Comparison with other studies was difficult due to the short duration of the study, and we decided to not combine the Lindberg study with the early part of the Howard study. Intravenous versus oral corticosteroids In the Chinese study (Zhang 1998) the exact duration of the study is not given. hormone treatment. Data collection and analysis Three authors Abametapir extracted the data from the selected articles and one other checked them. Main results Seven trials involving a total of 199 participants were included. A trial of adrenocorticotrophic hormone (43 participants) did not show any advantage compared with placebo for the treatment of ocular myasthenia gravis. Two double\blind trials compared prednisone with placebo for generalised myasthenia gravis. In the first (13 participants), the improvement was slightly greater in the prednisone group at six months. In the second (20 participants) which was a short\term trial, the improvement was significantly greater at two weeks. Two trials compared glucocorticosteroids with azathioprine (41 and 10 participants respectively). In one of these the rate of treatment failure was greater in the prednisone group. In a trial of glucocorticosteroids versus intravenous immunoglobulin (33 participants) no differences in treatment responses were encountered during a treatment period of 14 days. An open trial (39 participants) evaluating different corticosteroid doses revealed a shorter time to improvement in the high\dose group. None fulfilled the presently accepted standards of a high\quality trial. All these studies have risks of bias and have a weak statistical power. Authors’ conclusions Limited evidence from randomised controlled trials suggests that corticosteroid treatment offers short\term benefit in myasthenia gravis compared with placebo. This supports the conclusions of observational studies and expert opinion. Limited evidence from randomised controlled trials does not show any difference in efficacy between corticosteroids and either azathioprine or intravenous immunoglobulin. Plain language summary Corticosteroids for Rabbit Polyclonal to MAGI2 myasthenia gravis Myasthenia gravis is caused by the body’s antibodies impairing transmission of nerve impulses to muscles, resulting in fluctuating weakness and fatigue. Acute attacks can be life threatening because of swallowing or breathing difficulties. Seven randomised controlled trials which included Abametapir in all 199 participants are published. None fulfilled the presently accepted standards of a high\quality trial. All these studies have risks of bias and have a weak statistical power. Limited evidence from randomised controlled trials suggests that corticosteroids offer short\term benefit compared with placebo (dummy treatment). This supports the conclusions of observational studies and expert opinion. Limited evidence from randomised controlled trials does not show any difference in efficacy between corticosteroids and either azathioprine or intravenous immunoglobulin. All trials had design flaws which limit the strength of the conclusions. Further randomised controlled trials are needed. Background Acquired myasthenia gravis (MG) is an autoimmune disease in which Abametapir antibodies reduce the number of available acetylcholine receptors and thereby impair neuromuscular transmission. The annual incidence of MG is between 0.25 Abametapir and 2.00 per 100,000 population (Vincent 2003). The cardinal features of MG are weakness and fatigability of skeletal and extraocular muscles. In more than half of Abametapir cases the initial symptoms are ptosis and diplopia, often followed by involvement of bulbopharyngeal and skeletal muscles. The natural history of MG is characterised by exacerbations and more or less complete remissions. Respiratory and swallowing difficulties during myasthenic crisis are life\threatening and may require intubation and mechanical ventilation. In 382 patients whose disease began between 1940 and 1960, Grob (Grob 1981) reported death in 33%, remission in 11% and improvement in 20%. Recently, the death rate was reported to be less than 10% (Thomas 1997). Oosterhuis reported remission in 38% and improvement in 25% of 537 patients followed between 1960 and 1994 with changing treatment modalities (Oosterhuis 1997). Treatments tried include oral and intravenous glucocorticosteroids, azathioprine, ciclosporin, cyclophosphamide, methotrexate, intravenous immunoglobulin, plasma exchange (Hohlfeld 2003) and most recently mycophenolate mofetil (Chaudhry 2001; Ciafaloni 2001; Schneider 2001). The rationale for using corticosteroids is the autoimmune nature of.