Background It is well demonstrated that immunosuppressants can reduce, but not eliminate the risk of generalized development in ocular myasthenia gravis (OMG). In this study, we aimed to explore the predictive factors of generalized conversion of OMG patients who received immunosuppressive treatments. Methods OMG patients under immunosuppressive treatments in Tangdu Hospital from June 2008 to June 2012 were retrospectively reviewed. Baseline clinical characteristics were documented. Patients were followed up regularly by face-to-face interview and the main outcome measure was generalized conversion. The logistic regression analysis was performed to determine the predictive factors of generalization of OMG. Results Two hundred twenty-three eligible OMG patients completed the final follow-up visit and 38 (17.0%) progressed to generalized MG (GMG) at a median time to generalization of 0.9 year. Patients with adult onset and positive repetitive nerve stimulation (RNS) of facial or axillary nerve had higher conversion rate than those with juvenile onset and negative RNS (p = 0.001; p = 0.019; p = 0.015, respectively). Adult-onset patients converted earlier than juvenile-onset OMG patients (p = 0.014). Upon multivariate logistic regression analysis, age of onset (Odds ratio [OR] 1.023, 95% confidence interval [CI] 1.006–1.041, p = 0.007) and positive facial nerve RNS (OR 2.826, 95%CI 1.045–5.460, p = 0.038) were found to be positively associated with generalized development. Moreover, an obviously negative association was found for disease duration (OR 0.603, 95%CI 0.365–0.850, p = 0.019). Conclusions Age of onset, disease duration and facial nerve RNS test can predict generalized conversion of OMG under immunosuppressive therapy. Adult-onset, shorter disease duration and facial nerve RNS-positive OMG patients have a higher risk of generalized development.

Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been considered to be closely relevant to an inflammatory demyelinating disease of the central nervous system (CNS). Glial fibrillary acidic protein (GFAP) immunoglobulin G (IgG) has been identified as a biomarker for a novel autoimmune astrocytopathy. However, coexistence of MOG-IgG and GFAP-IgG is extremely unusual and only one patient has been described with simultaneous presence of MOG-IgG in serum and GFAP-IgG in cerebrospinal fluid (CSF). Herein, we reported the first case of overlapping syndrome of MOG-IgG-associated disease (MOG-AD) and autoimmune GFAP astrocytopathy in whom MOG-IgG and GFAP-IgG were detected both in serum and CSF. A 20-year-old male patient was referred to our department with the presentation of decreased vision, diplopia and weakness of right limb with unknown reasons. Magnetic resonance imaging (MRI) revealed multiple intracranial lesions presenting hypointensity on T1-weighted images, hyperintensity on T2-weighted and FLAIR images and patchy contrast enhancement. MOG-IgG and GFAP-IgG were detected both in serum and CSF, and the titers of both antibodies fluctuated with the severity of disease. Treatment strategy employing intravenous methylprednisolone pulse therapy followed by oral prednisone with slow tapering resulted in an improvement of his symptoms and a sustained remission. Coexistence of MOG-IgG and GFAP-IgG with distinct underlying pathogeneses necessitates the recommendations to screen all recognized pathogenic antibodies against CNS antigens when an autoimmune disease is suspected, since it shows great significance for definite diagnosis of disease and treatment strategy options.

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BackgroundGinsenoside Rd (GSRd), a main component of the root of Panax ginseng, exhibits anti-inflammation functions and decreases infarct size in many injuries and ischemia diseases such as focal cerebral ischemia. M1 Macrophages are regarded as one of the key inflammatory cells having functions for disease progression.MethodsTo investigate the effect of GSRd on renal ischemia/reperfusion injury (IRI) and macrophage functional status, and their regulatory role on mouse polarized macrophages in vitro, GSRd (10–100 mg/kg) and vehicle were applied to mice 30 min before renal IRI modeling. Renal functions were reflected by blood serum creatinine and blood urea nitrogen level and histopathological examination. M1 polarized macrophages infiltration was identified by flow cytometry analysis and immunofluorescence staining with CD11b+, iNOS+/interleukin-12/tumor necrosis factor-α labeling. For the in vitro study, GSRd (10–100 μg/mL) and vehicle were added in the culture medium of M1 macrophages to assess their regulatory function on polarization phenotype.ResultsIn vivo data showed a protective role of GSRd at 50 mg/kg on Day 3. Serum level of serum creatinine and blood urea nitrogen significantly dropped compared with other groups. Reduced renal tissue damage and M1 macrophage infiltration showed on hematoxylin–eosin staining and flow cytometry and immunofluorescence staining confirmed this improvement. With GSRd administration, in vitro cultured M1 macrophages secreted less inflammatory cytokines such as interleukin-12 and tumor necrosis factor-α. Furthermore, macrophage polarization-related pancake-like morphology gradually changed along with increasing concentration of GSRd in the medium.ConclusionThese findings demonstrate that GSRd possess a protective function against renal ischemia/reperfusion injury via downregulating M1 macrophage polarization.