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)

The patient with Parkinson' disease on chronic levodopa therapy, like the diabetic on insulin, is dependent on the drug. Like the diabetic, the patients with Parkinson's disease may run into problems during long-term treatment. Two have emerged as frequent and serious, an insidious and progressive loss of benefit and the appearance of progessively more severe fluctuations in disability. It is concluded that progression of the underlying pathology of the disease is probably responsible. Discovery of the exact causes for loss of benefit may provide a rational basis for new therapy.
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PMID:Success and problems of long-term levodopa therapy in Parkinson's disease. 6 68

Urinary excretion of catecholamines under insulin hypoglycemia was studied in cerebral infarct patients as well as in patients with Parkinson's disease and subjects with lumbar discopathy (control group). While in the last two categories of subjects a normal response to hypoglycemia, i.e., an increase in urinary excretion of epinephrine was noticed, no such increase was found in patients with cerebral infarction. The disorder is attributed to the unresponsiveness to hypoglycemia of the brain stem centers controlling epinephrine secretion.
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PMID:Unresponsiveness to hypoglycemia of centers controlling epinephrine release in cerebral infarct patients. 39 98

Carbohydrate metabolism and insulin secretion were investigated in 26 patients with Parkinson's disease before and during L-dopa treatment. Oral glucose tolerance tests were performed on 13 patients treated with L-dopa alone and on 7 patients treated with L-dopa combined with Carbidopa. Intravenous glucose tolerance tests were performed on additional 6 patients treated with L-dopa alone. Results indicate that chronic L-dopa administration does not modify glucose metabolism. It was observed only a significant decrease of insulin secretion after oral glucose in the early phase (15th day) of treatment with L-dopa alone. This temporary effect may be related to the peripheral conversion of L-dopa to dopamine since insulin secretion during combined therapy was normal. The mechanism by which L-dopa transiently inhibits insulin release is not clear. Perhaps the oral administration of L-dopa alone causes an alteration in some gastrointestinal functions which are involved in the handling of oral glucose.
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PMID:Effects of long-term L-dopa therapy on carbohydrate metabolism in patients with Parkinson's disease. 127 95

Researchers believe fetal tissue can be easily transplanted into and cure people with incurable debilitating diseases such as Parkinson's disease. In 1988, the Reagan Administration stopped funding transplantation research of fetal tissue from induced abortions. An advisory panel later decided that it is an acceptable public policy as long as certain conditions a re met. Yet the Bush Administration continued the ban. In 1992, it erroneously claimed that transplantation research could use alternative sources of fetal tissue. 1 alternative is fetal tissue obtained from ectopic pregnancies. Yet spontaneously aborted ectopic pregnancies tend not to produce recognizable or viable in culture fetal tissue and if they do the tissue has been ischemic for days. Ectopic pregnancies requiring surgical sterilization tend to be morphologically abnormal. The only likelihood of viable fetal tissue form ectopic pregnancies is a fetus with myocardial contractility before surgery. The administration also recommended use of fetal tissue from spontaneous abortions but these fetuses often have a major chromosomal or other fatal defect. Researchers cannot use chromosomally abnormal fetal tissue since it growth, development, and function are unreliable. Expulsion of the necrotic fetus tends to occur a couple of weeks after death. The Bush Administration also proposed use of tissue from stillbirths but their tissue tends to be nonviable and the tissue, even if it were viable, is generally not at the developmental stage needed for transplantation. The placenta and yolk sac were other suggested alternatives, but the placenta is likely to be less immunogenic than embryonic tissue. It can help develop certain cell lines which produce insulin or neurotransmitters like dopamine, however. The yolk sac could replace fetal liver cells in transplantation. Nevertheless the only advantage of using the suggested alternatives is the perception of them raising less ethical concern than fetal tissue from an induced abortion.
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PMID:Are there really alternatives to the use of fetal tissue from elective abortions in transplantation research? 143 88

The efficacy of intranasal apomorphine was assessed in seven patients with Parkinson's disease and severe levodopa (L-dopa)-related "off-period" disabilities. All patients responded favorably to treatment with intranasal apomorphine. The speed and the quality of motor response and the pharmacokinetic profile showed results similar to those seen after subcutaneous injection of apomorphine administered by insulin pen syringe. The simplicity in the technique of intranasal apomorphine administration was found to be superior by all patients.
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PMID:Intranasal apomorphine in parkinsonian on-off fluctuations. 158 Aug 9

