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Knowledge about the postintervention psychosocial status of myasthenia gravis (MG) is limited and based on questionnaire studies. In this study, the effects of improvement in muscle strength with plasmapheresis treatment on both quality of life (QoL) and psychological status of MG patients were studied. Between January 2008 and December 2009, 29 MG patients were enrolled to receive one course of plasmapheresis treatment. Differences in baseline and posttherapy clinical, laboratory, and psychosocial measures were determined. The mean MG score decreased from 7.8 points at baseline to 4.2 after plasmapheresis, accompanied by the mean antibody clearance of 56%. Psychosocial tests showed significant pre- and posttherapy differences in illness identity (mean scores 23.62 and 20.79 points, respectively) and disability (mean scores 11.28 and 7.63 points, respectively) (p < 0.01). No significant differences were found for the other indices. Although both anxiety and depression scores did not differ significantly, there was a clear change in patients, as evidenced by their decreases in severity after treatment. The mean mental components scores of QoL were still less than 40 after treatment, indicating that myasthenic patients need assistance in adapting to their disease. Thus, although plasmapheresis treatment achieved immediate improvement of myasthenic symptoms, reduced disability, and better illness identity, both emotional status and QoL did not differ significantly after intervention. Systematical evaluation for patients' illness perceptions and emotional problems are warranted and related strategies should be taken for long-term stabilization of psychosocial function.

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Thiazolidinediones (TZD) can cause adipose tissue accumulation and myocardial hypertrophy. This study aimed to determine if combined Metformin (Glucophage) and Rosiglitazone (Avandia) could reduce the risk of heart failure caused by Rosiglitazone in BALB/c mice. BALB/c mice were treated with oral Rosiglitazone/Metformin twice daily for four weeks. Metformin or Rosiglitazone alone and non-treated mice acted as double control. Myocardial hypertrophy and associated side effects of the combined therapy were determined through isolated heart and body weights. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were applied to evaluate expression of sulfonylurea receptor 2A (SUR2A) and Kir 6.2. The activities of peroxisome proliferator activated receptor a (PPARa) in the myocardium were also observed. Rosiglitazone/Metformin decreased body weight gain and food intake, and inhibited an increasing adipose ratio but did not reduce myocardial hypertrophy. Rosiglitazone increased Kir6.2/SUR2A, Kir6.2/SUR2B, and PPARa gene expression. The Rosiglitazone/Metformin combination further increased these gene expressions, especially PPARa. Metformin inhibits obesity but has no effect in reducing myocardial hypertrophy caused by Rosiglitazone. Whether Metformin can reduce side effects of TZDs in humans warrants further study.