PMID- 24200120
OWN - NLM
STAT- MEDLINE
DCOM- 20141128
LR  - 20211021
IS  - 1529-8027 (Electronic)
IS  - 1085-9489 (Print)
IS  - 1085-9489 (Linking)
VI  - 18
IP  - 4
DP  - 2013 Dec
TI  - Rapid and reversible responses to IVIG in autoimmune neuromuscular diseases 
      suggest mechanisms of action involving competition with functionally important 
      autoantibodies.
PG  - 275-96
LID - 10.1111/jns5.12048 [doi]
AB  - Intravenous immunoglobulin (IVIG) is widely used in autoimmune neuromuscular 
      diseases whose pathogenesis is undefined. Many different effects of IVIG have 
      been demonstrated in vitro, but few studies actually identify the mechanism(s) 
      most important in vivo. Doses and treatment intervals are generally chosen 
      empirically. Recent studies in Guillain-Barre syndrome and chronic inflammatory 
      demyelinating polyneuropathy show that some effects of IVIG are readily 
      reversible and highly dependent on the serum IgG level. This suggests that in 
      some autoantibody-mediated neuromuscular diseases, IVIG directly competes with 
      autoantibodies that reversibly interfere with nerve conduction. Mechanisms of 
      action of IVIG which most likely involve direct competition with autoantibodies 
      include: neutralization of autoantibodies by anti-idiotypes, inhibition of 
      complement deposition, and increasing catabolism of pathologic antibodies by 
      saturating FcRn. Indirect immunomodulatory effects are not as likely to involve 
      competition and may not have the same reversibility and dose-dependency. 
      Pharmacodynamic analyses should be informative regarding most relevant 
      mechanism(s) of action of IVIG as well as the role of autoantibodies in the 
      immunopathogenesis of each disease. Better understanding of the role of 
      autoantibodies and of the target(s) of IVIG could lead to more efficient use of 
      this therapy and better patient outcomes.
CI  - (c) 2013 The Authors. Journal of the Peripheral Nervous System published by Wiley 
      Periodicals, Inc. on behalf of Peripheral Nerve Society.
FAU - Berger, Melvin
AU  - Berger M
AD  - Departments of Pediatrics and Pathology, Case Western Reserve University, 
      Cleveland, OH, USA; Immunology Research and Development, CSL Behring, LLC, King 
      of Prussia, PA, USA.
FAU - McCallus, Daniel E
AU  - McCallus DE
FAU - Lin, Cindy Shin-Yi
AU  - Lin CS
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Peripher Nerv Syst
JT  - Journal of the peripheral nervous system : JPNS
JID - 9704532
RN  - 0 (Autoantibodies)
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Immunologic Factors)
SB  - IM
MH  - Animals
MH  - Autoantibodies/*metabolism
MH  - Autoimmune Diseases/complications/*therapy
MH  - Humans
MH  - Immunoglobulins, Intravenous/pharmacology/*therapeutic use
MH  - Immunologic Factors/pharmacology/*therapeutic use
MH  - Neuromuscular Diseases/complications/*therapy
MH  - Protein Binding/drug effects
PMC - PMC4285221
OTO - NOTNLM
OT  - Guillain-Barre syndrome
OT  - anti-idiotypes
OT  - autoimmune neuromuscular diseases
OT  - chronic inflammatory demyelinating polyneuropathy
OT  - intravenous immunoglobulin
OT  - multifocal motor neuropathy
EDAT- 2013/11/10 06:00
MHDA- 2014/12/15 06:00
CRDT- 2013/11/09 06:00
PHST- 2013/11/09 06:00 [entrez]
PHST- 2013/11/10 06:00 [pubmed]
PHST- 2014/12/15 06:00 [medline]
AID - 10.1111/jns5.12048 [doi]
PST - ppublish
SO  - J Peripher Nerv Syst. 2013 Dec;18(4):275-96. doi: 10.1111/jns5.12048.