Jama copd exacerbation steroids

Genetics play a role in the development of COPD. [9] It is more common among relatives of those with COPD who smoke than unrelated smokers. [9] Currently, the only clearly inherited risk factor is alpha 1-antitrypsin deficiency (AAT). [46] This risk is particularly high if someone deficient in alpha 1-antitrypsin also smokes. [46] It is responsible for about 1–5% of cases [46] [47] and the condition is present in about 3–4 in 10,000 people. [16] Other genetic factors are being investigated, [46] of which there are likely to be many. [11]

The symptoms of acute exacerbations are treated using short-acting bronchodilators. A course of corticosteroids, usually in tablet or intravenous rather than inhaled form, can speed up recovery. [1] The IV and oral forms of steroids have been found to be equivalent. [17] Antibiotics are often used but will only help if the exacerbation is due to an infection. [18] Antibiotics are indicated when a patient notes increased sputum production, [5] purulent sputum, [5] increased dyspnea , [5] has an elevated white count, or is febrile . Examples of first-line antibiotics are amoxicillin , [5] doxycycline [5] and co-trimoxazole . [5]

Noninferiority trials have serious inherent limitations , the main one being that (unlike in a superiority trial), given a finding of noninferiority, it is impossible to distinguish between true equivalence and poor execution or faulty pretrial a priori assumptions regarding expectations of benefit and event rates. In this particular trial, a 15% absolute difference in the primary outcome was arguably too large to use as a noninferiority threshold. That threshold implies acceptance of 1 additional COPD exacerbation for each 7 patients treated. If a superiority trial showed a week's extra steroids prevented 1 COPD exacerbation for 10 or even 20 patients treated (, a 5-10% noninferiority margin), I think many doctors and patients would endorse longer-course prednisone. This trial (as designed) would fail to detect that.

Patients in GOLD groups C and D should be prescribed a long-acting anticholinergic or a combination of an inhaled corticosteroid and long-acting beta 2 agonist. 3 Compared with tiotropium alone, fluticasone/salmeterol (Advair) improved daily symptom scores and decreased mortality (number needed to treat = 40), but increased the incidence of pneumonia (number needed to harm = 25) and did not change the rate of exacerbations. 33 Patients with poorly controlled symptoms should start triple therapy with an inhaled corticosteroid, long-acting anticholinergic, and long-acting beta 2 agonist. The data for triple therapy are inconsistent, with studies showing improvement in lung function and symptom scores but conflicting results regarding reduction in exacerbation rates compared with tiotropium alone. 28 , 34   A summary of initial treatment options and common medications is presented in Table 4 8 and Table 5 , 35 and patient instructions for inhaler use are reviewed in eFigure B .

Jama copd exacerbation steroids

jama copd exacerbation steroids

Patients in GOLD groups C and D should be prescribed a long-acting anticholinergic or a combination of an inhaled corticosteroid and long-acting beta 2 agonist. 3 Compared with tiotropium alone, fluticasone/salmeterol (Advair) improved daily symptom scores and decreased mortality (number needed to treat = 40), but increased the incidence of pneumonia (number needed to harm = 25) and did not change the rate of exacerbations. 33 Patients with poorly controlled symptoms should start triple therapy with an inhaled corticosteroid, long-acting anticholinergic, and long-acting beta 2 agonist. The data for triple therapy are inconsistent, with studies showing improvement in lung function and symptom scores but conflicting results regarding reduction in exacerbation rates compared with tiotropium alone. 28 , 34   A summary of initial treatment options and common medications is presented in Table 4 8 and Table 5 , 35 and patient instructions for inhaler use are reviewed in eFigure B .

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