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)

EEG-findings of a group of 95 patients suffering from Parkinson's disease were related to accompanying diseases inducing cerebral hypoxic hypoxidosis. The EEG in 59 to 74 per cent of our patients was abnormal but the changes were not specific. There was a correlation between age and EEG-abnormalities. On the other hand no association could be seen between EEG-changes and duration of the Parkinson's disease. At least 74 per cent of the patients suffered from concomitant cardiovascular complications and 36 of them had a severe pathologic EEG as well as a pathologic ECG. The results lead to the conclusion that in treatment of parkinsonian patients attention is to be paid to accompanying diseases as heart failure, angiopathy or anemia.
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PMID:[EEG in Parkinson's disease and cerebral hypoxia (author's transl)]. 41 49

Oxygen free radicals and other oxygen derived species (Superoxide, O2-; Hydroperoxide, HOO; Singlet oxygen, 1O2-; Hydroxyl radical, OH; and Hydrogen peroxide, H2O2) including lipid peroxides have been suggested as important causative agents of aging and several human diseases, including cancer, multiple sclerosis, Parkinson's disease, autoimmune disease, ischemia, anemia, senile dementia, asbestosis and in thalassemia. This paper aims to communicate some of the theories and rationales in aging process and thalassemia.
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PMID:Role of lipid peroxidation and antioxidants in aging process and thalassemia. 134 11

Retroperitoneal fibrosis has been observed in two patients with Parkinson's disease treated with bromocriptine. The patients complained of abdominal or lower back pain and presented with various degrees of renal insufficiency, with anuria in one. Laboratory evaluation furthermore showed an increased sedimentation rate and inflammatory anemia. Computerized tomography disclosed marked retroperitoneal thickening, and biopsy was performed in one patient. The symptoms appeared eighteen months and five years after treatment was started, at doses of 20 and 22.5 mg of bromocriptine daily. The medication was discontinued in both patients and steroid therapy was initiated, with resolution of all clinical, biological and radiological evidence of disease. This potential but rare complication of a widely prescribed drug warrants monitoring of renal function and sedimentation rate in patients undergoing bromocriptine treatment.
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PMID:Retroperitoneal fibrosis in two patients with Parkinson's disease treated with bromocriptine. 217 99

The fact that levodopa, a drug used for the treatment of Parkinson's disease induces a direct Coombs-positive reaction in about 15% of treated patients, indicating the presence of auto-antibodies against the patient's red blood cells (RBCs), is well known. Another known fact is that only 1% of those patients do actually develop auto-immune haemolytic anaemia. In this paper, we describe our findings utilizing the direct ELISA, a method for measuring the presence of IgM and IgG auto-antibodies on the patients' red blood cells (RBCs), as well as an indirect ELISA, testing the presence of antibodies in their serum. The tests were performed on 8 patients, 7 of whom had been receiving the drug for long periods of time. Our results show that the serum antibodies precede the bound antibodies in a significant fashion and that the severity of the anaemia is directly related to the amount of auto-antibodies. Since auto-antibodies do not seem to be directed against the drug itself, some modification of the RBC must occur. For this reason, we attempted to determine whether patients receiving the drug show any morphological changes of their RBCs which could be determined by scanning electron microscopy (SEM) and whether these changes could be related to direct and indirect ELISA. In most levodopa-treated patients, a small number of echinocytes could be observed by SEM, while in 1 patient who suffered a severe anaemic phase, a very high percentage of the RBCs were echinocytes and spherocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electron microscopy of red blood cells altered by auto-immunity-inducing drugs. 239 95

