Association of inflammatory cytokine gene polymorphisms with platelet recovery in idiopathic thrombocytopenic purpura patients after the eradication of Helicobacter pylori.
BACKGROUND
Idiopathic thrombocytopenic purpura (ITP) is associated with the cytokine response and dysregulation of the cytokine network. Gene polymorphisms of proinflammatory cytokines are associated with several diseases including ITP. Recently, the successful eradication of Helicobacter pylori has been reported to improve the platelet counts in some patients with ITP. The aim of this study was to elucidate the relationship between cytokine gene polymorphisms and platelet recovery in ITP patients after the eradication of H. pylori.


METHODS
Gastric H. pylori infection was confirmed using a culture method or specific IgG antibodies against H. pylori in the serum. Thirty-six adult H. pylori-positive ITP patients received antibiotic therapy for H. pylori. The response to treatment was defined as complete response (CR) if the platelet count was above 150 x 10(3)/microl and partial response (PR) if the platelet count increased by more than 50 x 10(3)/mul above the pretreatment count. Genomic DNA was extracted from peripheral blood and polymorphisms in IL-1B (-31, -511), IL-1RN (long or short), TNFA (-308) and TNFB (+252) were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).


RESULTS
Of the 36 ITP patients, twenty patients (responders) exhibited a platelet response after successful H. pylori eradication therapy, but the other patients (nonresponders) did not. There were no statistical differences in the frequencies of polymorphisms in IL-1B, IL-1RN and TNFA genes between responders and nonresponders. In contrast, the frequency of responders in ITP patients with the TNFB G/G or G/A genotype was significantly higher (69.6%) than that with the TNFB A/A genotype (30.8%).


CONCLUSIONS
The TNFB (+252) G/G or G/A genotype may therefore be a good predictor of platelet recovery in ITP patients after the eradication of H. pylori.
Suzuki
Takayoshi
T
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Japan. takayosh@is.icc.u-tokai.ac.jp
Matsushima
Masashi
M
Shirakura
Katsuya
K
Koike
Jun
J
Masui
Aya
A
Takagi
Atsushi
A
Shirasugi
Yukari
Y
Ogawa
Yoshiaki
Y
Shirai
Takayuki
T
Mine
Tetsuya
T
D000368:Aged; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D000942:Antigens, Bacterial / Q000097:blood; D001426:Bacterial Proteins / Q000097:blood; D016207:Cytokines / Q000235:genetics*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy* / Q000276:immunology; D016480:Helicobacter pylori; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D053590:Interleukin 1 Receptor Antagonist Protein / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics; D008233:Lymphotoxin-alpha / Q000235:genetics; D008297:Male; D008875:Middle Aged; D012150:Polymorphism, Restriction Fragment Length; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000150:complications* / Q000276:immunology* / Q000382:microbiology; D012074:Remission Induction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D000900:Anti-Bacterial Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D016207:Cytokines; C507763:IL1RN protein, human; D007074:Immunoglobulin G; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D008233:Lymphotoxin-alpha; D014409:Tumor Necrosis Factor-alpha; C080866:cagA protein, Helicobacter pylori