monoiodotyrosine has been researched along with Pituitary-Neoplasms* in 4 studies
4 other study(ies) available for monoiodotyrosine and Pituitary-Neoplasms
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Follow-up of prolactin levels in long-term oestrogen-treated male-to-female transsexuals with regard to prolactinoma induction.
As in laboratory animals, long-term oestrogen treatment in the human male might induce prolactinomas. We here report on PRL levels in 142 male-to-female transsexuals, treated with 100 mg cyproterone acetate and 100 micrograms ethinyloestradiol per day for 6-108 months (median 52). PRL levels varied markedly between individuals. No relation with age and length of treatment period was found. In 42 subjects in whom PRL levels were followed serially, a slight fall was measured after 12-15 months of treatment. Galactorrhoea, present in 10 of 142 subjects, was unrelated to PRL levels. In 34 subjects in whom PRL levels were measured during treatment and 3 weeks after withdrawal, PRL levels fell significantly. Dopamine in doses of 0.1 microgram/kg/min and 1.0 microgram/kg/min was administered to six subjects with PRL levels greater than 1000 mU/l and six subjects with PRL levels less than 500 mU/l. No difference in the percentage decrease of PRL levels was found between these two groups. However, administration of monoiodotyrosine, an inhibitor of central dopamine synthesis, to these two groups, induced a significantly smaller release of PRL (expressed as percentage change) in subjects with PRL greater than 1000 mU/l than in those with PRL less than 500 mU/1 possibly indicating a loss of control of central dopaminergic regulation. These findings suggest that the risk of inducing prolactinomas through cross-gender hormone treatment is likely to be small. Topics: Adolescent; Adult; Cyproterone; Cyproterone Acetate; Dopamine; Ethinyl Estradiol; Female; Galactorrhea; Humans; Male; Middle Aged; Monoiodotyrosine; Pituitary Neoplasms; Pregnancy; Prolactin; Time Factors; Transsexualism | 1985 |
Role of defective dopaminergic inhibition of prolactin secretion in the pathogenesis of prolactinoma.
Prolactinomas pose an increasingly frequent therapeutic dilemma for the clinician. The neurosurgeon caring for the prolactinoma-bearing patient must stay abreast of the most current basic research concerning the pathogenesis of these often difficult tumors. A fascinating and dynamic line of research involves the possibility that prolactinomas arise secondary to a flaw in the normally inhibitory dopaminergic neurohypophyseal axis. The details of this hypothesis are presented, the current literature surrounding this topic is reviewed, and a brief synthesis of the available theoretical models of prolactinoma pathogenesis is provided. Topics: Autoantibodies; Carbidopa; Dopamine; Female; Humans; Hypothalamo-Hypophyseal System; Levodopa; Metoclopramide; Monoiodotyrosine; Neural Inhibition; Nomifensine; Pituitary Neoplasms; Prolactin; Radioligand Assay; Receptors, Dopamine | 1985 |
Prolactin and thyrotropin response to blockade of dopamine synthesis by monoiodotyrosine in subjects with postpartum and pathological hyperprolactinemia.
To better understand the state of dopamine (DA) neurotransmission in the tuberoinfundibular DA system (TIDA), monoiodotyrosine (3-iodo-L-tyrosine, MIT), a potent inhibitor of DA synthesis, was acutely administered to 8 normal women, 7 postpartum women, 8 women with pathological hyperprolactinemia and 5 women after successful removal of a prolactinoma. The effects on plasma prolactin (PRL) and thyrotropin (TSH) were compared to those induced in the same subjects by the DA receptor antagonist domperidone (DOM). MIT (1 gpo) and DOM (10 mg iv) induced qualitatively similar hormonal responses, although the PRL- and TSH-releasing effects of DOM were always greater than those of MIT. In control subjects, MIT treatment induced a consistent rise in plasma PRL (peak increment 45.2 +/- 13 ng/ml at 120 min); in the same subjects DOM induced a prompter and higher PRL response, (peak increment 147.8 +/- 26 ng/ml at 30 min). MIT failed to alter plasma TSH levels, while DOM induced a significant rise in plasma TSH. In postpartum women MIT induced a prompter and higher PRL rise than that occurring in controls (peak increment 180.3 +/- 20 ng/ml at 90 min), though also in this instance DOM proved to be a more potent PRL releaser (peak increment 345.7 +/- 88 ng/ml at 30 min) than MIT. MIT was unable to stimulate TSH secretion, while DOM induced a significant rise in plasma TSH. In women with pathological hyperprolactinemia MIT failed to alter baseline PRL levels while DOM slightly increased them (peak increment 14.7 +/- 3 ng/ml at 30 min).(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Adenoma; Adult; Animals; Binding, Competitive; Domperidone; Dopamine; Female; Humans; In Vitro Techniques; Male; Monoiodotyrosine; Pituitary Gland, Anterior; Pituitary Neoplasms; Postpartum Period; Pregnancy; Prolactin; Rats; Rats, Inbred Strains; Receptors, Dopamine; Thyrotropin | 1985 |
Prolactin response to dopamine synthesis inhibition using monoiodotyrosine in subjects on oral contraceptives and patients with pathological hyperprolactinemia.
Topics: Adolescent; Adult; Contraceptives, Oral; Contraceptives, Oral, Combined; Dopamine; Dopamine Antagonists; Female; Humans; Monoiodotyrosine; Pituitary Neoplasms; Prolactin | 1983 |