Population aging is continuously increasing in Italy and in the World. Individuals aged 60 years or more are currently 10,500,000 and will be 13,000,000 in 2015. Life quality in geriatric ages includes the maintenance of sexual power: according to recent data (Carrol et al., 1992), 80% of impotence cases are due to organic causes. In addition, the use of drugs can cause impotence. Among them tiazidic diuretics may cause an increase of sexual disturbances. Other drugs with this potential are digitalis, antihypertensive drugs (particularly beta blockers), major and minor tranquillizers, antidepressant, H2 receptor antagonists, antiparkinsonian cholinergic drugs and estrogens employed in the treatment of prostate tumors. Diseases of geriatric age that can alter sexual power are diabetes mellitus, ischemic heart disease for the accompanying depression and for the use of antidepressants; severe hypertension is complicated by impotence in 15% of cases. Among neurological diseases Parkinson's disease and multiple sclerosis can be causes of sexual dysfunctions. Patients on hemodialysis can be impotent, with recent data (Soloh et al 1992) showing that erythropoietin treatment of anemia also improve sexual dysfunctions. Prevention from a geriatric standpoint should be base on action on known risk factor as smoking, alcohol abuse and dislipidemias and with the activation of a close drug vigilance.
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PMID:[Andrologic problems and internal pathology in the elderly]. 825 79

A case of familial juvenile parkinsonism with dementia, orthostatic hypotension, neurogenic bladder and constipation was reported. He had been in a good health until the age of 28 when a finger tremor occurred on effort to hold hands in a definite position, and disturbances in gait and speech were noted. These symptoms were relieved by levodopa treatment followed by dyskinesia and motor fluctuations. Three years later, he complained of faintness, constipation and urinary frequency. The neurological examination revealed mentally sound male with masked face, tremor and rigidity in his extremities, and short step gait with lateropulsion. Urodynamic study showed uninhibited bladder. In the following years, orthostatic hypotension, dysuria and urinary retention developed gradually. He became mentally loose and was unable to take medicines appropriately. When in the Nishiojiya Byoin National Sanatorium, he tried to snake out the hospital many times. His parents and a brother suffered from Parkinson's disease and juvenile parkinsonism, respectively, suggesting an autosomal dominant inheritance. On admission to our hospital, he was apathetic. He had masked face, bilateral postural tremor, frozen gait and dyskinesia in the right lower extremity. Little bradykinesia or rigidity was noted. His muscle tone and deep tendon reflexes were decreased but neither muscular wasting, weakness, ataxia nor sensory disturbance was observed. Laboratory data including ceruloplasmin, copper, dopamine-beta-hydroxylase and lysosomal enzyme activities were normal except for mild anemia. A cranial CT scan revealed mild cortical atrophy in the frontal and temporal lobes, but nerve conduction study and cortical evoked potentials showed no abnormality. While in the hospital, his mental functions deteriorated to the state of dementia and orthostatic hypotension became apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial juvenile parkinsonism with dementia and autonomic failure--a case report]. 833 79

Pleurisy of initially unknown origin was found in a patient who was treated with bromocriptine for Parkinson's disease for 6 years. At presentation, bilateral pleural thickening existed that caused severe restriction of pulmonary function. There were an elevated erythrocyte sedimentation rate, polyclonal hypergammaglobulinaemia, increased levels of acute phase proteins and anaemia. After withdrawal of the bromocriptine the patient's complaints as well as the laboratory parameters markedly improved. Further loss of pulmonary function did not occur. However, the pleural thickening did not resolve, not even upon subsequent corticosteroid treatment, probably due to fibrosis. Together, these findings strongly suggest a causative role of bromocriptine. The results of the laboratory studies suggested an immunopathogenetic mechanism, but in vitro lymphocyte-proliferation studies and skin patch tests with bromocriptine were negative. Bromocriptine should be considered as a cause of pleurisy. The drug must be stopped immediately upon the occurrence of pleural thickening in order to prevent impairment of pulmonary function. In addition, periodic laboratory and X-ray studies in patients on long-term bromocriptine treatment should be considered.
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PMID:Suggestive evidence for bromocriptine-induced pleurisy. 871 45

Serum erythropoietin (EPO) levels are partially controlled by the sympathetic outflow to the kidney. We have studied whether patients with multiple system atrophy (MSA), known to be associated with dysautonomia, are EPO-deficient. Eighteen MSA patients were studied along with 32 idiopathic Parkinson's disease (PD) patients, 23 controls with iron-deficiency anaemia, and 18 healthy individuals. Serum creatinine was normal in all groups. Mean haemoglobin (Hb) concentration in MSA patients was 13.7 +/- 1.7 g/dL. Four MSA patients had unexplained anaemia (minimum Hb: 10.5 g/dL) and abnormal autonomic function tests including significant postural hypotension, whereas none of the PD patients was anaemic. Serum EPO levels were suppressed in relation to anaemia in MSA patients compared to elevated EPO levels in iron-deficiency anaemia patients (difference of regression lines P < 0.001), indicating EPO deficiency in the anaemic MSA patients. Serum EPO levels in PD patients were within normal range. A subset of MSA patients has anaemia and postural hypotension, which may be associated with EPO deficiency. This may have therapeutic implications.
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PMID:Erythropoietin deficiency and anaemia in multiple system atrophy. 1129 75

