Prevalência da infecção pelo Helicobacter pylori e sua associação com a doença tireoidiana autoimune na infância e adolescência

• Ano de defesa: 2014
• Autor(a) principal: Lara Vieira Marcal
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Helicobacter pylori; Autoimune; Infância; Tireoide; Endocrinologia pediatrica; Infecções por helicobacter/complicações; Doenças da glândula tireóide/complicações; Infecções por helicobacter/epidemiologia; Saúde da criança; Criança; Adolescente; Saúde do adolescente
• Link de acesso: http://hdl.handle.net/1843/BUBD-9Q3GKY

The interaction between genetic susceptibility and environmental triggers seem to be of fundamental importance in the development of autoimmune thyroid disease (ATD). It is known that Helicobacter pylori (H. pylori) is potentially capable of producing systemic low-grade inflammatory status and inducing mechanisms of molecular mimicry. The association between H. pylori infection and ATD is controversial. The aim of this study was to investigate the association between H. pylori infection and ATD in children and adolescents. The study included 252 patients aged 1-19 years, including 27 patients with Hashimoto's thyroiditis (HT) and 9 patients with Graves' disease (GD); to compare ATD with autoimmune disease but without thyroid disease, 110 patients with type 1 diabetes mellitus (T1DM) were included and to compare ATD with thyroid disease without autoimmunity, 106 patients with congenital hypothyroidism (CH) were included. The prevalence of infection was determined by urea breath test labeled with carbon 13 (13C-UBT), as well as thyroid function by measurement of TSH, FT4 and FT3 and the presence of anti-thyroid antibodies: anti-thyroid peroxidase (anti- TPO), anti-thyroglobulin (anti-Tg) and anti-TSH-receptor (TRAb) were done. After adjusting for age, we have found prevalence of infection of 19.4% in patients with ATD, 21.9% in patients with T1DM and 34.9% in patients with HC. No difference was observed when the prevalence in children ATD was compared with those with T1DM (p=0.26). The prevalence in children with CH was higher than in ATD group, but without statistical significance (p = 0.08). Among patients with ATD, the H. pylori infection was not associated with serum TSH levels (p=0.20), FT4 (p = 0.09) and FT3 (p=0.24), nor with levels of anti-TPO (p=0.34), anti-Tg (p=1.00) and TRAb (p=0.65) antibodies. Among diabetic patients, there was no association between infection and TSH (p=0.91), FT4 (p=1.00) and FT3 (p=0.99), nor with the presence of anti-TPO (p=0.25) and TRAb (p=1.00). On the other hand, the diabetic H. pylori-positive patients were more often anti-Tg positive (p=0.04). In patients with HC, group in which higher prevalence of infection was found, there was a negative association between elevated FT3 and H. pylori infection (p=0.002), which remained after adjustment for age (p=0,04). In conclusion, no association was found between H. pylori infection and ATD: they either did not present a higher prevalence of infection, neither the infected with H. pylori showed a higher frequency of anti-thyroid antibodies or changes in thyroid function. Due to the higher prevalence of infection in patients with HC, one can hypothesize that children with this condition are more susceptible to H. pylori infection and once infected, have greater difficulty in absorption of levothyroxine. Finally, it is sensible to assume that isolated doses of TSH, FT4 and FT3 are not sufficient to determine or not if there is participation of infection in the functioning of the thyroid gland. Cohort studies to monitor thyroid function in serial blood dosage as well as studies evaluating the effect of H. pylori eradication are needed to increase knowledge about the involvement of H. pylori infection on thyroid function.