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Important pages


Sources

Source Author Title Publ. Year Bib. FN
Amm/Anzueto 2010 A. Anzueto Impact of exacerbations on COPD 2010 no no
Amm/Celli and Barnes 2007 B.R. Celli, P.J. Barnes Exacerbations of chronic obstructive pulmonary disease 2007 yes yes
Amm/Decramer et al 2011 Marc Decramer, Marc Miravitlles, David Price, Miguel Román-Rodríguez, Carl Llor, Tobias Welte, Roland Buhl, Daniel Dusser, Katerina Samara, Nikolaus Siafakas New horizons in early stage COPD - Improving knowledge, detection and treatment Elsevier 2011 no no
Amm/Puhan et al 2008 Milo A Puhan, Daniela Vollenweider, Johann Steurer, Patrick M Bossuyt, Gerben ter Riet Where is the supporting evidence for treating mild to moderate chronic obstructive pulmonary disease exacerbations with antibiotics? A systematic review BioMed Central 2008 yes yes
Amm/Sethi 2008 Sanjay Sethi The problems of meta-analysis for antibiotic treatment of chronic obstructive pulmonary disease, a heterogeneous disease: a commentary on Puhan et al 2008 yes yes
Amm/Sethi 2010 S. Sethi Infection as a comorbidity of COPD 2010 yes yes


Fragments (Plagiarism, reviewed)

No Fragment



Fragments (Plagiarism, unreviewed)

8 Fragments

[1.] Analyse:Amm/Fragment 007 12 - Diskussion
Bearbeitet: 25. December 2014, 20:27 Hindemith
Erstellt: 25. December 2014, 20:27 (Hindemith)
Amm, Celli and Barnes 2007, Fragment, KomplettPlagiat, SMWFragment, Schutzlevel, ZuSichten

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COPD is a condition that becomes clinically apparent in mid-to-late life. Comorbidity is relatively common in patients with COPD and this raises the issue as to whether such a comorbidity is age-related, related to a common factor, such as smoking and cardiovascular disease, due to the effect of drugs like corticosteroids and the development of diabetes, or a reflection of the increase in systemic inflammatory cytokine concentrations, which are a feature of COPD with systemic involvement. Data are emerging that the same inflammatory mediators are central to the pathogenesis of other diseases and, to illustrate this, focus was directed towards type 2 diabetes and cardiovascular diseases. COPD is a condition that becomes clinically apparent in mid-to-late life. Comorbidity is relatively common in patients with COPD and this raises the issue as to whether such a comorbidity is age-related, related to a common factor, such as smoking and cardiovascular disease, due to the effect of drugs like corticosteroids and the development of diabetes, or a reflection of the increase in systemic inflammatory cytokine concentrations, which are a feature of COPD with systemic involvement. Data are emerging that the same inflammatory mediators are central to the pathogenesis of other diseases and, to illustrate this, focus was directed towards type 2 diabetes and cardiovascular diseases.
Anmerkungen

The source is not mentioned here.

Sichter
(Hindemith)

[2.] Analyse:Amm/Fragment 011 01 - Diskussion
Bearbeitet: 25. December 2014, 21:03 Hindemith
Erstellt: 25. December 2014, 21:01 (Hindemith)
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[A group of patients with COPD exacerbation showed a moderate-to-large improvement] in all four domains of the Chronic Respiratory Disease Questionnaire after 10 days of treatment (Aaron SD et al, 2002). This improvement was not observed in patients who relapsed after treatment of exacerbation.

