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10.1097/MD.0000000000000954 http://scihub22266oqcxt.onion/10.1097/MD.0000000000000954 C4616492!4616492 !26061327     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26061327 &cmd=llinks): Failed to open stream: HTTP request failed! 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A Case of Stiff Person Syndrome: Immunomodulatory Effect of Benzodiazepines: Successful Rituximab and Tizanidine Therapy |pdf=|usr=}}{{26061327 }} gab.com Text A Case of Stiff Person Syndrome: Immunomodulatory Effect of Benzodiazepines: Successful Rituximab and Tizanidine Therapy JO: Medicine (Baltimore) http://www.kidney.de/pget.php?&tw=1&pmid=26061327 #FOAvip Stiff person syndrome (SPS) is a rare autoimmune disease. Most patients have high-titer antibodies against glutamate decarboxylase (GADAb), which is without practical value in disease monitoring. Benzodiazepines are the first line drugs, but long-term use is not well characterized. This report demonstrates ineffective benzodiazepine therapy of SPS that prompts tachyphylaxis, loss of responsiveness, and finally benzodiazepine withdrawal syndrome. Convulsion and anxiety correlate with high level of creatine phosphokinase (CK). Although tonus and spasm attacks were successfully controlled by tizanidine, glutamate release inhibitor, the immune response, and autoimmune diabetes development require the plasmapheresis, mycophenolat mofetil, and rituximab therapy that results in a significant decrease of GADAb, impaired glucose tolerance (IGT), lactate dehydrogenase (LDH), and CK normalization. Unfortunately, reintroduction of benzodiazepine was a source of rapid and high increase of CK, LDH, GADAb titer (up to 1:15,000), IGT, and SPS relapse. Contrary to previous publications, we observed IGT that correlated with high anti-GAD level, but without high immunogenetic susceptibility to haplotype human leukocyte antigens-DR3, DQw2. This preliminary observation and the last finding of immunomodulatory properties of peripheral benzodiazepine receptor suggest that increased antigenic stimulation during benzodiazepine therapy and glutamatergic hyperactivity could account for convulsions observed in SPS. Benzodiazepine withdrawal prompted alternative muscle relaxant therapy (tizanidine). Muscular and brain abnormalities observed in SPS indicate that noncardiac CK level may be a useful tool in SPS therapy monitoring. Twit Text FOAVip A Case of Stiff Person Syndrome: Immunomodulatory Effect of Benzodiazepines: Successful Rituximab and Tizanidine Therapy ????Medicine (Baltimore) http://www.kidney.de/pget.php?&tw=1&pmid=26061327 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26061327 #FOAvip English Wikipedia <ref>{{Cite pmid|26061327 }}</ref> A Case of Stiff Person Syndrome: Immunomodulatory Effect of Benzodiazepines: Successful Rituximab and Tizanidine Therapy #MMPMID26061327 Zdziarski P Medicine (Baltimore) 2015[Jun]; 94 (23 ): e954 PMID26061327 show ga Stiff person syndrome (SPS) is a rare autoimmune disease. Most patients have high-titer antibodies against glutamate decarboxylase (GADAb), which is without practical value in disease monitoring. Benzodiazepines are the first line drugs, but long-term use is not well characterized. This report demonstrates ineffective benzodiazepine therapy of SPS that prompts tachyphylaxis, loss of responsiveness, and finally benzodiazepine withdrawal syndrome. Convulsion and anxiety correlate with high level of creatine phosphokinase (CK). Although tonus and spasm attacks were successfully controlled by tizanidine, glutamate release inhibitor, the immune response, and autoimmune diabetes development require the plasmapheresis, mycophenolat mofetil, and rituximab therapy that results in a significant decrease of GADAb, impaired glucose tolerance (IGT), lactate dehydrogenase (LDH), and CK normalization. Unfortunately, reintroduction of benzodiazepine was a source of rapid and high increase of CK, LDH, GADAb titer (up to 1:15,000), IGT, and SPS relapse. Contrary to previous publications, we observed IGT that correlated with high anti-GAD level, but without high immunogenetic susceptibility to haplotype human leukocyte antigens-DR3, DQw2. This preliminary observation and the last finding of immunomodulatory properties of peripheral benzodiazepine receptor suggest that increased antigenic stimulation during benzodiazepine therapy and glutamatergic hyperactivity could account for convulsions observed in SPS. Benzodiazepine withdrawal prompted alternative muscle relaxant therapy (tizanidine). Muscular and brain abnormalities observed in SPS indicate that noncardiac CK level may be a useful tool in SPS therapy monitoring. |Adult [MESH] |Antibodies, Monoclonal, Murine-Derived/*therapeutic use [MESH] |Benzodiazepines/therapeutic use [MESH] |Clonidine/*analogs & derivatives/therapeutic use [MESH] |Diazepam/therapeutic use [MESH] |Drug Therapy, Combination [MESH] |Female [MESH] |Glutamate Decarboxylase [MESH] |Humans [MESH] |Immunologic Factors/*therapeutic use [MESH] |Muscle Relaxants, Central/*therapeutic use [MESH] |Remission Induction [MESH] |Rituximab [MESH]A Case of Stiff Person Syndrome: Immunomodulatory Effect of Benzodiaze(epmc).pdf DeepDyve Pubget Overpricing