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)

We measured regional cerebral blood flow (CBF) with single photon emission computed tomography and Xenon 133 in 8 patients with Parkinson's disease (stages I or II) before and after acute oral administration of 10 mg bromocriptine. Moreover, Columbia University Rating scale and neuropsychological tests were assessed before and after drug administration. Bromocriptine induced a significant (p less than 0.01) increase in CBF (+ 12 p. 100) in all the regions studied unrelated to pCO2 variations. The Columbia motor scale score decreased (by 16 p. 100) whereas those on the neuropsychological tests did not vary. There was no relationship between the improvement in motor performance and the increase in CBF. The results suggest that the effect of bromocriptine on CBF is not mediated by an action on the major dopaminergic pathways in the brain but rather by a direct effect on dopaminergic receptors located on cerebral vessels.
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PMID:[Effect of bromocriptine on cerebral blood flow in Parkinson's disease]. 342 Mar 54

This paper reviews the safety data on bromocriptine administration for 1 to 10 years at daily doses of 1.25 to 80 mg in over 1100 patients with pituitary hormone overproduction (mainly from prolactinomas and growth-hormone producing adenomas), at daily doses of 3.75 to 170 mg in over 700 patients with Parkinson's disease, and at daily doses of 2.5 to 20 mg in 28 patients with various other conditions. In addition, information is provided on the safety for mother and child of bromocriptine administered at daily doses of 2.5 to 35 mg throughout gestation (54 pregnancies) or during its later stages (39 pregnancies). The side-effects of long-term bromocriptine treatment are usually no different from those seen during short-term treatment; most of them are relatively benign, and they have been shown in virtually all patients to be reversible. Bromocriptine appears to have no harmful effect on hepatic, renal, haematologic, or cardiac functions. It is considered that a hitherto unknown, severe though rare side-effect of bromocriptine is unlikely to be reported after such long experience.
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PMID:The safety of bromocriptine in long-term use: a review of the literature. 351 79

The etiology, pathophysiology, diagnosis and clinical presentation, and clinical management of Parkinson's disease are reviewed. The cause of Parkinson's disease, a progressive, degenerative neurologic motor disorder, is unknown. Both endogenous and environmental factors appear to play a role. The clinical features of parkinsonism result from a depletion in dopaminergic transmission in the corpus striatum; the dopamine deficiency is caused by a loss of melanin-containing nerve cells within the substantia nigra and locus ceruleus. In the remaining neurons, hyalin-like masses called Lewy bodies increase in number, but the importance of this is unclear. The diagnosis of Parkinson's disease is based on the clinical presentation of the patient, which initially includes sensory complaints of aching pains, paresthesias, numbness, and coldness. As the disease progresses, the four classic symptoms become prominent: tremor, rigidity, bradykinesia, and postural difficulties. Drug therapy is the cornerstone of clinical management of Parkinson's disease, but no treatment has been found that will retard or reverse the disease. Therapy is usually initiated with anticholinergic agents such as biperiden hydrochloride or trihexyphenidyl hydrochloride with or without amantadine. The mainstay of therapy is levodopa, which is used in combination with dopa decarboxylase inhibitors to decrease the peripheral conversion of levodopa to dopamine. Bromocriptine is a dopamine agonist useful in treating Parkinson's disease. Therapy, which must continue for life, eventually becomes less effective or completely ineffective in all patients. Drug therapy has improved greatly the functional ability of patients with Parkinson's disease, but new agents that can extend the length of effective treatment or reverse the disease are needed.
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PMID:Current concepts in clinical therapeutics: Parkinson's disease. 353 Jun 16

Two multigravida patients with no prior psychiatric history were seen with postpartum psychosis, having received bromocriptine for inhibition of lactation. Bromocriptine given in high doses has been associated with psychosis in patients receiving the drug for Parkinson's disease. These cases demonstrate that bromocriptine may cause psychosis even when given in low doses.
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PMID:Postpartum psychosis induced by bromocriptine. 368 55

Bromocriptine (2-Br-alpha-ergocryptine), a partial ergoline derivative, is a dopamine agonist which has been used successfully in the treatment of hyperprolactinemia, acromegaly and Parkinson's disease. The main targets for the action of the drug are the hypothalamic, hypophyseal pathway and the striatum. These regions contain different populations of neurons which interact with each other in a complex way. In order to check the mechanism of these interactions in rats, we administered different neuroactive drugs together with bromocriptine. After a single intraperitoneal injection, bromocriptine concentration in the striatum was 13.1 +/- 2.9 ng/mg protein, and in the hypothalamus 13.9 +/- 0.8 ng/mg protein. The largest increase in the bromocriptine content in the striatum was found after the concomitant administration of naloxone, an opiate receptor blocker (21.2 +/- 2.5 ng/mg protein). The largest increase of the bromocriptine content in the hypothalamus was found after the concomitant injection of methysergide, a serotonin receptor blocker (27.8 +/- 2.6 ng/mg protein). Amantadine, diazepam and haloperidol caused the largest decrease in the two regions. The mechanism of interaction and therapeutic implication of these findings are discussed.
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PMID:Selective regional effect of various neuroactive drugs on bromocriptine concentration in the brain of rats. 381 35

