Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In eight subjects with Parkinson's disease under an optimal daily dose of L-dopa, acute administration of MIF-I (200 mg i.v.) did not ameliorate either the total disability score or the intellectual test PM 38 when evaluated in comparison with the effect induced by acute administration of a placebo. Also concomitant evaluation of the effect of MIF-I on the secretion of anterior pituitary hormones which are under dopaminergic control i.e., growth hormone and prolactin, did not reveal any potentiation of the L-dopa-induced stimulus.
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PMID:Failure of MIF-I to affect behavioral responses in patients with Parkinson's diseases under L-dopa therapy. 3 8

As assessed by changes of prolactin secretion in rat anterior pituitary cells in culture, estrogens can exert a potent antidopaminergic activity at the pituitary level. Androgens and progestins can reverse the effect of estrogens. An interaction of sex steroids at the hypothalamic level on dopamine release and at the pituitary level on dopamine action could also be demonstrated in vivo. Moreover, estrogens exert a similar antidopaminergic activity at the striatal level on dopaminergic agent-induced acetylcholine accumulation. The observation of a modulation by estrogens of the symptoms of Parkinson's disease and tardive dyskinesias suggests the implication of sex steroids in neurology, psychiatry and behavior.
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PMID:Influence of estrogens on tuberoinfundibular and striatal dopaminergic systems in the rat. 55 44

In the course of a clinical trial with 2alpha-bromoergocryptin in Parkinson's disease, the serum levels of several pituitary hormones have been studied in the assumption that the drug active on nigro-striatal dopaminergic system might also interfere with hypothalamus-protuberantial neurotransmission, and have effects on the function of the pituitary. No changes in serum levels of FSH, LH, STH and TSH were detected for every dose of the drug employed. Only prolactin serum levels diminished since the beginning of the treatment, the decrease being significant (p less than 0.05 and p less than 0.01). This effect on prolactin does not change in the dose range considered. Clinical improvement was observed for doses of drugs above 15 mg/day, whereas the effect on prolactin secretion occurred with the dose of 7.5 mg/day.
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PMID:Changes in pituitary hormones serum levels in bromocryptine-treated parkinsonian patients. 57 93

Lergotrile, an ergot alkaloid, has been shown to be effective in treating disorders associated with elevated serum prolactin levels (e.g., galactorrhea-amenorrhea). Lergotrile has also been found to be a potent dopaminergic agonist and thus to be effective in Parkinson's disease. This study describes the physiologic disposition of lergotrile after administration to human volunteers. N-14CH3-lergotrile was rapidly absorbed from the gastrointestinal tract. Lergotrile was detected at low concentrations in plasma when subjects received large doses over extended periods of time. The major portion of radioactivity in plasma was attributed to the presence of circulating metabolites of lergotrile. Lergotrile metabolities were eliminated in the feces (ca. 60%), urine (ca. 20%), and breath (ca. 7% as 14CO2). A metabolite in feces was identified as 13-OH-lergotrile (up to 30% of the dose). A metabolite in urine was formed by conversion of the C8-acetonitrile group of lergotrile to a carboxyl group (about 10% of the dose). The presence of 14CO2 in the expired air after administering N-14C-methyl-lergotrile indicated that the drug was N-demethylated to form norlergotrile.
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PMID:Physiologic disposition of lergotrile. 62 32

Bromocriptine was used for Parkinson's disease in 15 patients for 20 weeks. Immunoreactive plasma lutrophin (LH), follitrophin (FSH), prolactin, and somatotrophin (GH, growth hormone) concentrations were analysed before and during the treatment. Plasma prolactin levels were very markedly reduced during treatment. Plasma lutrophin levels were increased significantly in female patients, but not in male patients. No changes were noticed in follitrophin levels, but plasma somatotrophin levels were reduced during treatment. No correlations were found between the degree of clinical response and changes in plasma gonadotrophin and somatotrophin. This suggests that the effects of bromocriptine on extrapyramidal and neuroendocrine dopaminergic neurones are unrelated. We suggest careful and frequent controls of neuroendocrine secretion patterns in patients with Parkinson's disease who are treated with high doses of dopamine receptor stimulators, since the response of some pituitary hormones to bromocriptine are very marked.
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PMID:Plasma pituitary hormones in patients with Parkinson's disease treated with bromocriptine. 65 Feb 5

