736 201
( Immune thrombocytopenic purpura ) ( )
( Eradication therapy ) ( Cross mimicry )
( Platelet aggregation )
( i m m u n e thrombocytopenic purpura, ITP )
1
( lymphoproliferative diseases )
( Helicobacter pylori; H. Pylori ) 1983 Marshall Warren
3-7
( Sjogren's syndrome )
Helicobacter pylori
..
8
4 6
4
9 - 1 2
IgG 54.4%
13
( )
( )
( C L O test)
2 0 0 0 - 2
(Maastricht 2-2000 Consensus )
(MALToma )
( )
( NSAIDs )
14
( )
7 5 %
1 5 , 1 6
( / 1.2 -
1.7 )
17,18
19
(
[ HIV ] C [ HCV ] )
20
21,22
( American society of hematology )
23
8 5 %
( glycoprotein )
24 glycoprotein IIb/IIIa
Ib/IX IgG IgA 25
( antigen- presenting cells APC ) ( macrophage )
( dendritic cell )
T- ( T-helper cells ) B- ( B-lymphocyte )
1
( 30,000/mm2 )
1 , 2 0
26
Gasbarrini 1998
27
28
H. pylori
16 1126
470 250 53%29
3 0 - 3 2
( 70%10)
( 34%33 )
31
30,32
34
( strain )
35
( randomized controlled trial )
A ( Anti-
cytotoxin-associated gene A antibody; Anti-CagA Ab ) ( p = 0.04 )
A
36
( a m o x i - cillin + clarithromycin + PPI )
3 1 , 3 7
H+-K+-ATPase ( molecular mimicry )
38 ( cross mimicry )
A ( CagA anti- gen)
PAIgG ( platelet-associated im- munoglobulin G )
( )
PA I g G 3 9
A
3 6 , 4 0
A
55 kDa
40
55 kDa
55 kDa
( Platelet Aggregation )
( anti-H. pylori IgG ) von
Willebrand factor ( vWf ) vWf
glycoprotein Ib
( VacA ) CagA
41
( ) B- T-
( clone ) 3 8
T- ( clonality )
B- ( 2.9% )42
T-
T-
43
( ge- netic )
( major his- tocompatibility complex MHC )
HLA-DRB1
11 14 HLA-DQB1 03
H L A - D R B 1 03
HLA-DQB1 0342
HIV HCV
44
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Immune Thrombocytopenic Purpura and Infection
Cheng-Yao Lin, Wen-Tsung Huang, Chao-Jung Taso, and Chih-Hui Lee1
Immune thrombocytopenic purpura (ITP) is a disorder characterized by a low platelet count. The peripher- al blood platelets are conjugated with anti-platelet antibodies and then are destroyed by autoimmune system.
However, the definite causes and mechanisms of how to induce those auto-antibodies are not clear. The infec- tion of ( ) has been documented to be associated with peptic ulcers, gastric cancer and gastric lymphoma as well as some auto-immune diseases. And the marvelous finding has approached a new therapeutic milestone for those diseases. Recently, numerous studies have reported that: about half of ITP pa- tients simultaneously infected with will improve their platelet counts after successful eradication of their
infections. Theories of molecular cross mimicry, platelet aggregation and serological studies have tried to explain the relations and possible mechanism. Therefore, we might understand the causes and mechanisms of the evolution of auto-antibodies in ITP, and then conduct a new strategy to treat those ITP patients. ( J Intern Med Taiwan 2007; 18: 182-188 )
Division of Hemato-oncology, Department of Internal Medicine, Liouying Chi-Mei Hospital, Tainan County, Taiwan
1Department of FamilyMedicine, Liouying Chi-Mei Hospital, Tainan County, Taiwan
Helicobacter Pylori
Helicobacter Pylori H. Pylori
H. Pylori H. Pylori
