Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cause of the amenorrhea that occurs in patients with hyperprolactinemia is unknown. The involvement of endogenous opioid peptides in the inhibition of GnRH release as a central factor leading to the hypogonadotropic state has been recently described. This study analyzed the LH response to opiate receptor blockade by naloxone (4 mg, iv) in groups of subjects with amenorrhea due to hyperprolactinemia of different etiologies. Patients presenting with a PRL-secreting pituitary adenoma (n = 7), idiopathic hyperprolactinemia (n = 9), or hyperprolactinemia during pharmacological treatment for schizophrenia (n = 5) were studied. Furthermore, to evaluate whether high circulating PRL levels influence the activity of the opioid system after the menopause, a group of seven postmenopausal subjects was tested before and 1 week after the administration of metoclopramide (10 mg, three times a day), a dopamine receptor antagonist. Normal premenopausal women (n = 6) served as controls. Naloxone significantly increased plasma LH levels in both prolactinoma and idiopathic hyperprolactinemic patients (P less than 0.01 vs. basal and placebo). In neither of those groups was a significant correlation found between the plasma LH response to naloxone and basal plasma PRL levels. In contrast to pathological hyperprolactinemia, blockade of opiate receptors did not significantly change LH secretion in either amenorrheic women with pharmacologically induced hyperprolactinemia or postmenopausal women. These results suggest that the effect of hyperprolactinemia on opioid modulation of LH secretion is related to the nature of the hyperprolactinemic state, supporting the existence of increased opioid inhibition of LH levels in pathological hyperprolactinemia.
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PMID:Differences in the opioid control of luteinizing hormone secretion between pathological and iatrogenic hyperprolactinemic states. 288 Aug 62

Reported herein is the possible interaction between two drugs used to treat a man with a large prolactin-secreting pituitary adenoma. The patient had a long history of schizophrenia that was treated with many different medications, including phenothiazines. Evaluation of progressive lethargy led to the discovery of a large parasellar tumor and a prolactin level of 7,981 ng/ml. His serum prolactin level fell to the 400 ng/ml range during bromocriptine therapy but rose whenever the antipsychotic thioridazine was added to his regimen. A marked deterioration of his visual fields was noted after 3 months' therapy with both drugs, and this abnormality resolved five days after the thioridazine was stopped. The use of dopamine antagonists such as thioridazine in patients with prolactinoma may interfere with bromocriptine's action, resulting in potentially serious complications.
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PMID:Interactions between thioridazine and bromocriptine in a patient with a prolactin-secreting pituitary adenoma. 672 Jul 32

In humans, behavioral dopamine supersensitivity occurs in schizophrenia and in Parkinson's disease. In animals, behavioral dopamine supersensitivity is consistently associated with increased dopamine D2(High) receptors in homogenized striata in vitro. Because D2(High) receptors have not yet been detected in intact cells, we used [(3)H]domperidone to detect D2(High) sites in intact rat anterior pituitary adenoma culture cells. Although [(3)H]raclopride and [(3)H]spiperone did not detect D2(High) receptors in intact cells or in rat fresh striatal slices, [(3)H]domperidone readily detected D2(High) receptors, warranting an in vivo search for D2(High) variations in human diseases.
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PMID:Dopamine D2(High) receptors on intact cells. 1824 Oct 49