Organ-specific autoantibodies in children with Helicobacter pylori infection.
ABSTRACT We compared the prevalence of organ-specific autoantibodies in a group of Helicobacter pylori infected children and a group of uninfected children and investigated the relationship between the presence of relevant autoantibodies and the status of the target organs.
One hundred and twenty-four children with dyspepsia (54 boys, 70 girls; mean age 10.5 years; range 4-19) underwent gastroscopy: 56 had H. pylori infection (31 girls, 25 boys), while 68 (37 girls and 31 boys), were H. pylori-negative. All sera were tested for the presence of: parietal cell autoantibodies (PCA), intrinsic factor autoantibodies (IFA), microsomial autoantibodies, thyroglobulin autoantibodies, islet cell autoantibodies, glutamic acid decarboxylase autoantibodies, adrenal cortex autoantibodies, steroid-producing cell autoantibodies; gastrin, pepsinogen A, pepsinogen C and anti-H. pylori antibodies. The histological features and the ureA and cagA genes were also considered.
The frequency of organ-specific autoantibodies was higher in patients with H. pylori infection than in uninfected patients (chi2-test p < .0001). Specifically gastric autoantibodies were significantly higher: seven of the 56 H. pylori-positive children were PCA-positive and one was IFA-positive (chi2-test p = .0004). The presence of autoantibodies was not associated with any clinical or biohumoral signs of disease.
Our study detected a relationship between H. pylori infection in childhood and the presence of organ-specific autoantibodies unassociated with any clinical or biohumoral signs of disease. Helicobacter pylori infection in childhood could trigger the onset of clinical autoimmune gastritis, and/or other clinical autoimmune diseases.
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ABSTRACT: We studied the association of clinical and latent autoimmune diseases with circulating steroid-producing cells autoantibodies (SCA) in patients with premature ovarian failure (Group I). We investigated the presence of SCA in patients with organ-specific autoimmune diseases but without hypogonadism (Group II). We assessed whether SCA can be considered markers of hypergonadotrophic hypogonadism. In Groups I and II blood samples were taken at diagnosis. In a subset of patients with SCA without hypogonadism blood samples were taken at least yearly for 6 years for immunological and functional tests. Group I included 50 females, aged 16-39 years; Group II included 3677 patients, aged 6-79 years, divided into Subgroup IIA (99 with Addison's disease alone or associated with other endocrinopathies or with hypoparathyroidism) and Subgroup IIB (3578 with insulin-dependent diabetes mellitus or thyroid autoimmune diseases). The follow-up group included nine subjects, aged 5-31 years (seven females and two males). SCA and other organ-specific autoantibodies were detected by standard indirect immunofluorescence using normal human tissues or passive haemagglutination tests. Gonadal functional tests included evaluation of FSH and LH levels by a RIA method; adrenocortical function included evaluation of cortisol and ACTH plasma levels by a RIA method. Three subgroups were identified in Group I on the basis of clinical autoimmune disease. 9/50 (18%) patients were found to have an Addison's disease (Subgroup IA) and in this subgroup SCA were present in 7/9 (78%); 10/50 (20%) had other autoimmune diseases (Subgroup IB) and SCA were found in 1/10 (10%); 31/50 (62%) did not have other clinical autoimmune diseases (Subgroup IC) and 1/31 (3%) had SCA. SCA were significantly increased in Subgroup IA vs IB (P = 0.017) and vs IC (P = 0.00002). In Group II, SCA were found in 20/3677 (0.5%); in particular, SCA were detected in 18/99 (18%) of the patients in Subgroup IIA and in 2/3578 (0.06%) of the patients in Subgroup IIB. The frequency of SCA in Subgroup IIA was found to be significantly increased with respect to that found in Subgroup IIB (P = 0.001 x 10(-5)). During follow-up, 3/7 females (42.8%) but 0/2 males developed hypergonadotrophic hypogonadism with a latency period of 10, 13 and 15 years, respectively. Three females and two males lacked clinical Addison's disease at the beginning of the study, but during follow-up 1/3 female and 2/2 males developed clinical Addison's disease with a mean latency period of 13 months. The results confirm the strong relationship between premature ovarian failure and other clinical autoimmune diseases, as well as the strong link existing between primary ovarian failure, Addison's disease and antibodies to steroid-producing cells. The study also suggests that in females antibodies to steroid-producing cells are serological markers of both potential hypergonadotrophic hypogonadism, and Addison's disease; however, in males these antibodies may be considered only as markers of potential Addison's disease.Clinical Endocrinology 08/1993; 39(1):35-43. · 3.40 Impact Factor