A study by Connors JR et al (Connors AF Jr. et al, 1996) reported the quality of life outcomes in patients hospitalised with acute exacerbations of COPD. At 6 months, 54% of patients required assistance with at least one activity of daily living and 49% considered their health status to be fair or poor. No analysis was conducted on the relationship between readmissions and perceived quality of life. The recovery of HRQL parameters after an acute COPD exacerbation may be determined by several factors. Spencer et al (Spencer S et al, 2001) in exacerbated patients who did not relapse during follow-up experienced an improvement in the St George's Respiratory Questionnaire (SGRQ) of 11.8 units at 1 month and 17 units after 5 months of the onset of the exacerbation. These results indicate that the recovery of health status after an exacerbation may take longer than previously expected. In contrast, median recovery time for lung function after an exacerbation is 6 days and for symptoms is 7 days (Spencer S et al, 2001). However, this recovery may be influenced by the severity of the exacerbation. The more severe the exacerbation, the longer it takes to recover. Seemungal et al (Seemungal TA et al, 2000a) showed that only 75% of patients return to their baseline peak flow values 35 days after the episode. The SGRQ and Medical Research Council questionnaire were completed by patients at the end of the study. Exacerbations were more frequent in patients with frequent previous exacerbations with an odds ratio (OR) of 5.5. Using the median number of exacerbations, patients were classified as infrequent exacerbators (0–2) or frequent exacerbators (3–8). SGRQ total score was significantly worse in frequent exacerbators, with a mean difference of 14.8.

In multiple regression analyses, exacerbation frequency was strongly correlated with SGRQ total score and component scores. Miravitlles et al (Miravitlles M et al, 2004a) confirmed the impact of exacerbations on health status. Thus, these studies showed that patients who suffered more exacerbations had significantly worse SGRQ scores compared with infrequent exacerbators, and HRQL-related questionnaires offer complementary information to lung function and respiratory symptoms to monitor the [course of recovery of an exacerbation.]

A group of patients with COPD exacerbation showed a moderate-to-large improvement in all four domains of the Chronic Respiratory Disease Questionnaire after 10 days of treatment [18]. This improvement was not observed in patients who relapsed after treatment of exacerbation.

[page 115]

A study by CONNORS JR et al. [36] reported the quality of life outcomes in patients hospitalised with acute exacerbations of COPD. At 6 months, 54% of patients required assistance with at least one activity of daily living and 49% considered their health status to be fair or poor. No analysis was conducted on the relationship between readmissions and perceived quality of life. The recovery of HRQoL parameters after an acute COPD exacerbation may be determined by several factors. SPENCER et al. [33] in exacerbated patients who did not relapse during follow-up experienced an improvement in the St George’s Respiratory Questionnaire (SGRQ) of 11.8 units at 1 month and 17 units after 5 months of the onset of the exacerbation. These results indicate that the recovery of health status after an exacerbation may take longer than previously expected. In contrast, median recovery time for lung function after an exacerbation is 6 days and for symptoms is 7 days [33]. However, this recovery may be influenced by the severity of the exacerbation. The more severe the exacerbation, the longer it takes to recover. SEEMUNGAL et al. [37] showed that only 75% of patients return to their baseline peak flow values 35 days after the episode. The SGRQ and Medical Research Council questionnaire were completed by patients at the end of the study. Exacerbations were more frequent in patients with frequent previous exacerbations (OR 5.5, p=0.001). Using the median number of exacerbations, patients were classified as infrequent exacerbators (0–2) or frequent exacerbators (3–8). SGRQ total score was significantly worse in frequent exacerbators (mean difference 14.8; p<0.001) (fig. 1).

In multiple regression analyses, exacerbation frequency was strongly correlated with SGRQ total score and component scores. MIRAVITLLES et al. [6] confirmed the impact of exacerbations on health status. Thus, these studies showed that patients who suffered more exacerbations had significantly worse SGRQ scores compared with infrequent exacerbators, and HRQoL-related questionnaires offer complementary information to lung function and respiratory symptoms to monitor the course of recovery of an exacerbation.


6 Miravitlles M, Ferrer M, Pont A, et al. Effect of exacerbations on quality of life in patients with chronic obstructive pulmonary disease: a 2 year follow up study. Thorax 2004; 59: 387–395.

18 Aaron SD, Vandemheen KL, Clinch JJ, et al. Measurment of shortterm changes in dyspnoea and disease-specific quality of life following an acute COPD exacerbation. Chest 2002; 121: 688–696.

33 Spencer S, Calverley PMA, Burge S, et al. Health status deterioration in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001; 163: 122–128.

36 Connors AF Jr, Dawson NV, Thomas C, et al. Outcomes following acute exacerbation of severe chronic obstructive lung disease. The SUPPORT investigators (Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments). Am J Respir Crit Care Med 1996; 154: 959–967.