A case history of a patient who developed mammary cancer (T1N1bMo) after 5 1/2 years of continuous treatment with Levodopa for Parkinson's disease is presented. The prolactin inhibition by the Levodopa was verified, and the clinical and mammographic growth, the doubling time, and the labeling index of the tumor were determined. The results were not significantly different than those obtained from patients with breast cancer not under treatment with Levodopa. The rapid growth and evolution of this tumor suggests that prolactin does not have an inducer or promoter effect in mammary cancer.
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PMID:Breast cancer in a patient under levodopa treatment. 67 56

On the basis of a reassessment of the aetiopathogenetic problem and the neuroendocrine implications, the therapeutic effectiveness of a prolactin inhibitor, 2-alpha-Br-ergocryptine (CB 154), in Parkinson's disease is assessed. Five patients were treated for a total of two weeks using doses between 10 and 15 mg/die. CB 154 was found to act as a dopaminergic receptor agonist at nigro-striatal level, considerably improving tremor and rigidity and to a lesser extent bradykinesia and total disability.
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PMID:[Neuroendocrine aspects of Parkinson's disease. Therapeutic/effect of a prolactin inhibitor]. 103 12

Serum prolactin (HPR) levels are influenced by waking and sleep states, as reflected by surges in serum concentrations during daytime naps and nocturnal sleep. Other physiological causes of hyperprolactinemia include sexual activity, pregnancy, and lactation. Drugs may stimulate or inhibit HPR secretion. Pathological causes for HPR secretion include destructive lesions of the hypothalamus, prolactin-secreting neoplasms of the pituitary gland, lesions of the spinal cord, and occasionally Parkinson's disease. The most predictable postictal changes are increased serum cortisol levels and hyperprolactinemia. Serum HPR rises after virtually all generalized tonic-clonic seizures, most complex partial seizures, and some simple partial seizures. Absence and myoclonic seizures do not affect serum HPR levels. Repeated epileptic seizures and electroconvulsive therapy treatments produce successively less marked rises in serum HPR. The postictal elevation of serum cortisol has a longer latency than for HPR and follows an earlier rise in serum ACTH. Other postictal hormonal changes are much more variable. Because of the normal diurnal variation in serum cortisol levels and the relative delay in the postictal elevation of serum cortisol, HPR is more useful as a diagnostic measure of epileptic seizures. This application of HPR requires an understanding of other factors that influence serum HPR and the use of baseline serum HPR levels for comparison. HPR data must be correlated with behavioral and electroencephalographic events.
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PMID:The effect of seizures on hormones. 165 82

The bromocriptine-TRH test was performed in 11 patients with advanced Parkinson's disease and in 10 control subjects. Seven patients were receiving treatment with Levo-DOPA, which was discontinued 12 h prior to the test. Basal prolactin levels were 5.88 ng/ml in treated and 18.22 ng/ml in untreated patients as compared to 9.68 mg/ml in controls. Bromocriptine induced a similar reduction of about 60% in prolactin levels in all groups (3.28, 11.5 and 5.95 ng/ml, respectively). After TRH, prolactin levels increased to 13.8 ng/ml in controls and 15.2 ng/ml in patients treated with levo-DOPA. Untreated patients remained with prolactin below basal levels (11.6 ng/ml). We postulate that low basal levels of prolactin in patients treated with levo-DOPA reveal a residual suppressing effect of the drug. The sharp increase after TRH is related to a significant dopaminergic hypofunction as evidenced by clinical findings. A high sensitivity of dopaminergic receptors in the anterior hypofisis is suggested as an explanation for the findings of the test in the untreated patients.
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PMID:[Patients with Parkinson disease: functional analysis of dopamine receptors by bromocriptine- thyrotropin-releasing hormone test]. 184 16

Plasma profiles of prolactin, growth hormone, adrenocorticotropic hormone (ACTH) and cortisol were evaluated in a group of untreated patients with idiopathic Parkinson's disease and a group of healthy age-matched controls. Plasma integrated concentrations of all hormones except prolactin were significantly lower in the patients as compared with the controls; however, prolactin nocturnal peak concentration was significantly elevated in the patients; nocturnal growth hormone levels were significantly reduced in the Parkinson group; ACTH and cortisol plasma concentrations were also consistently lower during most of the day in the patients with Parkinson's disease. These data confirm the presence of a hypothalamic disturbance in patients with idiopathic Parkinson's disease, which can affect pituitary function.
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PMID:Plasma profiles of adrenocorticotropic hormone, cortisol, growth hormone and prolactin in patients with untreated Parkinson's disease. 185 13


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