The effects of insulin-induced hypoglycemia on catecholamine secretion were investigated in patients with various neurological disorders affecting the autonomic nervous system. In control subjects, insulin-induced hypoglycemia resulted in marked increases in plasma epinephrine and norepinephrine levels. Heart rates were increased within 15 minutes after the insulin injection which were associated with slight elevation and depression of systolic and diastolic blood pressure, respectively. In patients with upper level spinal cord lesions (C1-T6) of various etiology, Shy-Drager syndrome and familial amyloidosis, insulin-induced hypoglycemia failed to increase plasma epinephrine and norepinephrine levels and resulted in falls in systolic and/or diastolic blood pressure 15 minutes after the injection. Heart rates were increased at 30-45 minutes after the injection. In patients with lower spinal cord lesions (T10-L1), neurosyphilis or brain stem tumor with orthostatic hypotension, the catecholamine responses were normal and blood pressure did not fall during insulin-induced hypoglycemia. In patients with Parkinson's disease and spinocerebellar degeneration with autonomic symptoms catecholamine responses were not impaired. These findings suggest that any lesion involving the sympathetic efferent systems of baroreflex such as the spinal descending pathway, sympathetic preganglionic neuron and peripheral nervous system causes both impairment of catecholamine secretion and a fall in blood pressure during hypoglycemia, and that lesions in sympatho-afferent system may not affect the secretion of catecholamine and neural control of blood pressure.
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PMID:[Effects of insulin-induced hypoglycemia on catecholamine secretion and blood pressure in neurological disorders affecting autonomic nervous system]. 162 51

Energy expenditure was determined in 18 patients with Parkinson's disease, 6 healthy volunteers and 6 patients with essential tremor, age-matched, using the indirect calorimetric method which measures the gas exchange rate. The results showed a significant increase in the relative energy expenditure, i.e. the difference between absolute and predictable values from the Harris and Benedict equation, among the parkinsonian patients (+21 +/- 4.1 p. 100; mean +/- S.E.M.) as compared to the 2 control groups (-8.6 +/- 7 p. 100 and -2.1 +/- 4.1 p. 100 respectively; p less than 0.001). There was no correlation between the rate of energy expenditure and the duration or degree of severity of the disease, and particularly the occurrence and magnitude of weight loss, which is frequently observed during the course of the disease. The relative energy expenditure was not significantly different between untreated and treated parkinsonian patients (18.8 +/- 3 p. 100 and 24.5 +/- 6.2 p. 100 respectively). Further investigations were designed to determine whether the increased energy expenditure could reflect a functional impairment of the automatic nervous system. The integrity of the vagus nerve was tested by plotting vs time the plasma Pancreatic Polypeptide levels in response to insulin-induced hypoglycaemia. A physiological stimulation was obtained in the 8 parkinsonian patients studied. This is not the case in chronic autonomic failure. On the contrary, the relative energy expenditure was significantly decreased in the 6 patients that were given a beta-blocking drug, pindolol, 15 mg daily for 3 weeks (+30.7 +/- 4.3 p. 100 before and +21 +/- 4.2 p. 100 after treatment; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Increase of energy expenditure in Parkinson's disease]. 201 81

The in vitro effects of dopamine (DA) and insulin on -14C glucose oxidation (transport) in isolated rat adipocytes was studied. Low to intermediate concentrations of DA combined with low concentrations of insulin tended to stimulate glucose transport whilst high concentrations of DA combined with high concentrations of insulin produced inhibition of insulin stimulated glucose transport. The effect of DA on glucose transport was mediated via beta-adrenergic receptors, since propranolol, but not haloperidol or phentolamine, antagonised these effects of dopamine. These effects of dopamine on glucose transport may be relevant to the pathophysiology of Parkinson's disease and other neuropsychiatric conditions in which abnormalities of dopaminergic functions are thought to be of major pathogenic importance.
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PMID:Dopamine and insulin interact to modulate in vitro glucose transport in rat adipocytes. 306 82

Thirteen drug-free and not severely affected patients with idiopathic Parkinson's disease underwent an insulin-hypoglycaemia test, a TRH test and a levodopa test. The responses of growth hormone, prolactin, cortisol and thyrotropin were measured, and retested under stable therapy with levodopa and benserazide. Mean basal and stimulated hormonal concentrations were in the normal range before and during therapy. Minor abnormalities were observed in individual cases, but did not indicate a hypothalamic dopamine deficit.
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PMID:Effect of hypoglycaemia, TRH and levodopa on plasma growth hormone, prolactin, thyrotropin and cortisol in Parkinson's disease before and during therapy. 308 17

The authors, after a survey on literature and an extensive epidemiological study on the problems of parkinsonism, report the results from their retrospective and prospective study on the incidence and clinical characteristics of diabetes mellitus, developed in the process of Parkinson's disease. Diabetes mellitus was established in 180 patients (7.77%) out of 2315 patients with parkinsonism studied from Sofia and the district of Lovetch. The majority of the diabetics are males, aged between 61 and 70, with non-insulin dependent type of diabetes (second type). The patients with light and moderately grave diabetes, predominated--most often clinically not manifested and diagnosed by determination of carbohydrate tolerance. As far as the character of parkinson syndrome in the patients with developed diabetes mellitus is concerned, most often patients with parkinsonism with mixed tremor-rigid form are referred to, with a duration of the disease from 3 to 5 years. The incidence and character of cardiovascular disturbances were studied in the patients with parkinsonism that developed diabetes mellitus.
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PMID:[Diabetes mellitus in parkinsonism patients]. 359 Jul 33


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