria/ Risk Factors No underlying structural disease Pathogens Usually viral Suggested Therapy None; consider macrolide or tetracycline
  • Viral Pathogens Associated With Acute COPD Exacerbations RSV = respiratory syncytial virus. Sethi S. Infect Dis Clin Pract . 1998;7:S300–S308. 10% 10% 18% 20% 25% 35% 0 10 20 30 40 Influenza Parainfluenza Rhinovirus Coronavirus Adenovirus RSV Proportion of Acute Viral Exacerbations
  • AECOPD Proposed Classification of Patients (cont’d) * Possible beta-lactam resistance. Baseline Clinical Status II. Simple chronic bronchitis Criteria/ Risk Factors FEV 1 >50% increased sputum volume/ purulence Pathogens H influenzae M catarrhalis S pneumoniae* Suggested Therapy Amoxicillin Adapted from Wilson R. Chest . 1995;108:53S–57S.
  • AECOPD Proposed Classification of Patients (cont’d) * Resistance to beta-lactams common. Baseline Clinical Status III. Complicated chronic bronchitis Criteria/ Risk Factors As for Class II + any one of: FEV 1 <50%, advanced age, ≥4 exacerbations/yr, significant co- morbidity Pathogens H influenzae M catarrhalis S pneumoniae * Suggested Therapy Quinolone Penicillin +  -lactamase inhibitor 2nd- or 3rd-gen. cephalosporin 2nd-gen. macrolide Adapted from Wilson R. Chest . 1995;108:53S–57S.
  • AECOPD Proposed Classification of Patients (cont’d) Baseline Clinical Status IV. Chronic bronchial infection Criteria/ Risk Factors Class III + continuous sputum throughout the year Pathogens H influenzae M catarrhalis S pneumoniae Enterobacteriae spp P aeruginosa Suggested Therapy Quinolone Adapted from Wilson R. Chest . 1995;108:53S–57S.
  • “ The Downward Spiral” COPD Airway obstruction Exacerbation Mucus hypersecretion Continued smoking Lung inflammation Alveolar destruction Impaired mucus clearance Submucosal gland hypertrophy Exacerbation Exacerbation Hypoxemia DEATH
  • Asthma Management Step Symptoms Day/Night FEV1 & PEF (% predicted) PEF variability Medication PRN SABA ≥ 80% <20% < 2 days per week/Nocturnal symptoms < 2 nights per month 1 Mild Intermittent Low-dose ICS ≥ 80% 20-30% >2 x per week but <1 time day/Nocturnal symptoms >2 nights/month 2 Mild Persistent LABA + low to moderate dose ICS  60%  80% >30% Daily/Nocturnal symptoms  1 per week 3 Moderate LABA + high-dose ICS Consider LTM corticosteroids as needed (taper to lowest dose)  60%  30% Continual daytime/frequent nocturnal symptoms 4 Severe
  • Importance of early treatment with inhaled corticosteroids in asthma <2 2-3 3-5 >5 Annual change in FEV 1 %pred Agertoft & Pedersen. Respir Med 1994; 88:373-81 Years that symptoms started before treatment
  • Relative Risk of Hospitalization in the United States Donahue et al. JAMA . 1997;277:887-891. Prescriptions per Person-Year Relative Risk None 1-2 2-3 3-5 5-8 8+ 0-1  2 -Agonists Total ICS 0 1 2 3 4 5 6 7 8 Age 0-17 Age 18-44 Age 45+ Total Age 0-17 Age 18-44 Age 45+
  • Low-dose ICS and the Prevention of Death from Asthma No. of Canisters of Inhaled Corticosteroids per Yr. Rate Ratio for Death from Asthma Suissa S et al. N Engl J Med. 2000;343:332-336.
    • ICS protects patients from asthma-related deaths
    • Users of > 6 canisters/yr. Had a death rate ~ 50% lower than non-users of ICS
    • Death rate decreased by 21% for each additional ICS canister used during the previous year.
    2.5 2.0 1.5 1.0 0.5 0.0 1 2 3 4 5 6 7 8 9 10 11 12
  • Beclomethasone Comparison Study: FEV 1 Placebo Montelukast sodium Beclomethasone Weeks in active treatment 0 3 6 9 12 15 0 5 10 15 Mean change in FEV 1 (%) Washout * P < 0.01 beclomethasone vs montelukast and placebo. † P < 0.001 vs placebo. * † Malmstrom K, et al. Ann Intern Med. 1999;130:487-495.
  •  
  • Patients Treated With ADVAIR ™ Diskus ® 250/50 Had a Significantly Greater Improvement in FEV 1 Mean  in FEV 1 from Baseline (%) *Differs from FP 250, salmeterol 50, placebo at endpoint; P  0.003 Doses in mcg b.i.d. Shapiro G, et al. Am J Respir Crit Care Med. 2000;161:527-534. 30 25 20 15 10 5 0 -5 Endpoint Week -5% [-0.11L] ADVAIR 250/50 FP 250 Salmeterol 50 Placebo 23% [0.48L] * 13% [0.25L] 4% [0.05L] 2 4 6 8 10 12
  • Patients Treated With ADVAIR ™ Diskus ® 250/50 Were Less Likely to be Withdrawn for Worsening Asthma *Differs from FP 250, salmeterol 50, placebo; P  0.002 Doses in mcg b.i.d. Shapiro G, et al. Am J Respir Crit Care Med. 2000;161:527-534. 1.0 0.8 0.6 0.4 0.2 0 0 7 14 21 28 35 42 49 56 63 70 77 84 Study Day Placebo FP 250 ADVAIR 250/50 Salmeterol 50 Probability of Remaining in Study 4% * 22% 38% 62%
  • Anti-IgE
    • Monoclonal Ab to IgE
    • Reduces circ. IgE, # of IgE receptors on basophils & Reduces early & late phase response
    • Ag stimulated histamine release, bronchial rxt, & sputum eosinophilia
    • Reduces exacerbation rate while allowing steroid withdrawal
  • Asthma & COPD Summary
    • Both disorders of airways obstruction
    • Both inflammatory
    • COPD is progressive
    • 1 st line therapy for asthma are ICS
    • 1 st line therapy for COPD are BD
    • Attend to comorbidities