37 Seemungal TA, Donaldson GC, Bhowmik A, et al. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000; 161: 1608–1613.

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith)

[3.] Analyse:Amm/Fragment 014 04 - Diskussion
Bearbeitet: 25. December 2014, 20:33 Hindemith
Erstellt: 25. December 2014, 20:30 (Hindemith)
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Economic impact of exacerbations

Some studies have determined that hospitalisation costs represent 40–57% of total direct costs generated by patients with COPD, and this percentage may be as high as 63% in severe patients (Hilleman DE et al, 2000). Since acute exacerbations are the main cause of hospitalisation among COPD patients, it is evident that the economic burden of acute exacerbations is considerable. Observational studies performed in primary care centres observed that 16–22% of patients having exacerbations were admitted during 1 year (Pena VS et al, 2000). The costs of exacerbations that require hospitalisation increase dramatically compared with those that can be treated in an ambulatory setting. An analysis derived from a clinical trial in patients with COPD demonstrated that the 15% of exacerbations requiring hospital admission generated 90% of the costs associated with exacerbations (Miravitlles M et al, 2002). In a recent study in primary care in Spain, the mean total cost of an acute exacerbation of COPD was estimated to be US$159, with the main part being due to hospitalisations, which represented 58% of the total cost, followed by the drug costs amounting to 32% of the total (Miravitlles M et al, 2005). Failure implies a cost that is three times higher than the cost of management of the exacerbation, particularly due to the high cost of hospitalisation. If the percentage of relapses could be reduced, especially in severe cases, or if switching a patient from parenteral to oral therapy could reduce the length of hospital stay, valuable resources could be saved. The costs of managing acute exacerbations of chronic bronchitis are high, particularly because of the high costs associated with relapse (Feenstra TL et al, 2001; Jacobson L et al, 2000). Strategies to improve the outcome of ambulatory treatment of exacerbations should be very cost-effective, especially in more severe patients who are at increased risk of being admitted to hospital as a consequence of therapeutic failure.

Economic consequences

Some studies have determined that hospitalisation costs represent 40–57% of total direct costs generated by patients with COPD, and this percentage may be as high as 63% in severe patients [85]. [...] Since acute exacerbations are the main cause of hospitalisation among COPD patients, it is evident that the economic burden of acute exacerbations is considerable. Observational studies performed in primary care centres observed that 16–22% of patients having exacerbations were admitted during 1 yr [86]. The costs of exacerbations that require hospitalisation increase dramatically compared with those that can be treated in an ambulatory setting. An analysis derived from a clinical trial in patients with COPD demonstrated that the 15% of exacerbations requiring hospital admission generated 90% of the costs associated with exacerbations [87]. In a recent study in primary care in Spain, the mean total cost of an acute exacerbation of COPD was estimated to be US$159, with the main part being due to hospitalisations, which represented 58% of the total cost, followed by the drug costs amounting to 32% of the total [88]. [...] Failure implies a cost that is three times higher than the cost of management of the exacerbation, particularly due to the high cost of hospitalisation. If the percentage of relapses could be reduced, especially in severe cases, or if switching a patient from parenteral to oral therapy could reduce the length of hospital stay, valuable resources could be saved. [...] The costs of managing acute exacerbations of chronic bronchitis are high, particularly because of the high costs associated with relapse [89, 90]. Strategies to improve the outcome of ambulatory treatment of exacerbations should be very cost-effective, especially in more severe patients who are at increased risk of being admitted to hospital as a consequence of therapeutic failure.


85 Hilleman DE, Dewan N, Malesker M, Friedman M. Pharmacoeconomic evaluation of COPD. Chest 2000; 118: 1278–1285.

86 Pena VS, Miravitlles M, Gabriel R, et al. Geographic variations in prevalence and underdiagnosis of COPD: results of the IBERPOC multicentre epidemiological study. Chest 2000; 118: 981–989.

87 Miravitlles M, Murio C, Guerrero T, Gisbert R. Pharmacoeconomic evaluation of acute exacerbations of chronic bronchitis and COPD. Chest 2002; 121: 1449–1455.

