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author:("scharlach, M")
1.  How should COPD patients exercise during respiratory rehabilitation? Comparison of exercise modalities and intensities to treat skeletal muscle dysfunction 
Thorax  2005;60(5):367-375.
Background: Physical exercise is an important component of respiratory rehabilitation because it reverses skeletal muscle dysfunction, a clinically important manifestation of COPD associated with reduced health-related quality of life (HRQL) and survival. However, there is controversy regarding the components of the optimal exercise protocol. A study was undertaken to systematically evaluate and summarise randomised controlled trials (RCTs) comparing different exercise protocols for COPD patients.
Methods: Six electronic databases, congress proceedings and bibliographies of included studies were searched without imposing language restrictions. Two reviewers independently screened all records and extracted data on study samples, interventions and methodological characteristics of included studies.
Results: The methodological quality of the 15 included RCTs was low to moderate. Strength exercise led to larger improvements of HRQL than endurance exercise (weighted mean difference for Chronic Respiratory Questionnaire 0.27, 95% CI 0.02 to 0.52). Interval exercise seems to be of similar effectiveness as continuous exercise, but there are few data on clinically relevant outcomes. One small RCT which included patients with mild COPD compared the effect of high and low intensity exercise (at 80% and 40% of the maximum exercise capacity, respectively) and found larger physiological training effects from high intensity exercise.
Conclusions: Strength exercise should be routinely incorporated in respiratory rehabilitation. There is insufficient evidence to recommend high intensity exercise for COPD patients and investigators should conduct larger high quality trials to evaluate exercise intensities in patients with moderate to severe COPD.
PMCID: PMC1758898  PMID: 15860711
2.  What is the impact of the ACE gene insertion/deletion (I/D) polymorphism on the clinical effectiveness and adverse events of ACE inhibitors? – Protocol of a systematic review 
BMC Medical Genetics  2004;5:23.
The Angiotensin Converting Enzyme (ACE) insertion/deletion (I/D) polymorphism has received much attention in pharmacogenetic research because observed variations in response to ACE inhibitors might be associated with this polymorphism. Pharmacogenetic testing raises the hope to individualise ACE inhibitor therapy in order to optimise its effectiveness and to reduce adverse effects for genetically different subgroups. However, the extent of its effect modification in patients treated with ACE inhibitors remains inconclusive. Therefore our objective is to quantify the effect modification of the insertion/deletion polymorphism of the angiotensin converting enzyme gene on any surrogate and clinically relevant parameters in patients with cardiovascular diseases, diabetes, renal transplantation and/or renal failure.
Systematic Review. We will perform literature searches in six electronic databases to identify randomised controlled trials comparing the effectiveness and occurrence of adverse events of ACE inhibitor therapy against placebo or any active treatment stratified by the I/D gene polymorphism. In addition, authors of trials, experts in pharmacogenetics and pharmaceutical companies will be contacted for further published or unpublished data. Hand searching will be accomplished by reviewing the reference lists of all included studies. The methodological quality of included papers will be assessed. Data analyses will be performed in clinically and methodologically cogent subgroups. The results of the quantitative assessment will be pooled statistically where appropriate to produce an estimate of the differences in the effect of ACE inhibitors observed between the three ACE genotypes.
This protocol describes a strategy to quantify the effect modification of the ACE polymorphism on ACE inhibitors in relevant clinical domains using meta-epidemiological research methods. The results may provide evidence for the usefulness of pharmacogenetic testing for individualised ACE inhibitor therapy.
PMCID: PMC518966  PMID: 15361261

Results 1-2 (2)