Treatment of inclusion body myositis: is low-dose intravenous immunoglobulin the solution?

Inclusion body myositis (IBM), the most common inflammatory myopathy in the elderly, is often resistant to various forms of therapy. Placebo-controlled treatment trials with high dose intravenous immunoglobulins (IVIG) have shown disease amelioration in some but not all patients. Here, we present the informative case of a 70-year-old woman with diagnosed inclusion body myositis that showed progressive muscle weakness without treatment and following immuno-suppressive treatment with corticosteroids and azathioprine. A trial with low-dose intravenous immunoglobulins was started at that time. The patient responded rapidly to low dose IVIG treatment with amelioration of muscle strength and normalization of CK serum activities. Our results demonstrate that IBM patients may respond to low-dose IVIG treatment which has important clinical and economic consequence

Antibodies to the Junctional Adhesion Molecule Cause Disruption of Endothelial Cells and Do Not Prevent Leukocyte Influx into the Meninges after Viral or Bacterial Infection

A hallmark of infectious meningitis is the invasion of leukocytes into the subarachnoid space. In experimental meningitis triggered by tumor necrosis factor—α and interleukin-1β, the interaction of leukocytes with endothelial cells and the subsequent migration of the cells through the vessel wall can be inhibited by an antibody to the junctional adhesion molecule (JAM). In contrast to the cytokine-induced meningitis model, anti-JAM antibodies failed to prevent leukocyte influx into the central nervous system after infection of mice with Listeria monocytogenes or lymphocytic choriomeningitis virus. Furthermore, in bacterial meningitis, anti-JAM IgG antibodies, but not Fab fragments, caused disruption of the endothelium. Likewise complement-dependent antibody-mediated cytotoxicity was observed in cultured brain endothelial cells treated with anti-JAM IgG but not with its Fab fragmen

High resolution proton magnetic resonance spectroscopy of human cervical mucus

High resolution 1H NMR spectroscopy is a powerful method for qualitative and quantitative analysis of the highly viscous human cervical mucus (CM). Up to 23 compounds could be identified in this study and can be observed in the 1H NMR spectra of native mucus without the need of any complicated preparative chemistry. Storage conditions could be excluded as a possible reason for variations observed between different samples. pH values decreased after freezing and storing at 253 K. For NMR studies, lyophilization proved to be most useful, allowing the determination of the water content, replacement of H2O by D2O, and most importantly, absolute quantification of low molecular mass compounds. In a small collective of women the concentrations of some of the small constituents of the CM are strongly correlated; an example is the mutual positive correlation of taurine, citrate and creatinine. In conclusion, high resolution 1H NMR spectroscopy is a valid method to investigate mucus composition and to determine absolute concentrations of low molecular mass compounds in CM

Antibodies to the Junctional Adhesion Molecule Cause Disruption of Endothelial Cells and Do Not Prevent Leukocyte Influx into the Meninges after Viral or Bacterial Infection

A hallmark of infectious meningitis is the invasion of leukocytes into the subarachnoid space. In experimental meningitis triggered by tumor necrosis factor—α and interleukin-1β, the interaction of leukocytes with endothelial cells and the subsequent migration of the cells through the vessel wall can be inhibited by an antibody to the junctional adhesion molecule (JAM). In contrast to the cytokine-induced meningitis model, anti-JAM antibodies failed to prevent leukocyte influx into the central nervous system after infection of mice with Listeria monocytogenes or lymphocytic choriomeningitis virus. Furthermore, in bacterial meningitis, anti-JAM IgG antibodies, but not Fab fragments, caused disruption of the endothelium. Likewise complement-dependent antibody-mediated cytotoxicity was observed in cultured brain endothelial cells treated with anti-JAM IgG but not with its Fab fragmen