title: Pyridostigmine and metoclopramide do not restore the TSH response to TRH inhibited by L-thyroxine treatment in children with goiter.
abstract: To define the role of somatostatin and dopamine in TSH suppression induced by L-thyroxine, 16 children (12 F, 4 M) on suppressive doses of L-thyroxine (3-4 microg/kg/day) for endemic goiter were studied. Firstly a conventional TRH test was performed in all subjects, in order to evaluate TSH, PRL and GH (basal study). A week later a second TRH test was carried out; one hour before the test, however, group A (9 patients) was given 60 mg pyridostigmine bromide po (pyridostigmine study) and group B (7 patients) 10 mg metoclopramide po (metoclopramide study). In the basal study, TSH was suppressed in both groups and levels did not increase following TRH administration, while PRL increased significantly and GH levels remained stable. In the pyridostigmine study, TSH levels did not increase following TRH administration, while PRL and GH levels were both significantly raised. In the metoclopramide study, TSH and GH levels were not raised following TRH administration, while a significantly greater increase of PRL was observed. In conclusion, suppressive doses of L-thyroxine inhibit the TSH response to TRH, while they do not seem to affect GH and PRL secretion. Somatostatin and/or dopamine do not seem to play a significant role in the L-thyroxine-induced TSH suppression.
authors.affiliation: Pediatric Department, Regional Hospital of Bolzano, Italy. G.Radetti@ntt.it
authors.forename: G
authors.initials: G
authors.lastname: Radetti
authors.forename: S
authors.initials: S
authors.lastname: Bernasconi
authors.forename: M
authors.initials: M
authors.lastname: Bozzola
authors.forename: C
authors.initials: C
authors.lastname: Volta
authors.forename: G
authors.initials: G
authors.lastname: Tonini
authors.forename: L
authors.initials: L
authors.lastname: Gentili
authors.forename: F
authors.initials: F
authors.lastname: Rigon
mesh_terms: D000293:Adolescent; D002648:Child; D018679:Cholinergic Agonists / Q000494:pharmacology*; D004298:Dopamine / Q000502:physiology; D018492:Dopamine Antagonists / Q000494:pharmacology*; D005260:Female; D006042:Goiter / Q000188:drug therapy*; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D007700:Kinetics; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology; D011388:Prolactin / Q000097:blood; D011729:Pyridostigmine Bromide / Q000494:pharmacology; D013004:Somatostatin / Q000502:physiology; D013972:Thyrotropin / Q000097:blood*; D013973:Thyrotropin-Releasing Hormone; D013974:Thyroxine / Q000097:blood / Q000494:pharmacology* / Q000627:therapeutic use; D014284:Triiodothyronine / Q000097:blood
chemical_list: D018679:Cholinergic Agonists; D018492:Dopamine Antagonists; D014284:Triiodothyronine; D019382:Human Growth Hormone; D013004:Somatostatin; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D013972:Thyrotropin; D011729:Pyridostigmine Bromide; D008787:Metoclopramide; D013974:Thyroxine; D004298:Dopamine