88 Miravitlles M, Ferrer M, Pont A, et al. Characteristics of a population of COPD patients identified from a population-based study. Focus on previous diagnosis and never smokers. Respir Med 2005; 99: 985–995.

89 Feenstra TL, van Genugten ML, Hoogenveen RT, Wouters EF, Rutten-van Molken MP. The impact of aging and smoking on the future burden of chronic obstructive pulmonary disease: a model analysis in the Netherlands. Am J Respir Crit Care Med 2001; 164: 590–596.

90 Jacobson L, Hertzman P, Lofdahl CG, Skoogh BE, Lindgren B. The economic impact of asthma and chronic obstructive pulmonary disease (COPD) in Sweden in 1980 and 1991. Respir Med 2000; 94: 247–255.

Anmerkungen

The source is not mentioned here.

Sichter
(Hindemith)

[4.] Analyse:Amm/Fragment 023 07 - Diskussion
Bearbeitet: 25. December 2014, 21:05 Hindemith
Erstellt: 25. December 2014, 20:42 (Hindemith)
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Early studies based on culture of respiratory secretions and serological tests revealed that about one-third of exacerbations were related to bacterial infection. However, in the remaining cases, the aetiology appeared to be uncertain; specifically, the significance of bacterial isolation from sputum was unclear (Gump DW et al, 1976). A causal relationship between bacteria and exacerbation was largely discredited when longitudinal studies showed similar rates of isolation of Streptococcus pneumoniae and Haemophilus influenzae from sputum during both acute exacerbations and stable disease (Fagon JY et al, 1996; Gump DW et al, 1976; McHardy VU et al, 1980; Smith CB et al, 1976; Tager I et al, 1975). A significant limitation of these studies was their failure to differentiate among strains within a bacterial species (Sethi S et al, 2002), as the technology was not available at that time for such differentiation. Consequently, changes in strains within a species in the airways of individual patients over time were undetected.

In recent years, new research techniques, including molecular typing, have led to renewed interest in the area of bacteria and COPD. Recent studies have used more sophisticated diagnostic tools and the application of molecular technologies to further explore a causal relationship between infection and exacerbation. Acquisition of new bacterial strains from the environment has been shown to be the major driver of exacerbations (Veeramachaneni SB et al, 2006). In this model, following acquisition of a new bacterial strain, the balance between the virulence of the pathogen and the host lung defence determines the degree of excess airway and systemic inflammation engendered by the bacterial pathogen. The degree of increased inflammation in turn determines the extent of symptoms, which, if they lead to the patient seeking [healthcare, are diagnosed as an acute exacerbation.]

Early studies based on culture of respiratory secretions and serological tests revealed that about one-third of exacerbations were related to viral infection. However, in the remaining cases, the aetiology appeared to be uncertain; specifically, the significance of bacterial isolation from sputum was unclear [4]. A causal relationship between bacteria and exacerbation was largely discredited when longitudinal studies showed similar rates of isolation of Streptococcus pneumoniae and Haemophilus influenzae from sputum during both acute exacerbations and stable disease [4–8]. A significant limitation of these studies was their failure to differentiate among strains within a bacterial species [9], as the technology was not available at that time for such differentiation. Consequently, changes in strains within a species in the airways of individual patients over time were undetected.

In recent years, new research techniques, including molecular typing, have led to renewed interest in the area of bacteria and COPD. Recent studies have used more sophisticated diagnostic tools and the application of molecular technologies to further explore a causal relationship between infection and exacerbation.

[...]

An alternative model that is now well supported with empirical evidence is based on the premise that acquisition of new bacterial strains from the environment is the major driver of exacerbations (fig. 2) [12]. In this model, following acquisition of a new bacterial strain, the balance between the virulence of the pathogen and the host lung defence determines the degree of excess airway and systemic inflammation engendered by the bacterial pathogen. The degree of increased inflammation in turn determines the extent of symptoms, which, if they lead to the patient seeking healthcare, are diagnosed as an acute exacerbation.


