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Submitted on June 7, 2005
Accepted on October 24, 2005
Department of Pediatric Sciences, University of Pavia and IRCCS Policlinico San Matteo, Pavia, Immunohematology and Transfusion Center, IRCCS Policlinico S. Matteo, Pavia, Institute of Internal Medicine, Spedali Civili, Brescia, Clinical Epidemiology and Biometry Unit, IRCCS Policlinico San Matteo, Pavia, Department of Pathology, University of Pavia and IRCCS Policlinico San Matteo, Pavia, Italy
* To whom correspondence should be addressed. E-mail: d.larizza{at}smatteo.pv.it.
Context and objective: Pathogenesis of autoimmune thyroid disease (ATD) is multifactorial. Hp infection has been proposed to be involved in non gastrointestinal conditions and reported more frequent in ATD-adult patients.
We evaluated the prevalence of Hp antibodies in young ATD-patients and investigated on the possibility that a susceptible immunogenetic profile could influence the development of ATD in subjects with Hp infection.
Subjects and methods: We retrospectively studied 90 children with ATD (median age 11.2 yr), 70 age and sex-matched healthy subjects as controls and 65 patients with Turner syndrome (TS) (median age 18.8 yr).
Antibodies to Hp were determined at diagnosis in ATD-patients and, in Turner patients, at the last control in cases without ATD and before the appearance of thyroid autoantibodies in the others. Serological and molecular HLA typing for class I and II polymorphisms was performed.
Results: Prevalence of positive Hp serology resulted significantly higher in ATD-patients than in controls (P = 0.032). No association was found between individual HLA alleles and Hp serology. HLA-A1, B8 and DRB1*0301 were found significantly associated to ATD. A significant interaction between HLA-DRB1*0301 and Hp infection was present in ATD-patients and not in controls (P = 0.007), suggesting that the copresence of these two factors might favor ATD development. Similar phenomenon was observed in TS patients (P = 0.02), cumulative Mantel test P = 0.0001.
Conclusions: Another target of Hp-elicited immune-inflammatory response might be thyroid gland in subjects with a peculiar immunogenetic profile so that ATD may be a consequence. Our findings suggest the opportunity of eradicating Hp infection in children with ATD and/or with susceptible HLA alleles.
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| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |