Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned?
Autor(a) principal: | |
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Data de Publicação: | 2005 |
Outros Autores: | , , , |
Tipo de documento: | Relatório |
Idioma: | eng |
Título da fonte: | Arquivos Brasileiros de Endocrinologia & Metabologia (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302005000300021 |
Resumo: | Long term use of high doses of estrogen and the presence of chronic hyperprolactinemia may, at least in the rat, provoke lesions in the tuberoinfundibular dopaminergic (TIDA) neurons responsible for the control of prolactin (Prl) secretion. This occurrence, which is not yet well documented in humans, may have taken place in a patient on chronic oral hormonal contraceptive (OC) treatment who was seen for primary hypothyroidism, hyperprolactinemia and a pituitary mass. After thyroid hormone replacement, OC withdrawn and bromocriptine treatment, this patient could not maintain normal Prl levels, unless continuously treated with a dopaminergic agonist even when MRI was indicative of a normal situation. Function of TIDA neurons was investigated by TRH test (200µg IV) performed before and after treatment with 25mg carbidopa plus 250mg L-dopa every 4 hours for one day. Basal TSH was normal (3.9µU/mL) whereas basal Prl was high (67.5 ng/mL); both TSH and Prl levels appropriately increased after TRH: peaks 31.8µU/mL and 157.8 ng/mL, respectively. After treatment with carbidopa/L-dopa, basal TSH (1.6µU/mL) and Prl (34ng/mL) decreased and the response to TRH was partially blocked (10.3µU/mL and 61ng/mL, respectively). In spite of a normal response, we discuss the possibility that the persistence of hyperprolactinemia is due to lesion of the TIDA neurons produced by the long term use of high doses of estrogens and by the presence of chronic hyperprolactinemia. |
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Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned?HypothyroidismHyperprolactinemiaEstrogenDopaminePituitaryLong term use of high doses of estrogen and the presence of chronic hyperprolactinemia may, at least in the rat, provoke lesions in the tuberoinfundibular dopaminergic (TIDA) neurons responsible for the control of prolactin (Prl) secretion. This occurrence, which is not yet well documented in humans, may have taken place in a patient on chronic oral hormonal contraceptive (OC) treatment who was seen for primary hypothyroidism, hyperprolactinemia and a pituitary mass. After thyroid hormone replacement, OC withdrawn and bromocriptine treatment, this patient could not maintain normal Prl levels, unless continuously treated with a dopaminergic agonist even when MRI was indicative of a normal situation. Function of TIDA neurons was investigated by TRH test (200µg IV) performed before and after treatment with 25mg carbidopa plus 250mg L-dopa every 4 hours for one day. Basal TSH was normal (3.9µU/mL) whereas basal Prl was high (67.5 ng/mL); both TSH and Prl levels appropriately increased after TRH: peaks 31.8µU/mL and 157.8 ng/mL, respectively. After treatment with carbidopa/L-dopa, basal TSH (1.6µU/mL) and Prl (34ng/mL) decreased and the response to TRH was partially blocked (10.3µU/mL and 61ng/mL, respectively). In spite of a normal response, we discuss the possibility that the persistence of hyperprolactinemia is due to lesion of the TIDA neurons produced by the long term use of high doses of estrogens and by the presence of chronic hyperprolactinemia.Sociedade Brasileira de Endocrinologia e Metabologia2005-06-01info:eu-repo/semantics/reportinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302005000300021Arquivos Brasileiros de Endocrinologia & Metabologia v.49 n.3 2005reponame:Arquivos Brasileiros de Endocrinologia & Metabologia (Online)instname:Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)instacron:SBEM10.1590/S0004-27302005000300021info:eu-repo/semantics/openAccessCasulari,Luiz AugustoCelotti,FábioNaves,Luciana A.Domingues,LucíliaPapadia,Carlaeng2005-10-13T00:00:00Zoai:scielo:S0004-27302005000300021Revistahttps://www.aem-sbem.com/ONGhttps://old.scielo.br/oai/scielo-oai.php||abem-editoria@endocrino.org.br1677-94870004-2730opendoar:2005-10-13T00:00Arquivos Brasileiros de Endocrinologia & Metabologia (Online) - Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)false |
