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10.1212/NXI.0000000000000096 http://scihub22266oqcxt.onion/10.1212/NXI.0000000000000096 C4386794!4386794!25866831     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Neurol+Neuroimmunol+Neuroinflamm 2015 ; 2 (3): ä Nephropedia Template TP {{tp|p=25866831|t=2015. Clinical course and treatment of anti-HMGCR antibody?associated necrotizing autoimmune myopathy |pdf=|usr=}}{{25866831}} gab.com Text Clinical course and treatment of anti-HMGCR antibody associated necrotizing autoimmune myopathy JO: Neurol Neuroimmunol Neuroinflamm http://www.kidney.de/pget.php?&tw=1&pmid=25866831 #FOAvip Objective:: We examined a cohort of Australian patients with statin exposure who developed a necrotizing autoimmune myopathy (NAM) associated with a novel autoantibody against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) and describe the clinical and therapeutic challenges of managing these patients and an optimal therapeutic strategy. Methods:: Clinical, laboratory, EMG, and histopathologic results and response to immunomodulation are reported in 6 Australian patients with previous statin exposure and antibodies targeting HMGCR. Results:: All patients presented with painless proximal weakness following statin therapy, which persisted after statin cessation. Serum creatine kinase (CK) levels ranged from 2,700 to 16,200 IU/L. EMG was consistent with a myopathic picture. Muscle biopsies revealed a pauci-immune necrotizing myopathy. Detailed graphical representation of the clinical course of these patients showed a close association with rising CK and an increase in clinical weakness signifying relapses, particularly upon weaning or ceasing steroids. All 6 patients were responsive to initial steroid therapy, with 5 relapsing upon attempts to wean steroids. Both CK and clinical strength improved with the reinstitution of immunotherapy, in particular steroids and IV immunoglobulin (IVIg). All patients required treatment with varying multiagent immunosuppressive regimens to achieve clinical remission, including prednisone (n = 6), IVIg (n = 5), plasmapheresis (n = 2), and additional therapy including methotrexate (n = 6), cyclophosphamide (n = 2), rituximab (n = 2), azathioprine (n = 1), and cyclosporine (n = 1). Conclusions:: Recognition of HMGCR antibody?associated NAM is important because these patients are responsive to immunosuppression, and early multiagent therapy and a slow and cautious approach to withdrawing steroids may improve outcomes. Twit Text FOAVip Clinical course and treatment of anti-HMGCR antibody associated necrotizing autoimmune myopathy ????Neurol Neuroimmunol Neuroinflamm http://www.kidney.de/pget.php?&tw=1&pmid=25866831 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25866831 #FOAvip English Wikipedia <ref>{{Cite pmid|25866831}}</ref> Clinical course and treatment of anti-HMGCR antibody?associated necrotizing autoimmune myopathy #MMPMID25866831 Ramanathan S; Langguth D; Hardy TA; Garg N; Bundell C; Rojana-Udomsart A; Dale RC; Robertson T; Mammen AL; Reddel SW Neurol Neuroimmunol Neuroinflamm 2015[Jun]; 2 (3): ä PMID25866831show ga Objective:: We examined a cohort of Australian patients with statin exposure who developed a necrotizing autoimmune myopathy (NAM) associated with a novel autoantibody against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) and describe the clinical and therapeutic challenges of managing these patients and an optimal therapeutic strategy. Methods:: Clinical, laboratory, EMG, and histopathologic results and response to immunomodulation are reported in 6 Australian patients with previous statin exposure and antibodies targeting HMGCR. Results:: All patients presented with painless proximal weakness following statin therapy, which persisted after statin cessation. Serum creatine kinase (CK) levels ranged from 2,700 to 16,200 IU/L. EMG was consistent with a myopathic picture. Muscle biopsies revealed a pauci-immune necrotizing myopathy. Detailed graphical representation of the clinical course of these patients showed a close association with rising CK and an increase in clinical weakness signifying relapses, particularly upon weaning or ceasing steroids. All 6 patients were responsive to initial steroid therapy, with 5 relapsing upon attempts to wean steroids. Both CK and clinical strength improved with the reinstitution of immunotherapy, in particular steroids and IV immunoglobulin (IVIg). All patients required treatment with varying multiagent immunosuppressive regimens to achieve clinical remission, including prednisone (n = 6), IVIg (n = 5), plasmapheresis (n = 2), and additional therapy including methotrexate (n = 6), cyclophosphamide (n = 2), rituximab (n = 2), azathioprine (n = 1), and cyclosporine (n = 1). Conclusions:: Recognition of HMGCR antibody?associated NAM is important because these patients are responsive to immunosuppression, and early multiagent therapy and a slow and cautious approach to withdrawing steroids may improve outcomes. äClinical course and treatment of anti-HMGCR antibody?associated necrot(epmc).pdf DeepDyve Pubget Overpricing