Buprenorphine is a low molecular weight, lipophilic, opioid analgesic. Recently, a transdermal matrix patch formulation of buprenorphine has become available in three dosage strengths designed to release buprenorphine at 35, 52.5 and 70 micro g/h over a 72-hour period. At least satisfactory analgesia with minimal requirement for rescue medication (=0.2 mg/day sublingual buprenorphine) was achieved by 34-50% of patients with chronic pain treated with transdermal buprenorphine 35, 52.5 or 70 micro g/h and 31% of placebo recipients, in one double-blind, placebo-controlled, randomised trial. In one trial involving patients unsuccessfully treated with weak opioids or morphine, 36.6% and 47.5% of buprenorphine 35 micro g/h and 52.5 micro g/h recipients, respectively, experienced at least satisfactory analgesia and received =0.2 mg/day of sublingual buprenorphine compared with 16.2% of placebo recipients (both p = 0.032). The requirement for rescue medication was reduced from baseline in >50% of patients treated with transdermal buprenorphine, in two trials. Furthermore, despite the availability of rescue medication to all patients, those receiving transdermal buprenorphine tended to experience greater pain relief, reduced pain intensity and longer pain-free sleep. Transdermal buprenorphine was generally well tolerated. Systemic adverse events were typical of opioid treatment or were attributable to the underlying disease.
Experimental and epidemiological evidence supports the hypothesis that exposure to mycobacteria has the potential to suppress the development of asthma and/or atopy and there are reports in the Chinese medical literature of repeated vaccination with inactivated BCG being effective in the management of asthma. Forty-three patients with stable moderately severe asthma who were skin prick test positive to house dust mite were randomized to receive two intradermal injections of either phosphate-buffered saline (placebo), heat-killed Mycobacterium vaccae (0.5 mg), or delipidated deglycolipidated Mycobacterium vaccae (DDMV) (0.05 mg). Markers of asthma severity were measured for 3 mo and blood eosinophil, IgE levels, and the T cell proliferative and cytokine responses were monitored. There were no significant differences between either treatment group and the placebo group for any of the outcome variables. There was also no difference between the treatment groups and placebo for eosinophil, IgE levels, or the T cell proliferative and cytokine response. The results indicate no effect of low dose intradermal DDMV or M. vaccae on asthma severity in patients with established asthma.
* Omalizumab is a recombinant humanised monoclonal antibody which specifically binds to the C epsilon3 domain of immunoglobulin (Ig) E, the site of high-affinity IgE receptor binding. * Improvements in asthma symptoms and health-related quality-of-life, and a significant reduction in the frequency of asthma exacerbations were seen in allergic asthmatic patients treated with omalizumab. * Omalizumab was also effective in the treatment of children with allergic asthma demonstrating improvements in health-related quality-of-life and significant dosage reductions of inhaled corticosteroids. * Administration of omalizumab to patients with allergic rhinitis resulted in a rapid dose-dependent suppression of serum free IgE levels. * Omalizumab significantly improved health-related quality-of-life and nasal symptoms in patients with seasonal allergic rhinitis. Antihistamine requirements were also significantly reduced following treatment. * Adverse events were infrequent in clinical trials of omalizumab, and not significantly different from placebo. The most frequent drug-related event was mild to moderate urticaria.
Pioglitazone is an antihyperglycaemic agent that, in the presence of insulin resistance, increases hepatic and peripheral insulin sensitivity, thereby inhibiting hepatic gluconeogenesis and increasing peripheral and splanchnic glucose uptake. Pioglitazone is generally well tolerated, weight gain and oedema are the most common emergent adverse events, and there are no known drug interactions between pioglitazone and other drugs. In clinical trials in patients with type 2 diabetes mellitus, pioglitazone as monotherapy, or in combination with metformin, repaglinide, insulin or a sulphonylurea, induced both long- and short-term improvements in glycaemic control and serum lipid profiles. Pioglitazone was also effective in reducing some measures of cardiovascular risk and arteriosclerosis. Pioglitazone thus offers an effective treatment option for the management of patients with type 2 diabetes.
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