Effect of H. pylori infection and CagA status on leukocyte counts and liver function tests: extra-gastric manifestations of H. pylori infection.
BACKGROUND
It has been suggested that H. pylori infection is associated with abnormalities in total leukocyte count as well as the number of basophils and lymphocytes. In addition, CagA seropositivity has been associated with an increase in serum transaminase (SGOT) values. The aim of this study was to confirm the findings of previous subgroup analyses in patients before and after treatment for H. pylori infection and to ascertain whether the abnormalities reversed following successful treatment.


METHODS
Blood counts and serum transaminase levels were obtained prior to and following treatment of H. pylori infection of H. pylori-infected duodenal ulcer patients. CagA status was assessed by Western blot of the H. pylori isolates obtained from the patients.


RESULTS
Ninety-four ulcer patients were studied, including 77 with CagA-positive H. pylori isolates (82%) and 17 with CagA-negative H. pylori isolates. All study parameters remained within normal limits both before and after therapy. There were no significant changes in any study parameter in those who failed therapy. Successful therapy resulted in a significant fall in total white cell count (7413 +/- 520 cmm to 6738 +/- 410 cmm, for pretreatment vs. cured, respectively, p = 0.04) and was almost entirely accounted for by a reduction in the number of circulating polymorphonuclear leukocytes (4595 +/- 370 cmm to 3855 +/- 270 cmm for pretreatment vs. cured, respectively, p = 0.015). The pretreatment SGOT and basophil count were significantly higher in those with CagA-positive H. pylori (SGOT = 23 +/- 1 vs. 18.5 +/- 1 U). Successful or failed therapy with follow-up for 3 months post therapy did not result in a significant change of SGOT levels.


CONCLUSIONS
We confirmed an increase in total leukocyte count and number of polymorphonuclear leukocytes in those with H. pylori infection. We also confirmed higher SGOT levels with CagA-positive H. pylori infection, but the failure to resolve within 3 months of cure of the infection makes it unlikely to be a direct result of the H. pylori infection.
Graham
D Y
DY
VA Medical Center, Baylor College of Medicine, Houston, TX 77030, USA.
Osato
M S
MS
Olson
C A
CA
Zhang
J
J
Figura
N
N
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000378:metabolism*; D015153:Blotting, Western; D017291:Clarithromycin / Q000627:therapeutic use; D004381:Duodenal Ulcer / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology* / Q000503:physiopathology; D016481:Helicobacter Infections / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000737:chemistry / Q000302:isolation & purification*; D006801:Humans; D007958:Leukocyte Count; D008111:Liver Function Tests; D009853:Omeprazole / Q000627:therapeutic use; D016896:Treatment Outcome
D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori; D017291:Clarithromycin; D009853:Omeprazole