4 Gump DW, Phillips CA, Forsyth BR, et al. Role of infection in chronic bronchitis. Am Rev Respir Dis 1976; 113: 465–474.

5 McHardy VU, Inglis JM, Calder MA, et al. A study of infective and other factors in exacerbations of chronic bronchitis. Br J Dis Chest 1980; 74: 228–238.

6 Smith CB, Golden C, Klauber MR, et al. Interactions between viruses and bacteria in patients with chronic bronchitis. J Infect Dis 1976; 134: 552–561.

7 Fagon JY, Chastre J. Severe exacerbations of COPD patients: the role of pulmonary infections. Semin Respir Infect 1996; 11: 109–118.

8 Tager I, Speizer FE. Role of infection in chronic bronchitis. N Engl J Med 1975; 292: 563–571.

9 Sethi S, Evans N, Grant BJ, et al. New strains of bacteria and exacerbations of chronic obstructive pulmonary disease. N Engl J Med 2002; 347: 465–471.

12 Veeramachaneni SB, Sethi S. Pathogenesis of bacterial exacerbations of COPD. COPD 2006; 3: 109–115.

Anmerkungen

The source is not mentioned here.

Note that in the first sentence "viral" was changed to "bacterial". From the abstract of the original source Gump et al. (1976): "One third (33.6 per cent) of the 116 exacerbations observed could be related to viral infection or Mycoplasma pneumoniae (1 exacerbation)."

Sichter
(Hindemith)

[5.] Analyse:Amm/Fragment 044 03 - Diskussion
Bearbeitet: 27. December 2014, 00:29 Hindemith
Erstellt: 25. December 2014, 20:03 (Hindemith)
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On the other hand, Sachs et al (Sachs APE et al, 1995) included patients of younger age, mild underlying disease and asthma. Not surprisingly, only 11% of their exacerbations were associated with a positive bacterial culture, rather than the usual 40% to 50%. Not surprisingly, antibiotics were of no benefit in this study and, in their placebo arm, there was a 93% resolution rate compared with 55% in the Anthonisen study (Anthonisen NR et al, 1987).

Severity of exacerbations

These systematic reviews considered non-severe exacerbations based on the site of treatment, that is, outpatient treatment. This classification is clearly very broad as the site of care will vary among countries and healthcare systems as well as with patient and physician preferences. Furthermore, over time, changes in healthcare delivery and results of outcome studies can change the site of care for the same severity of exacerbation. As Sethi states (Sethi S, 2008) a 40-year-old smoker without underlying airway obstruction, infrequent exacerbations and free of comorbid conditions would have been included as a mild-to-moderate exacerbation. On the other hand, a patient with severe COPD, frequent exacerbations and comorbid conditions who does not require hospitalization would also be classified as a mild-to-moderate exacerbation. In the former patient, it is possible that host immunity can adequately deal with the infection and the exacerbation will spontaneously resolve. In the latter patient, such resolution is less likely and complications are more frequent. Grouping these patients together can lead to confusing and contradictory results.

The severity of an exacerbation is a complicated concept, constituted by at least two factors, the severity of the underlying COPD and the acute change induced by the exacerbation itself. Therefore, a patient with severe underlying COPD will have significant clinical consequences from a relatively small change from the baseline state, while a patient with mild COPD will tolerate a much larger change in symptoms and lung function. It is evident that we need more objective measures of severity of exacerbations.

Severity of exacerbations

Puhan et al have grouped together mild and moderate exacerbations based on the site of treatment, that is, outpatient treatment. This classification is clearly very broad as the site of care will vary among countries and healthcare systems as well as with patient and physician preferences. Furthermore, over time, changes in healthcare delivery and results of outcome studies can change the site of care for the same severity of exacerbation. A 40-year-old smoker without underlying airway obstruction, infrequent exacerbations and free of comorbid conditions would have been included as a 'mild to moderate' exacerbation. On the other hand, a patient with severe COPD, frequent exacerbations and comorbid conditions who does not require hospitalization would also be classified as a 'mild to moderate exacerbation'. In the former patient, it is possible that host immunity can adequately deal with the infection and the exacerbation will spontaneously resolve. In the latter patient, such resolution is less likely and complications are more frequent. Grouping these patients together can lead to confusing and contradictory results.