Bromocriptine is an ergopeptine derivative and dopamine agonist that predominantly stimulates the striatal D2 non-adenyl cyclase-linked dopamine receptors. Bromocriptine, unlike other dopamine agonists, has mixed "agonist-antagonist" properties at these receptors. The striatal dopamine receptors exist in two different affinity states: a low and a high affinity state. Bromocriptine, unlike other dopamine agonists, does not differentiate between the low and the high affinity state of the D2 receptors, and bromocriptine does not induce a conformational change in these receptors. Bromocriptine, in low doses, is effective in patients with mild to moderate Parkinson's disease, while bromocriptine in higher doses is needed in patients with advanced disease. Both in low doses and in high doses, bromocriptine combined with levodopa is usually more effective than bromocriptine alone. The efficacy of low dose (5-30 mg/day) and high dose (31-100 mg/day) bromocriptine alone and with levodopa was examined in 27 studies encompassing 790 patients. Forty-six % of the studies were done in a double blind manner. In four studies of 79 patients, low dose bromocriptine (16 mg/day) without levodopa resulted in improvement in 58% of the patients. Only 9% of the patients experienced adverse effects. Most of the patients (63%) and mild or moderate Parkinson disease. In seven studies of 143 patients, high dose bromocriptine (56 mg/day) without levodopa resulted in improvement in 62% of patients, but with 27% having adverse effects. Most of these patients (77%) had mild or moderate disease. Diurnal oscillations in performance, the "wearing off" or "on-off" effect, were not seen during treatment with bromocriptine alone. In nine studies of 201 patients, low dose bromocriptine (23 mg/day) and levodopa resulted in improvement in 71% of patients with 26% having adverse effects. Most of these patients (66%) had advanced disease, and many had diurnal oscillations in performance. In seven studies of 367 patients, high dose bromocriptine (48 mg/day) and levodopa resulted in improvement in 58% with 37% having adverse effects. Most of these patients (85%) had advanced disease. The increased effectiveness of bromocriptine in combination with levodopa may be explained as follows. Bromocriptine by itself does not discriminate between the low and the high affinity states of the dopamine receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bromocriptine in Parkinson disease. 390 Oct 46

We studied the effects of bromocriptine therapy (mean dosage, 56.0 mg daily) for 12 months in five patients with both Parkinson's disease and hypertension. Therapy improved neurologic manifestations and reduced both supine and standing systolic blood pressures and standing diastolic blood pressure with no consistent change in heart rate. Transient episodes of orthostatic hypotension appeared in two cases. Domperidone (60 mg daily for 1 month) did not abolish the antihypertensive effect of bromocriptine, suggesting that central dopaminergic or alpha-adrenolytic mechanisms are involved in this effect. Bromocriptine may be useful in the treatment of hypertension in patients with Parkinson's disease.
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PMID:Parkinson's disease and hypertension: chronic bromocriptine treatment. 405 53

Bromocriptine (CB-154) and the 8-alpha-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5-75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1-60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of "total disability score' at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and "on-off' effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effect including mental changes (for with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and "on-off' effects than bromocriptine.
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PMID:Adjuvant treatment of Parkinson's disease with dopamine agonists: open trial with bromocriptine and CU 32-085. 618 Jan 42

Bromocriptine, a specific dopamine receptor agonist, has been used for the treatment of various hyperprolactinemic conditions and as adjunctive therapy for acromegaly (with or without concomitant hyperprolactinemia) and Parkinson's disease. Bromocriptine is extremely effective in suppressing prolactin secretion regardless of the cause, in restoring gonadal function and fertility, and in decreasing the size of prolactin-secreting pituitary tumors. Most patients with acromegaly have clinical improvement with this drug. When bromocriptine is added to a regimen of levodopa or carbidopa, patients with Parkinson's disease frequently have additional clinical improvement and, in most patients, the levodopa or carbidopa dose can be reduced. Withdrawal of bromocriptine therapy is associated in most patients with reversal of its beneficial effects--return of hyperprolactinemia, return of excess growth hormone secretion, and exacerbation of Parkinson's disease.
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PMID:Drugs five years later. Bromocriptine. 622 5

From a personal case and a review of the literature, it is recalled that bromocriptine may induce pleuropulmonary fibrosis. The various presentations of this condition are described. The index patient is a 56-year-old man, with Parkinson disease and a negative history for respiratory disease, who was taking bromocriptine in a high dose (60 mg/d). Under this treatment, he exhibited weight loss and an inflammatory syndrome and developed interstitial pneumopathy with secondary pleuropulmonary fibrosis, which resolved in part once therapy was discontinued. Bromocriptine, which is an ergot alcaloid with dopaminergic properties, has been used since 1965 in therapy. Its indications, which at the outset were restricted to endocrinology, were extended in 1972 to Parkinson disease, with a significant increase in dosages from 1979. Its responsibility in pleuropulmonary fibroses was suspected in 1981 by Rinne on data from 5 patients. As of now, 8 cases have been reported. All are Parkinson patients who, after a variable time interval (15 days to 3 years), developed a uniform picture of pleuropulmonary disease with rapidly increasing dyspnea upon exertion and deterioration of general health. These features mirror inflammation then fibrosis of the pleura and lung tissue, which results in a variable degree of chronic restrictive respiratory failure. The course is equally uniform, with partial resolution under corticosteroid therapy and more or less significant residual fibrosis at discontinuation of treatment. Immunoallergic rather than toxic or vasomotor mechanisms seem involved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pleuropulmonary fibrosis and bromocriptine]. 632 51


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