Polyglandulární aktivace autoimunity jako projev subklinických endokrinopatií
[Polyglandular activation of autoimmnunity as a manifestation of subclinical endocrinopathies]
Jazyk čeština Země Česko Médium print
Typ dokumentu anglický abstrakt, časopisecké články
PubMed
17419310
- MeSH
- autoimunitní polyglandulární syndromy imunologie MeSH
- autoimunitní tyreoiditida imunologie MeSH
- autoprotilátky biosyntéza MeSH
- lidé středního věku MeSH
- lidé MeSH
- nadledviny imunologie MeSH
- ovarium imunologie MeSH
- testis imunologie MeSH
- únava etiologie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- anglický abstrakt MeSH
- časopisecké články MeSH
- Názvy látek
- autoprotilátky MeSH
BACKGROUND: Autoimmune thyropathies belong to the most frequently occurring autoimmune endocrinopathies. Autoimmune thyropathies occur either independently or linked to known polyglandular syndromes of type I-III. METHODS AND RESULTS: During the last decade, we observed a group of patients with autoimmune thyroiditis, in which autoimmune endocrinopathies were mutually associated and named the symptoms of this group "polyglandular activation of autoimmunity". The frequency of the occurrence of autoantibodies against other endocrine organs in this group was determined and the most frequent was the occurrence of the autoantibodies against steroid producing cells - anti-ovary 28 %, anti-adrenal 23 %, anti-testes 12 %. Considering the most frequent occurrence of autoantibodies against steroid producing cells, attention has been paid namely to patients with autoimmune thyroiditis and a concurrent occurrence of anti-adrenal autoantibodies. In the foreground of the clinical picture of these patients were dysregulations on the metabolic and circulation levels together with symptoms of discomfort (subfebrile condition, arthralgia and fatigue). Heavy fatigue of these patients was linked to the changes of levels and mutual ratio of melatonin and serotonin and regarding autoantibodies, mainly autoantibodies against steroid producing cells, namely against the particular cells of the layers of adrenal cortex played a role. CONCLUSIONS: The presence of autoantibodies influenced also the functional response, namely the ACTH/cortisol ratio. Autoantibodies detected were not anti-21-hydroxylase autoantibodies, typical for autoimmune polyglandular syndrome II, but antibodies against antigens of other molecular weight.