The severity of an exacerbation is a complicated concept, constituted by at least two factors, the severity of the underlying COPD and the acute change induced by the exacerbation itself. Therefore, a patient with severe underlying COPD will have significant clinical consequences from a relatively small change from the baseline state, while a patient with mild COPD will tolerate a much larger change in symptoms and lung function. It is evident that we need more objective measures of severity of exacerbations. [...]

[...]

[...] As is evident from this comparison, Sachs et al [5] included patients of younger age, mild underlying disease and asthma. Not surprisingly, only 11% of their exacerbations were associated with a positive bacterial culture, rather than the usual 40% to 50%. Not surprisingly, antibiotics were of no benefit in this study and, in their placebo arm, there was a 93% resolution rate compared with 55% in the Anthonisen study [4].


4. Anthonisen NR, Manfreda J, Warren CPW, Hershfield ES, Harding GKM, Nelson NA: Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease. Ann Intern Med 1987, 106:196-204.

5. Sachs APE, Koeter GH, Groenier KH, Waaij D van der, Schiphuis J, Jong BMd: Changes in symptoms, peak expiratory flow, and sputum flora during treatment with antibiotics of exacerbations in patients with chronic obstructive pulmonary disease in general practice. Thorax 1995, 50:758-763.

Anmerkungen

The source mentioned somewhere in the middle of the copied text, but it is not clear to the reader that the entire passage spanning three paragraphs is taken from the source verbatim.

Sichter
(Hindemith)

[6.] Analyse:Amm/Fragment 046 01 - Diskussion
Bearbeitet: 25. December 2014, 20:19 Hindemith
Erstellt: 25. December 2014, 20:18 (Hindemith)
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Allegra et al (Allegra L et al, 2001) did conduct a placebo-controlled trial where they used a 5-day time-point, showing a substantial benefit of antibiotics.

The adequacy of the traditional goals of treatment of an exacerbation, recovery to baseline clinical status and the prevention of complications, are being questioned because of several new observations. These include realization of the importance of exacerbations in the course of COPD, the role of infection in exacerbations, the high rates of relapse with an adequate initial clinical response, and the role played by chronic infection in the pathogenesis of COPD. Today, confining our goal in the treatment of COPD exacerbations to short-term resolution of symptoms would be analogous to treating acute myocardial infarction with the only aim being resolution of chest pain.

Allegra et al [11] did conduct a placebo-controlled trial where they used a 5-day time-point, showing a substantial benefit of antibiotics, which was excluded from the analysis by Puhan et al.

The adequacy of the traditional goals of treatment of an exacerbation, recovery to baseline clinical status and the prevention of complications, are being questioned because of several new observations. These include realization of the importance of exacerbations in the course of COPD, the role of infection in exacerbations, the high rates of relapse with an adequate initial clinical response, and the role played by chronic infection in the pathogenesis of COPD. Today, confining our goal in the treatment of COPD exacerbations to short-term resolution of symptoms would be analogous to treating acute myocardial infarction with the only aim being resolution of chest pain.


11. Allegra L, Blasi F, de Bernardi B, Cosentini R, Tarsia P: Antibiotic treatment and baseline severity of disease in acute exacerbations of chronic bronchitis: a re-evaluation of previously published data of a placebo-controlled randomized study. Pulm Pharmacol Ther 2001, 14:149-155.

Anmerkungen

The source is not mentioned here.

Sichter
(Hindemith)

