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10.1111/bcpt.12366

http://scihub22266oqcxt.onion/10.1111/bcpt.12366
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C4409821!4409821!25515181
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suck abstract from ncbi


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pmid25515181      Basic+Clin+Pharmacol+Toxicol 2015 ; 116 (4): 291-307
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  • Diagnosis and Pharmacotherapy of Stable Chronic Obstructive Pulmonary Disease: The Finnish Guidelines #MMPMID25515181
  • Kankaanranta H; Harju T; Kilpeläinen M; Mazur W; Lehto JT; Katajisto M; Peisa T; Meinander T; Lehtimäki L
  • Basic Clin Pharmacol Toxicol 2015[Apr]; 116 (4): 291-307 PMID25515181show ga
  • The Finnish Medical Society Duodecim initiated and managed the update of the Finnish national guideline for chronic obstructive pulmonary disease (COPD). The Finnish COPD guideline was revised to acknowledge the progress in diagnosis and management of COPD. This Finnish COPD guideline in English language is a part of the original guideline and focuses on the diagnosis, assessment and pharmacotherapy of stable COPD. It is intended to be used mainly in primary health care but not forgetting respiratory specialists and other healthcare workers. The new recommendations and statements are based on the best evidence available from the medical literature, other published national guidelines and the GOLD (Global Initiative for Chronic Obstructive Lung Disease) report. This guideline introduces the diagnostic approach, differential diagnostics towards asthma, assessment and treatment strategy to control symptoms and to prevent exacerbations. The pharmacotherapy is based on the symptoms and a clinical phenotype of the individual patient. The guideline defines three clinically relevant phenotypes including the low and high exacerbation risk phenotypes and the neglected asthma?COPD overlap syndrome (ACOS). These clinical phenotypes can help clinicians to identify patients that respond to specific pharmacological interventions. For the low exacerbation risk phenotype, pharmacotherapy with short-acting ?2-agonists (salbutamol, terbutaline) or anticholinergics (ipratropium) or their combination (fenoterol?ipratropium) is recommended in patients with less symptoms. If short-acting bronchodilators are not enough to control symptoms, a long-acting ?2-agonist (formoterol, indacaterol, olodaterol or salmeterol) or a long-acting anticholinergic (muscarinic receptor antagonists; aclidinium, glycopyrronium, tiotropium, umeclidinium) or their combination is recommended. For the high exacerbation risk phenotype, pharmacotherapy with a long-acting anticholinergic or a fixed combination of an inhaled glucocorticoid and a long-acting ?2-agonist (budesonide?formoterol, beclomethasone dipropionate?formoterol, fluticasone propionate?salmeterol or fluticasone furoate?vilanterol) is recommended as a first choice. Other treatment options for this phenotype include combination of long-acting bronchodilators given from separate inhalers or as a fixed combination (glycopyrronium?indacaterol or umeclidinium?vilanterol) or a triple combination of an inhaled glucocorticoid, a long-acting ?2-agonist and a long-acting anticholinergic. If the patient has severe-to-very severe COPD (FEV1 < 50% predicted), chronic bronchitis and frequent exacerbations despite long-acting bronchodilators, the pharmacotherapy may include also roflumilast. ACOS is a phenotype of COPD in which there are features that comply with both asthma and COPD. Patients belonging to this phenotype have usually been excluded from studies evaluating the effects of drugs both in asthma and in COPD. Thus, evidence-based recommendation of treatment cannot be given. The treatment should cover both diseases. Generally, the therapy should include at least inhaled glucocorticoids (beclomethasone dipropionate, budesonide, ciclesonide, fluticasone furoate, fluticasone propionate or mometasone) combined with a long-acting bronchodilator (?2-agonist or anticholinergic or both).
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