EFFECT OF HELICOBACTER-PYLORI INFECTION AND CAGA STATUS ON LEUKOCYTE COUNTS AND LIVER-FUNCTION TESTS - EXTRA-GASTRIC MANIFESTATIONS OF HELICOBACTER-PYLORI INFECTION

Background. It has been suggested that H. pylori infection is associat ed with abnormalities in total leukocyte count as well as the number o f 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 ana lyses in patients before and after treatment for H. pylori infection a nd to ascertain whether the abnormalities reversed following successfu l 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. Res ults. 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 befo re and after therapy. There were no significant changes in any study p arameter 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 w as almost entirely accounted for by a reduction in the number of circu lating polymorphonuclear leukocytes (4595 +/- 370 cmm to 3855 +/- 270 cmm for pretreatment vs. cured, respectively, p = 0.015). The pretreat ment SCOT and basophil count were significantly higher in those with C agA-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 res ult in a significant change of SCOT levels. Conclusions. We confirmed an increase in total leukocyte count and number of polymorphonuclear l eukocytes 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.