dc.title.none.fl_str_mv |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? |
title |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? |
spellingShingle |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? Casulari,Luiz Augusto Hypothyroidism Hyperprolactinemia Estrogen Dopamine Pituitary |
title_short |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? |
title_full |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? |
title_fullStr |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? |
title_full_unstemmed |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? |
title_sort |
Persistence of hyperprolactinemia after treatment of primary hypothyroidism and withdrawal of long term use of estrogen: are the tuberoinfundibular dopaminergic neurons permanently lesioned? |
author |
Casulari,Luiz Augusto |
author_facet |
Casulari,Luiz Augusto Celotti,Fábio Naves,Luciana A. Domingues,Lucília Papadia,Carla |
author_role |
author |
author2 |
Celotti,Fábio Naves,Luciana A. Domingues,Lucília Papadia,Carla |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Casulari,Luiz Augusto Celotti,Fábio Naves,Luciana A. Domingues,Lucília Papadia,Carla |
dc.subject.por.fl_str_mv |
Hypothyroidism Hyperprolactinemia Estrogen Dopamine Pituitary |
topic |
Hypothyroidism Hyperprolactinemia Estrogen Dopamine Pituitary |
description |
Long term use of high doses of estrogen and the presence of chronic hyperprolactinemia may, at least in the rat, provoke lesions in the tuberoinfundibular dopaminergic (TIDA) neurons responsible for the control of prolactin (Prl) secretion. This occurrence, which is not yet well documented in humans, may have taken place in a patient on chronic oral hormonal contraceptive (OC) treatment who was seen for primary hypothyroidism, hyperprolactinemia and a pituitary mass. After thyroid hormone replacement, OC withdrawn and bromocriptine treatment, this patient could not maintain normal Prl levels, unless continuously treated with a dopaminergic agonist even when MRI was indicative of a normal situation. Function of TIDA neurons was investigated by TRH test (200µg IV) performed before and after treatment with 25mg carbidopa plus 250mg L-dopa every 4 hours for one day. Basal TSH was normal (3.9µU/mL) whereas basal Prl was high (67.5 ng/mL); both TSH and Prl levels appropriately increased after TRH: peaks 31.8µU/mL and 157.8 ng/mL, respectively. After treatment with carbidopa/L-dopa, basal TSH (1.6µU/mL) and Prl (34ng/mL) decreased and the response to TRH was partially blocked (10.3µU/mL and 61ng/mL, respectively). In spite of a normal response, we discuss the possibility that the persistence of hyperprolactinemia is due to lesion of the TIDA neurons produced by the long term use of high doses of estrogens and by the presence of chronic hyperprolactinemia. |
publishDate |
2005 |
dc.date.none.fl_str_mv |
2005-06-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/report |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
report |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302005000300021 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302005000300021 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0004-27302005000300021 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Endocrinologia e Metabologia |
publisher.none.fl_str_mv |
Sociedade Brasileira de Endocrinologia e Metabologia |
dc.source.none.fl_str_mv |
Arquivos Brasileiros de Endocrinologia & Metabologia v.49 n.3 2005 reponame:Arquivos Brasileiros de Endocrinologia & Metabologia (Online) instname:Sociedade Brasileira de Endocrinologia e Metabologia (SBEM) instacron:SBEM |
instname_str |
Sociedade Brasileira de Endocrinologia e Metabologia (SBEM) |
instacron_str |
SBEM |
institution |
SBEM |
reponame_str |
Arquivos Brasileiros de Endocrinologia & Metabologia (Online) |
collection |
Arquivos Brasileiros de Endocrinologia & Metabologia (Online) |
repository.name.fl_str_mv |
Arquivos Brasileiros de Endocrinologia & Metabologia (Online) - Sociedade Brasileira de Endocrinologia e Metabologia (SBEM) |
repository.mail.fl_str_mv |
||abem-editoria@endocrino.org.br |
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1754734807976247296 |