The infection by Helicobacter pylori strains expressing CagA is highly prevalent in women with autoimmune thyroid disorders.
H. pylori infection is putatively associated with extra-digestive disorders and may also play a role in the development of autoimmune thyroid diseases (ATD). It was recently found that monoclonal antibodies to an H. pylori strain with cagA-positivity reacted with follicular cells of the thyroid gland, and that an H. pylori organism possessing the cag pathogenicity island carried a gene encoding for an endogenous peroxidase. The aims of this study was (1); To ascertain whether the infection by strains endowed with an increased inflammatory potential (those expressing CagA) could further enhance the risk of developing ATD (2); To verify the possible existence of an immune cross-reactivity between autoantibodies to peroxidase and thyroglobulin and H. pylori antigens (3). To establish whether thyroid colloid antigens could cross-react with an anti-H. pylori serum. The study was partly designed retrospectively. We examined 41 consecutive women with ATD, and, as a control, 33 consecutive age- and socio-economic class-matched women without autoimmune thyroid disorders, living in the same area as patients, occurred at the same institution in the same period (six months). Both patients and controls were examined serologically for H. pylori infection and CagA status by Western blotting. Some serum samples were absorbed with H. pylori to determine whether the antibody levels decreased. Colloid proteins were resolved electrophoretically and matched with a hyperimmune serum raised in rabbits against a CagA-positive H. pylori. Thirty-two patients (78.0%) tested seropositive for H. pylori infection, vs. 16 controls (48.4%) (P = 0.008, OR = 3.78, RR = 1.61). The prevalence of anti-CagA antibodies was 71.8% in infected patients, and 50% in infected controls (P = 0.161, n.s.). The overall prevalence of infection by CagA-positive H. pylori was significantly higher in patients with ATD (23/41, or 56.0%) than that in controls (8/33, or 24.2%) (P = 0.006, OR = 3.99, RR = 2.31). The other tests gave negative or inexplicable results.


CONCLUSIONS
CagA-positive H. pylori infection increases the risk of ATD development.
Figura
N
N
Institute of Internal Medicine, University of Siena, Policlinico le Scotte, Italy. figura@unisi.it
Di Cairano
G
G
Lorè
F
F
Guarino
E
E
Gragnoli
A
A
Cataldo
D
D
Giannace
R
R
Vaira
D
D
Bianciardi
L
L
Kristodhullu
S
S
Lenzi
C
C
Torricelli
V
V
Orlandini
G
G
Gennari
C
C
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000276:immunology / Q000378:metabolism; D001426:Bacterial Proteins / Q000096:biosynthesis* / Q000276:immunology; D003102:Colloids / Q000378:metabolism; D005260:Female; D006111:Graves Disease / Q000097:blood / Q000276:immunology / Q000382:microbiology*; D006360:Heat-Shock Proteins / Q000276:immunology; D016481:Helicobacter Infections / Q000097:blood / Q000453:epidemiology* / Q000276:immunology / Q000378:metabolism; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007106:Immune Sera / Q000378:metabolism; D008875:Middle Aged; D015995:Prevalence; D011817:Rabbits; D012189:Retrospective Studies; D013967:Thyroiditis, Autoimmune / Q000097:blood / Q000276:immunology / Q000382:microbiology*; D014510:Urease / Q000276:immunology
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D003102:Colloids; D006360:Heat-Shock Proteins; D007106:Immune Sera; C080866:cagA protein, Helicobacter pylori; D014510:Urease