[7.] Analyse:Amm/Fragment 048 10 - Diskussion
Bearbeitet: 25. December 2014, 23:02 Hindemith
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Many head-to-head trials of antibiotics for mild to moderate COPD exacerbations have been conducted although evidence from randomised placebo-controlled trials never showed that antibiotics were effective at all. So, in this case, the evaluation of antibiotics did not follow the general principle that placebo-controlled trials must have shown that the treatment is better than the placebo, before head-to-head trials are to be conducted (ICH Steering Committee, 2000). Probably, this is due to the pharmaceutical industry pressure. In general, big pharma tends to favour placebo-controlled trials in order to show large effects and to avoid direct comparison with competitors. Once a treatment, such as antibiotics for COPD exacerbations, is established in clinical practice an attractive market is available. If a company wants to enter this market it needs to provide a trial showing clinical non-inferiority of a new antibiotic and some advantages in terms of adverse effects or costs. This will make it relatively easy to get approval from regulatory agencies, as long as the drug is safe. The Helsinki Declaration emphasises the great importance of conducting experimental studies for medical progress. However, it also states that one should be very careful before embarking on randomised trials with placebo controls because research participants have a right to the best available treatment (World Medical Association, 2000). Worries about the 'unethical use of placebo' continue (Fergusson D et al, 2005; Michels KB et al, 2003). However, the present thesis tackles the reverse scenario. Might there be cases where experimental treatment did not show superiority over [placebo but where the placebo controls were abandoned nevertheless, thus exposing patients to adverse effects and society to healthcare expenditures not offset by any beneficial effects.] The Helsinki Declaration emphasises the great importance of conducting experimental studies for medical progress. However, it also states that one should be very careful before embarking on randomised trials with placebo controls because research participants have a right to the best available treatment [1]. Worries about the 'unethical use of placebo' continue [2,3]. However, what about the reverse scenario? Might there be cases where experimental treatment did not show superiority over placebo but where the placebo controls were abandoned nevertheless, thus exposing patients to adverse effects and society to healthcare expenditures not offset by any beneficial effects?

[page 4]

Our historical analysis showed that many head-to-head trials of antibiotics for mild to moderate COPD exacerbations have been conducted although evidence from randomised placebo-controlled trials never showed that antibiotics were effective at all. So, in this case, the evaluation of antibiotics did not follow the general principle that placebo-controlled trials must have shown that the treatment is better than the placebo or a sham procedure, before head-to-head trials are to be conducted [9].

[page 5]

In general, the pharmaceutical industry tends to favour placebo-controlled trials in order to show large effects and to avoid direct comparison with competitors. In situations like this, however, where comparisons with placebo do not favour a drug, the pharmaceutical industry might be more interested in head-to-head trials. Once a treatment, such as antibiotics for COPD exacerbations, is established in clinical practice an attractive market is available. If a company wants to enter this market it needs to provide a trial showing clinical non-inferiority of a new antibiotic and some advantages in terms of adverse effects or costs. Hence, chance aside, even a new antibiotic lacking specific activity will not be inferior to any established antibiotic in COPD outpatients. This will make it relatively easy to get approval from regulatory agencies, as long as the drug is safe.


1. World Medical Association: Declaration of Helsinki: ethical principles for medical research involving human subjects. JAMA 2000, 284:3043-3045.

2. Fergusson D, Glass KC, Hutton B, Shapiro S: Randomized controlled trials of aprotinin in cardiac surgery: could clinical equipoise have stopped the bleeding? Clin Trials 2005, 2:218-229.

3. Michels KB, Rothman KJ: Update on unethical use of placebos in randomised trials. Bioethics 2003, 17:188-204.

9. ICH Steering Committee: Harmonised tripartite guideline: choice of control group and related issues in clinical trials (E10). International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use: Geneva 2000 [1].

Anmerkungen

The source is not mentioned here.

Sichter
(Hindemith)

[8.] Analyse:Amm/Fragment 112 01 - Diskussion
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Quelle: Decramer et al 2011
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[In the Lung Health Study II, which compared triamcinolone acetonide 600 μg or placebo bid in] 1,116 patients with mild-to-moderate COPD, active treatment had, again, a non-significant effect on the rate of decline in FEV1. Nevertheless, there was a significant reduction in respiratory symptoms with triamcinolone acetonide and in visits to a physician due to respiratory illness (Group LHSR, 2000). A post-hoc analysis of the ISOLDE trial of 751 patients treated with fluticasone proprionate 500 μg or placebo bid showed that, in 391 patients with an FEV1 ≥ 50% predicted, fluticasone propionate had no impact on the number of exacerbations per patient per year, at 1.5 versus 1.8. However, the proportion of patients with more than one exacerbations/year treated with oral corticosteroids was reduced significantly with active treatment, at 8% versus 16% for placebo (Jones PW et al, 2003). In the ISOLDE trial as a whole, the annual rate of decline in FEV1 was similar in both groups (Burge PS et al, 2000).

