ABSTRACT
OBJECTIVES: To ascertain whether the use of oral glucosamine influences symptoms or functional outcomes in patients with chronic low back pain (LBP) thought to be related to spinal osteoarthritis (OA). DESIGN: Systematic review of randomised control trials. Searches were performed up to March 2011 on Medline, AMED, CINHAL, Cochrane and EMBASE with subsequent reference screening of retrieved studies. In addition, the grey literature was searched via opensigle. Included studies were required to incorporate at least one of the Cochrane Back Pain Review Group's outcome measures as part of their design. Trials with participants over 18 years with a minimum of 12 weeks of back pain, in combination with radiographic changes of OA in the spine, were included. Studies were rated for risk-of-bias and graded for quality. RESULTS: 148 studies were identified after screening and meeting eligibility requirements, and three randomised controlled trials (n=309) were included in the quantitative synthesis. The review found that there was low quality but generally no evidence of an effect from glucosamine on function, with no change in the Roland-Morris Disability Questionnaire score in all studies. Conflicting evidence was demonstrated with pain scores with two studies showing no difference and one study with a high risk-of-bias showing both a statistically and clinically significant improvement from taking glucosamine. CONCLUSIONS: On the basis of the current research, any clinical benefit of oral glucosamine for patients with chronic LBP and radiographic changes of spinal OA can neither be demonstrated nor excluded based on insufficient data and the low quality of existing studies.
ABSTRACT
1. The aim of this study was to investigate the mechanisms by which histamine causes nasal blockage. Histamine, 40-800 microg, intranasally into each nostril, induced significant blockage of the nasal airway in normal human subjects, as measured by acoustic rhinometry. 2. Oral pretreatment with cetirizine, 5-30 mg, the H1 antagonist, failed to reverse completely the nasal blockage induced by histamine, 400 microg. 3. Dimaprit, 50-200 microg, the H2 agonist, intranasally, caused nasal blockage, which was reversed by oral pretreatment with ranitidine, 75 mg, the H2 antagonist. 4. A combination of cetirizine, 20 mg, and ranitidine, 75 mg, caused greater inhibition of the nasal blockage caused by histamine, 400 microg, than cetirizine alone. In the presence of both antagonists, there was residual histamine-induced nasal blockage. 5. R-alpha-methylhistamine (R-alpha-MeH), 100-600 microg, the H3 agonist, intranasally, caused nasal blockage, which was not inhibited by either cetirizine or ranitidine. 6. Thioperamide, 700 microg, the H3 antagonist, intranasally, reversed the R-alpha-MeH-induced nasal blockage. Thioperamide alone had no significant action on the nasal blockage induced by histamine, 400 and 1000 microg, but, in the presence of cetirizine, 20 mg, thioperamide further reduced the histamine-induced nasal blockage. 7. Corynanthine, 2 mg, the alpha1-adrenoceptor antagonist, administered intranasally, caused nasal blockage. 8. Corynanthine produced a greater increase in nasal blockage when in combination with bradykinin compared to its combination with R-alpha-MeH. 9. There appears to be a contribution of H1, H2 and H3 receptors to histamine-induced nasal blockage in normal human subjects. The sympathetic nervous system actively maintains nasal patency and we suggest that activation of nasal H3 receptors may downregulate sympathetic activity.