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ABSTRACT: Whilst upper gastrointestinal disturbances are frequently observed in patients with diabetes mellitus, little is known about the prevalence of Helicobacter pylori infection and peptic disease in these patients. To evaluate prevalence of Helicobacter pylori infection and peptic disease lesions in diabetics with dyspeptic symptoms. Study population comprises 74 consecutive diabetes mellitus patients with dyspepsia and 117 consecutive non diabetic dyspeptic patients. Upon enrolment, each patient completed an interview screening questionnaire to obtain information concerning presence and severity of dyspepsia. All patients underwent upper gastrointestinal endoscopy with biopsy specimens being collected from gastric antrum and body Helicobacter pylori was evaluated in each patient by rapid urease test and histology (Giemsa). Gastritis was classified according to the Sydney System. Statistical analysis was performed by chi-square, Fisher exact or t test and logistic regression analysis. A p value <0.05 was considered significant. Prevalence of Helicobacter pylori infection was found to be significantly higher in diabetics than in controls. The prevalence rate of endoscopic lesions was comparable in the two groups, but the association between endoscopic lesions and Helicobacter pylori infection was significantly higher in diabetics. Overall, the presence of chronic gastritis, both non atrophic and atrophic, as well as intestinal metaplasia were comparable in the two groups of patients, whilst the association between chronic gastritis and Helicobacter pylori infection or gastritis activity were significantly higher in diabetics. In neither group, was any correlation found between severity of dyspepsia and presence of endoscopic lesions, chronic gastritis or Helicobacter pylori infection. These data show a higher prevalence of Helicobacter pylori infection in diabetes mellitus patients with dyspepsia. Helicobacter pylori infection was significantly associated both with the presence of endoscopic lesions and chronic gastritis in diabetic patients, but not in the controls.Digestive and Liver Disease 01/2001; 33(1):21-9. · 3.16 Impact Factor
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ABSTRACT: Across populations of children, Helicobacter pylori prevalence ranges from under 10% to over 80%. Low prevalence occurs in the U.S., Canada, and northern and western Europe; high prevalence occurs in India, Africa, Latin America, and eastern Europe. Risk factors include socioeconomic status, household crowding, ethnicity, migration from high prevalence regions, and infection status of family members. H. pylori infection is not associated with specific symptoms in children; however, it is consistently associated with antral gastritis, although its clinical significance is unclear. Duodenal ulcers associated with H. pylori are seldom seen in children under 10 years of age. H. pylori-infected children demonstrate a chronic, macrophagic, and monocytic inflammatory cell infiltrate and a lack of neutrophils, as compared with the response observed in adults. The effect of H. pylori infection on acid secretion in children remains poorly defined. The events that occur during H. pylori colonization in children should be studied more thoroughly and should include urease activity, motility, chemotaxis, adherence, and downregulation of the host response. The importance of virulence determinants described as relevant for disease during H. pylori infection has not been extensively studied in children. Highly sensitive and specific methods for the detection of H. pylori in children are needed, especially in younger pediatric populations in which colonization is in its early phases. Criteria for the use of eradication treatment in H. pylori-infected children need to be established. Multicenter pediatric studies should focus on the identification of risk factors, which can be used as prognostic indicators for the development of gastroduodenal disease later in life.Archives of Medical Research 01/2000; 31(5):431-69. · 2.08 Impact Factor