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   3 entiating the two disease entities (AMAN and AIDP) and focuses our attention on particular DR beta/DQ
     4 l distribution of DR13 allelic forms between AIDP and AMAN cases may suggest that there are different
  
     6  observed an identical diagnostic shift from AIDP to axonal GBS with modified criteria as that descri
  
  
  
  
    11 greater than 1:100, 60% of AMAN versus 4% of AIDP patients had IgG anti-GD1a antibodies; with a cutof
    12 ction was detected in 81% of AMAN and 50% of AIDP patients, and anti-ganglioside antibodies were comm
  
  
    15  criteria, we identified comparable rates of AIDP (56.2% vs. 58.7%; p=0.70), axonal GBS (35.1% vs. 36
    16 e inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN) being the
  
  
    19 e inflammatory demyelinating polyneuropathy (AIDP), the attack appears directed against a component o
    20 matory demyelinating polyradiculoneuropathy (AIDP) (71.5% vs. 72%; p=1), axonal GBS (17.5% vs. 14.7%;
    21 matory demyelinating polyradiculoneuropathy (AIDP) subtype resembles experimental autoimmune neuritis
  
  
  
    25 topes were associated with susceptibility to AIDP (p = 0.009 and p = 0.004, respectively), and the DQ
    26 ods, 47 patients with AMAN, 25 patients with AIDP, and 97 healthy controls were studied for the distr
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