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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0020550,
umls-concept:C0025853,
umls-concept:C0039082,
umls-concept:C0040160,
umls-concept:C0231491,
umls-concept:C0301625,
umls-concept:C0439611,
umls-concept:C0442027,
umls-concept:C0684224,
umls-concept:C0871261,
umls-concept:C1280500,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1709630,
umls-concept:C1955398,
umls-concept:C2911692
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pubmed:issue |
49
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pubmed:dateCreated |
1981-3-27
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pubmed:abstractText |
The TSH response to exogenous TRH may be diminished or absent not only on overt hyperthyroidism but also in other situations, e.g. obesity, old age, multinodular goiter and depression. To elucidate the possible role of dopaminergic control of the TSH response to TRH in such patients, the oral TRH test (40 mg) was performed with and without simultaneous administration of metoclopramide (10 mg i.v.) in 20 patients known to have diminished or absent response to oral TRH (delta TSH < 1.0 mU/l). All patients had euthyroid basal levels of FT4-index and T3, and may thus be assumed to have "preclinical hyperthyroidism" (TSH suppression syndrome). In 11 patients the history suggested they were free of symptoms of mental depression, while 9 patients were considered by two independent examiners to have various degrees of depression. The TSH response to TRH in depressive patients was significantly increased when the dopamine-receptor-blocker metoclopramide (MCL) wad added. The delta TSH rose from 0.6 +/- 0.3 mU/l (SEM) without MCL to 8.8 +/- 1.8 mU/l with MCL (p < 0.002). In contrast, MCL failed to enhance the TSH response in non-depressive patients: the delta TSH was 0.7 +/- 0.3 mU/l without MCL, and with MCL 2.1 +/- 0.9 mU/l (n.s.). Thus the dopaminergic system appears to play a major role in modulating the sensitivity of the pituitary to TRH stimulation. In clinically doubtful situations, the combined metoclopramide-TRH test may be used to distinguish patients with a diminished or absent TSH response as a consequence of depression (central dopaminergic suppression) from patients with "preclinical hyperthyroidism" where the TSH response is suppressed by feedback control of TSH by thyroid hormones (thyroid autonomy).
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pubmed:language |
ger
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0036-7672
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
6
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pubmed:volume |
110
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1877-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:6779375-Adult,
pubmed-meshheading:6779375-Aged,
pubmed-meshheading:6779375-Feedback,
pubmed-meshheading:6779375-Female,
pubmed-meshheading:6779375-Humans,
pubmed-meshheading:6779375-Hyperthyroidism,
pubmed-meshheading:6779375-Male,
pubmed-meshheading:6779375-Metoclopramide,
pubmed-meshheading:6779375-Middle Aged,
pubmed-meshheading:6779375-Thyrotropin,
pubmed-meshheading:6779375-Thyrotropin-Releasing Hormone
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pubmed:year |
1980
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pubmed:articleTitle |
[Effect of the dopamin antagonist metoclopramide on the TSH response after oral TRH in the TSH suppression syndrome ("preclinical hyperthyroidism"). Preliminary report].
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pubmed:publicationType |
Journal Article,
English Abstract,
Research Support, Non-U.S. Gov't
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