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1 ed by DNA-based technology in 34 control, 12 AIDP, and 31 AMAN cases.
2                                     AMAN and AIDP have an immunologic basis, and some cases are assoc
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
5 s associated with protection (p = 0.05) from AIDP.
6  observed an identical diagnostic shift from AIDP to axonal GBS with modified criteria as that descri
7                                           In AIDP patients, the DRB1*1301 allele showed a significant
8 he DRB1*1301 allele was not increased, as in AIDP patients.
9      The role of T-cell-mediated immunity in AIDP remains unclear and there is evidence for the invol
10 es were closely associated with AMAN but not AIDP.
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
13  results suggest that at least some forms of AIDP are complement mediated.
14 ntal in understanding the pathophysiology of AIDP.
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
17 e inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN).
18 e inflammatory demyelinating polyneuropathy (AIDP) pattern of Guillain-Barre syndrome.
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
22 :100) were detected in both the AMAN and the AIDP forms (57% vs 35%, NS).
23 :1,000, 24% of AMAN patients and none of the AIDP patients had IgG anti-GD1a antibodies.
24                                        Three AIDP subjects who were autopsied had had symptoms for 3
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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