Another study done by Godoy and Rabinstein27 recommended a second cycle of IVIG for treating severe forms of GBS. gastroenteritis. Unfortunately, antiganglioside antibodies (GM1 and GD1a) were not tested in our patient. Guillain-Barr syndrome is usually a heterogeneous disorder that occurs in healthy people with no known association with autoimmune or systemic diseases.9 In AMAN, the disease appears to be a humoral-mediated disorder with an antibody-mediated attack driven by molecular mimicry.10 On the contrary, the immunopathogenesis of AIDP is less clear with lack of specific antibody markers.11 In this form of GBS, a wide range of viruses and bacteria can incite an antibody, although a common antigenic stimulus or a specific antibody biomarker is difficult to find.12 The rapid recovery in our case could be explained by the nodopathy theory caused by impaired conduction at the node of Ranvier, possibly due to loss of sodium channel function. Injury of the nodal axolemma with axonal degeneration is due to nodal immunoglobulin G (IgG) deposition as well as complement and membraneCattack complex formation.13 In patients presenting with a clinical picture suggestive of GBS, MRI scanning of the spine has Salvianolic Acid B been commonly Salvianolic Acid B performed to exclude other causes of paralysis and to assess for gadolinium enhancement of nerve roots in the conus medullaris and cauda equina. In normal patients around the precontrast images, the spinal cord and nerve roots in the thecal sac appear normal with no enhancement after gadolinium administration because of the bloodCnerve barrier or bloodCbrain barrier. The enhancement of the thickened anterior and posterior nerve roots in patients with GBS indicates a breakdown of the bloodCnerve barrier with inflammatory infiltration.14 Qualitative evaluation of the contrast enhancement (mild, moderate, or severe) has been studied with a correlation between the severity of the disease and the degree of the enhancement of the spinal nerve root. The contrast enhancement is usually more prominent in the anterior root of the spinal cord.15 Although nonspecific, some recent studies have suggested serial contrast-enhanced MRI imaging as a useful tool to monitor the response to therapy.16 In fact, persistent Salvianolic Acid B contrast enhancement was the motive to repeat the cycles of intravenous infusion of IVIG in our patient. The presence of gadolinium enhancement in the MRI done after initiation of aggressive therapy could be an indication of Mouse monoclonal antibody to hnRNP U. This gene belongs to the subfamily of ubiquitously expressed heterogeneous nuclearribonucleoproteins (hnRNPs). The hnRNPs are RNA binding proteins and they form complexeswith heterogeneous nuclear RNA (hnRNA). These proteins are associated with pre-mRNAs inthe nucleus and appear to influence pre-mRNA processing and other aspects of mRNAmetabolism and transport. While all of the hnRNPs are present in the nucleus, some seem toshuttle between the nucleus and the cytoplasm. The hnRNP proteins have distinct nucleic acidbinding properties. The protein encoded by this gene contains a RNA binding domain andscaffold-associated region (SAR)-specific bipartite DNA-binding domain. This protein is alsothought to be involved in the packaging of hnRNA into large ribonucleoprotein complexes.During apoptosis, this protein is cleaved in a caspase-dependent way. Cleavage occurs at theSALD site, resulting in a loss of DNA-binding activity and a concomitant detachment of thisprotein from nuclear structural sites. But this cleavage does not affect the function of theencoded protein in RNA metabolism. At least two alternatively spliced transcript variants havebeen identified for this gene. [provided by RefSeq, Jul 2008] the continuous immune attack on roots and peripheral nerves. Further research should be done to address the question of whether patients who do not respond to the first cycle of IVIG and continue to demonstrate gadolinium enhancement on MRI deserve repeating the therapy. Guillain-Barr syndrome is usually a potentially life-threatening condition that requires a multidisciplinary approach consisting of general medical care and immune modulation therapy.17 General medical care includes monitoring of cardiopulmonary and hemodynamic functions, prophylaxis for deep vein thrombosis, management of bladder and bowel dysfunction, passive and active physiotherapy, and psychosocial support.18 In addition, pain management is extremely important using nonsteroidal anti-inflammatory medications and/or opioids. Respiratory failure requiring mechanical ventilation may develop in 20% to 30% of patients. The major causes of death in this condition are contamination, autonomic instability, and pulmonary embolism.19 Immune-modulating treatment with IVIG or PLEX is the mainstay of treatment. They have proved to be efficacious in improving outcomes and hastening recovery. They should be started as soon as possible prior to irreversible nerve damage occurrence. Intravenous immunoglobulin is usually given at a dose of 400 mg/kg daily for 5 days. Plasma exchange is usually performed in Salvianolic Acid B 5 sessions at a rate of 200 to 250 mL/kg on alternate days. It is usually well known that PLEX and IVIG are equally effective. However, IVIG is preferred in many centers because of its widespread availability and good tolerability. Intravenous immunoglobulin is usually more expensive than PLEX, and combined PLEX with IVIG is usually no better than PLEX or IVIG alone.20 Although IVIG has been used for more than 35 years in the field of autoimmunity, how concentrated intravenous nonhost immunoglobulins produce their clinical effect remains unknown.21 It seems that different mechanisms of action are relevant to different disorders. These include direct immune-modulating effects such as reduced T-cell proliferation, suppressed various pro-inflammatory cytokines, and induction of lymphocytes and monocytes apoptosis. Other effects include decreased endogenous immunoglobulin production, suppressed B-cell differentiation, and accelerated IgG catabolism. In addition, therapeutic immunoglobulins inhibit Fc region-mediated antibody production and modulate anti-idiotypic networks. Other direct mechanisms include action on oligodendrocyteCprogenitors.