| pubmed-article:3291425 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3291425 | lifeskim:mentions | umls-concept:C0004364 | lld:lifeskim |
| pubmed-article:3291425 | lifeskim:mentions | umls-concept:C0040128 | lld:lifeskim |
| pubmed-article:3291425 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:3291425 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:3291425 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:3291425 | pubmed:dateCreated | 1988-8-1 | lld:pubmed |
| pubmed-article:3291425 | pubmed:abstractText | As for other autoimmune diseases it is discussed also for immune hyperthyroidism (Basedow's disease) and immune thyroiditis, whether factors such as stress and infections with viruses and bacteria may lead to a disturbance of the immune tolerance in persons genetically predisposed. In Basedow's disease antibodies against the TSH-receptor cause an uncontrolled stimulation of the function of the thyroid gland. One year after the end of an antithyroid drug treatment, e.g. with thiamazol, a recidivation rate of circa 50% develops. There are no criteria which may predict the clinical development of an individual after the end of the treatment with a sufficient reliability. This applies particularly also to the measurement of the TSH receptor antibodies and the suppression test at the end of treatment (Alexander's test). According to the experiences of author moreover patients with small and large goitres and with different degrees of Basedow's orbitopathy do not show any difference in the frequency of the recidivations. In the immune thyroiditis a series of antibody-dependent and lymphocyte-dependent processes may lead to a decreased function of the thyroid gland. This includes the interaction of antibodies with the complement system or with the killer cells (ADCC), the direct decomposition of the cells of the thyroid gland by certain subgroups of lymphocytes and the occurrence of blocking antibodies against the TSH receptor. In patients in whom antibodies were made evident may develop a hypothyroidism. But many patients also for ever remain euthyroid. These observations and experimental data suggest that the cell of the thyroid gland also itself must be "susceptible" to the destruction by the antibodies and lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
| pubmed-article:3291425 | pubmed:language | ger | lld:pubmed |
| pubmed-article:3291425 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3291425 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:3291425 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3291425 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3291425 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3291425 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:3291425 | pubmed:issn | 0044-2542 | lld:pubmed |
| pubmed-article:3291425 | pubmed:author | pubmed-author:SchleusenerHH | lld:pubmed |
| pubmed-article:3291425 | pubmed:author | pubmed-author:KotullaPP | lld:pubmed |
| pubmed-article:3291425 | pubmed:author | pubmed-author:FinkeRR | lld:pubmed |
| pubmed-article:3291425 | pubmed:author | pubmed-author:BognerUU | lld:pubmed |
| pubmed-article:3291425 | pubmed:author | pubmed-author:SchwanderJJ | lld:pubmed |
| pubmed-article:3291425 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3291425 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:3291425 | pubmed:volume | 43 | lld:pubmed |
| pubmed-article:3291425 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3291425 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3291425 | pubmed:pagination | 133-9 | lld:pubmed |
| pubmed-article:3291425 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:3291425 | pubmed:meshHeading | pubmed-meshheading:3291425-... | lld:pubmed |
| pubmed-article:3291425 | pubmed:meshHeading | pubmed-meshheading:3291425-... | lld:pubmed |
| pubmed-article:3291425 | pubmed:meshHeading | pubmed-meshheading:3291425-... | lld:pubmed |
| pubmed-article:3291425 | pubmed:meshHeading | pubmed-meshheading:3291425-... | lld:pubmed |
| pubmed-article:3291425 | pubmed:meshHeading | pubmed-meshheading:3291425-... | lld:pubmed |
| pubmed-article:3291425 | pubmed:meshHeading | pubmed-meshheading:3291425-... | lld:pubmed |
| pubmed-article:3291425 | pubmed:meshHeading | pubmed-meshheading:3291425-... | lld:pubmed |
| pubmed-article:3291425 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:3291425 | pubmed:articleTitle | [Etiology and pathogenesis of autoimmune diseases of the thyroid gland]. | lld:pubmed |
| pubmed-article:3291425 | pubmed:affiliation | Endokrinologischen Abteilung, Freie Universität Berlin. | lld:pubmed |
| pubmed-article:3291425 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3291425 | pubmed:publicationType | English Abstract | lld:pubmed |
| pubmed-article:3291425 | pubmed:publicationType | Review | lld:pubmed |