The MISTRAL study, published in 2006, randomised 1,010 COPD patients to tiotropium 18 μg or placebo once daily for 1 year. Among 426 patients with an FEV1 > 50% predicted, tiotropium was associated with a significant reduction in the number of exacerbations per patient per year, at 1.2 versus 2, alongside which there was a nonsignificant reduction in the number of patients experiencing one or more exacerbations in patients with mild COPD (Dusser D et al, 2006). For the BRONCUS study, 523 COPD patients were randomly assigned to N-acetylcysteine 600 mg daily or placebo and followed-up for 3 years. N-acetylcysteine was found to have, compared with placebo, no significant effects on either the decline in FEV1 or the decline in vital capacity in 389 participants with GOLD stage II COPD (Decramer M et al, 2005).

In the Lung Health Study II, which compared triamcinolone acetonide 600 μg or placebo bid in 1116 patients with mild-to-moderate COPD, active treatment had, again, a non-significant effect on the rate of decline in FEV1. Nevertheless, there was a significant reduction in respiratory symptoms with triamcinolone acetonide, at 21.1 per 100 person-years versus 28.2 per 100 person-years for placebo (p = 0.005), and in visits to a physician due to respiratory illness, at 1.2 per 100 person-years versus 2.1 per 100 person-years for placebo (p Z 0.03).63

A post-hoc analysis of the ISOLDE trial of 751 patients treated with fluticasone proprionate 500 μg or placebo bid showed that, in 391 patients with an FEV1 ≥ 50% predicted, fluticasone propionate had no impact on the number of exacerbations per patient per year, at 1.47 versus 1.75 (p = 0.45). However, the proportion of patients with ≥1 exacerbations/year treated with oral corticosteroids was reduced significantly with active treatment, at 8% versus 16% for placebo (p = 0.02).64 In the ISOLDE trial as a whole, the annual rate of decline in FEV1 was 50 ml/year in the fluticasone propionate group and 59 ml/year in the placebo group (p Z 0.16). Again, the study was powered to detect only a difference of only 20 ml/year.65

For the BRONCUS study, 523 COPD patients were randomly assigned to N-acetylcysteine (NAC) 600 mg daily or placebo and followed-up for 3 years. NAC was found to have, compared with placebo, no significant effects on either the decline in FEV1 or the decline in vital capacity (VC) in 389 participants with GOLD Stage II COPD. Mean decline in FEV1 was 6 ml/year higher with NAC (p Z 0.589) and 12 ml/year higher in VC (p Z 0.538).66

The MISTRAL study, published in 2006, randomised 1010 COPD patients to tiotropium 18 μg or placebo once daily for 1 year. Among 426 patients with an FEV1 >50% predicted, tiotropium was associated with a significant reduction in the number of exacerbations per patient per year, at 1.21 versus 1.97 (p < 0.001), alongside which there was a nonsignificant reduction in the number of patients experiencing ≥1 exacerbation in patients with mild COPD.67


63. Lung Health Study Research Group. Effect of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med 2000;343:1902e9.

64. Jones PW, Willits LR, Burge PS, Calverley PM. Disease severity and the effect of fluticasone propionate on chronic obstructive pulmonary disease exacerbations. Eur Respir J 2003;21:68e73.

65. Burge PS, Calverley PM, Jones PW, Spencer S, Anderson JA, Maslen TK. Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ 2000;320:1297e303.

66. Decramer M, Rutten-van Molken M, Dekhuijzen PN, Troosters T, van Herwaarden C, Pellegrino R, et al. Effects of N-acetylcysteine on outcomes in chronic obstructive pulmonary disease (Bronchitis Randomized on NAC Cost-Utility Study, BRONCUS): a randomised placebo-controlled trial. Lancet 2005;365:1552e60.

67. Dusser D, Bravo ML, Iacono P. The effect of tiotropium on exacerbations and airflow in patients with COPD. Eur Respir J 2006;27:547e55.

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