Cochrane Db Syst Rev
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Cochrane Db Syst Rev · Jan 2008
ReviewMetal protein attenuating compounds for the treatment of Alzheimer's disease.
Alzheimer's disease (AD) may be caused by the formation of extracellular senile plaques comprised of beta-amyloid (Ass). In vitro and mouse model studies have demonstrated that metal protein attenuating compounds (MPACs) promote the solubilisation and clearance of Ass. ⋯ There is an absence of evidence as to whether clioquinol (PBT1) has any positive clinical benefit for patients with AD, or whether the drug is safe. We have some concerns about the quality of the study methodology, particularly the randomisation (subjects in the active treatment group had higher mean pre-morbid IQ as measured by the NART and this may have biased the results), the secondary analyses of results stratified by baseline disease severity and whether the study was adequately powered for the analysis of the other data collected on Ass, zinc and copper levels.
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Cochrane Db Syst Rev · Jan 2008
Review Meta AnalysisHawthorn extract for treating chronic heart failure.
Hawthorn extract is advocated as an oral treatment option for chronic heart failure. Also, the German Commission E approved the use of extracts of hawthorn leaf with flower in patients suffering from heart failure graded stage II according to the New York Heart Association. ⋯ These results suggest that there is a significant benefit in symptom control and physiologic outcomes from hawthorn extract as an adjunctive treatment for chronic heart failure.
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This review is one in a series of Cochrane reviews of interventions for shoulder disorders. ⋯ Based upon our review of 14 trials examining heterogeneous interventions and all susceptible to bias, we cannot draw firm conclusions about the effectiveness or safety of surgery for rotator cuff disease. There is "Silver" (www.cochranemsk.org) level evidence from three trials that there are no significant differences in outcome between open or arthroscopic subacromial decompression and active non-operative treatment for impingement. There is also "Silver" level evidence from six trials that there are no significant differences in outcome between arthroscopic and open subacromial decompression although four trials reported earlier recovery with arthroscopic decompression.
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Cochrane Db Syst Rev · Jan 2008
ReviewInhaled nitric oxide for acute chest syndrome in people with sickle cell disease.
Acute chest syndrome has been defined as a new infiltrate visible on chest radiograph associated with one or more symptoms, such as fever, cough, sputum production, tachypnea, dyspnea, or new-onset hypoxia. Symptoms and complications of this syndrome, whether of infectious or non-infectious origin, vary quite widely in people with sickle cell disease. Lung infection tends to predominate in children, whilst infarction appears more common in adults. However, these are often interrelated and may occur concurrently. The differences in clinical course and severity are suggestive of multiple causes for acute chest syndrome. Successful treatment depends principally on high-quality supportive care. The syndrome and its treatment have been extensively studied, but the response to antibiotics, anticoagulants, and other conventional therapies remains disappointing. The potential of inhaled nitric oxide as a treatment option has more recently provoked considerable interest. Nitric oxide appears to play a major role in both the regulation of vascular muscle tone at the cellular level and in platelet aggregation (clumping). Much of the pathophysiology of sickle cell disease is consistent with a mechanism of nitric oxide depletion and although there has been extensive research on the pathophysiology of acute chest syndrome, the possible therapeutic role of inhaled nitric oxide for acute chest syndrome in sickle cell disease is still to be determined. ⋯ There is a need for well-designed, adequately-powered randomised controlled trial to assess the benefits and risks of this form of treatment as an adjunct to established therapies.
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People with cystic fibrosis and pancreatic insufficiency are at risk of fat soluble vitamin deficiency as these vitamins (A, D, E and K) are co-absorbed with fat. Thus, some cystic fibrosis centres routinely administer these vitamins as supplements but the centres vary in their approach of addressing the possible development of deficiencies in these vitamins. Vitamin A deficiency causes predominantly eye and skin problems while supplementation of vitamin A to excessive levels may cause harm to the respiratory and skeletal systems in children. Thus a systematic review on vitamin A supplementation in people with cystic fibrosis would help guide clinical practice. ⋯ As there were no randomised or quasi-randomised controlled trials identified, we cannot draw any conclusions on the benefits (or otherwise) of regular administration of vitamin A in people with cystic fibrosis. Until further data are available, country or region specific guidelines on the use of vitamin A in people with cystic fibrosis should be followed.