While the results of CHM on HRQoL for stable COPD sufferers were promising, they need to be interpreted with caution due to methodological problems, which should be addressed in future trials.
In this retrospective study, clinical data including clinical manifestations, routine blood tests, chest radiographic imaging from 77 severe cases of SARS treated with integrated Chinese and Western medicine were collected and statistically analyzed. Twenty-nine (37.6%) patients were admitted to the intensive care unit, non-invasive ventilation was used in 40 (51.9%) cases, and invasive ventilatory procedure was performed in eight (10.3%) cases. Seventy (90.9%) patients were clinically cured and seven (9.0%) died. The duration of defervescence was 8.3 +/- 5.0 days after admission. In the early stage, normal leucocyte count was seen in 46 (75.4%) of the 61 patients tested, decreased leucocyte count in 13 (21.3%) and elevated leucocyte count in only two (3.2%) cases. A decreased lymphocyte count was also seen in 23 (37.7%) cases of the 61 patients tested on admission, and by day 14, the number of patients with decreased lymphocyte count (1.11 +/- 0.66 x 10(9)) increased to 32 (47.7%) in 67 cases examined. Neutral granulocyte count was normal or decreased in 58 (95.0%) patients on admission, but elevated from the 7th day onward and peaked on day 21 in 32 (65.3%) of the 49 cases tested. All of the blood abnormalities returned to normal in the convalescent stage. Twenty-nine (37.6%) of the 77 severe cases of SARS patients demonstrated an extensive lung involvement. In comparison with the non-severe SARS cases, this group of patients showed significantly more pneumonic air-space opacities and ground glass-like changes on the chest radiographs (p < 0.05, chi2 test). The role Chinese medicine played in the treatment of SARS was discussed.
Objective. To evaluate the efficacy and safety of oral Huangqi
formulae for the treatment of stable COPD. Methods. The major
databases were searched until September 2010 and supplemented with
a manual search. Randomized controlled trials (RCTs) of oral
Huangqi formulae that reported on lung function, St. George's
Respiratory Questionnaire, symptom improvement and/or frequency of
exacerbations were extracted by two reviewers. The Cochrane tool
was used for the assessment of risk of bias in the included
trials. Data were analyzed with RevMan 5.1.2 software. Results. 25
RCTs (1,661 participants) were included. Compared with
conventional therapy (CT) alone, oral Huangqi formulae plus CT
increased FEV1, and a similar result was found comparing Huangqi
formulae with no treatment. Improvements in SGRQ total score,
COPD-related symptoms and reduction of frequency of exacerbations
were found in patients receiving Huangqi formulae plus CT compared
to those receiving CT alone or CT plus placebo. No serious adverse
events were reported. However, there were some methodological
inadequacies in the included studies. Conclusions. The benefits of
Huangqi formulae for stable COPD were promising, but its efficacy
and safety have not been established due to methodological
weakness and possible bias in the reported results. Further
rigorously designed studies are warranted.
Jianpiyifei II granule (JPYF II) is an oriental herbal formula used clinically in China to treat chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the anti-inflammatory and antioxidative activities of JPYF II in a mouse model of COPD induced by lipopolysaccharide (LPS) and cigarette smoke (CS) and in RAW264.7 cells stimulated with cigarette smoke extract (CSE). Mice were given LPS via intratracheal instillation on days 1 and 15 and exposed to CS generated from 4 cigarettes/day for 28 days. The mice were treated with 0.75, 1.5, or 3 g/kg/d JPYF II by intragastric administration in low, middle, and high dose groups, respectively, for two weeks. RAW264.7 cells were stimulated by CSE and treated with JPYF II at doses of 12.5, 25, or 50 μg/mL. In the mouse model of LPS and CS-induced COPD, JPYF II decreased inflammatory cell counts in broncho alveolar lavage fluid (BALF), in addition to mRNA expression of proinflammatory cytokines and metalloproteinases (MMPs) in lung tissues. In addition, JPYF II elevated catalase (CAT) and glutathione peroxidase (GSH-Px) activities and reduced the levels of malondialdehyde (MDA) and IκBα and p65 phosphorylation and inflammatory cell infiltration in the lung tissues. In RAW264.7 cells stimulated with CSE, JPYF II inhibited the mRNA levels of inflammatory mediators and the phosphorylation of IκBα and p65. Our results suggest that JPYF II enhanced anti-inflammatory and antioxidative activities in a mouse model of COPD induced by LPS and CS and in RAW264.7 cells stimulated with CSE via inhibition of the NF-κB pathway.
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