Different tissues display distinct sensitivities to defective mitochondrial oxidative phosphorylation (OXPHOS). Tissues highly dependent on oxygen such as the cardiac muscle, skeletal and smooth muscle, the central and peripheral nervous system, the kidney, and the insulin-producing pancreatic beta-cell are especially susceptible to defective OXPHOS. There is evidence that defective OXPHOS plays an important role in atherogenesis, in the pathogenesis of Alzheimer's disease, Parkinson's disease, diabetes, and aging. Defective OXPHOS may be caused by abnormal mitochondrial biosynthesis due to inherited or acquired mutations in the nuclear (n) or mitochondrial (mt) deoxyribonucleic acid (DNA). For instance, the presence of a mutation of the mtDNA in the pancreatic beta-cell impairs adenosine triphosphate (ATP) generation and insulin synthesis. The nuclear genome controls mitochondrial biosynthesis, but mtDNA has a much higher mutation rate than nDNA because it lacks histones and is exposed to the radical oxygen species (ROS) generated by the electron transport chain, and the mtDNA repair system is limited. Defective OXPHOS may be caused by insufficient fuel supply, by defective electron transport chain enzymes (Complexes I - IV), lack of the electron carrier coenzyme Q10, lack of oxygen due to ischemia or anemia, or excessive membrane leakage, resulting in insufficient mitochondrial inner membrane potential for ATP synthesis by the F0F1-ATPase. Human tissues can counteract OXPHOS defects by stimulating mitochondrial biosynthesis; however, above a certain threshold the lack of ATP causes cell death. Many agents affect OXPHOS. Several nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit or uncouple OXPHOS and induce the 'topical' phase of gastrointestinal ulcer formation. Uncoupled mitochondria reduce cell viability. The Helicobacter pylori induces uncoupling. The uncoupling that opens the membrane pores can activate apoptosis. Cholic acid in experimental atherogenic diets inhibits Complex IV, cocaine inhibits Complex I, the poliovirus inhibits Complex II, ceramide inhibits Complex III, azide, cyanide, chloroform, and methamphetamine inhibit Complex IV. Ethanol abuse and antiviral nucleoside analogue therapy inhibit mtDNA replication. By contrast, melatonin stimulates Complexes I and IV and Gingko biloba stimulates Complexes I and III. Oral Q10 supplementation is effective in treating cardiomyopathies and in restoring plasma levels reduced by the statin type of cholesterol-lowering drugs.
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PMID:Mitochondrial medicine--molecular pathology of defective oxidative phosphorylation. 1131 62

The prevalence and severity of coronary atherosclerosis increase dramatically with age, so that more than half of all deaths in persons aged over 65 are due to coronary arterial disease (CAD) and about three fourths of all deaths from CAD occur in the elderly. The aims of our study were, first, to detect myocardial ischemia development in elderly versus younger patients undergoing treatment for known CAD through the use of both conventional treadmill testing and 201T1 scintigraphy, and second, to determine the relationship between the above non-invasive tests and angiographically confirmed important coronary artery disease (iCAD). A database of 606 patients (355 men and 251 women) who had undergone coronary angiography, exercise ECG testing (ETT) using the treadmill Bruce protocol, and 201T1 scintigraphy, was reviewed retrospectively. All patients had displayed clinical expression of CAD with or without the existence of an old myocardial infarction (MI). The patients were from both sexes (440 men and 252 women) and divided into two groups, according to age. Group A was composed of 265 patients aged over 65 (170 men, 95 women, mean age = 70.3 +/- 5.3 years). Group B was composed of 341 patients aged under 65 (185 men, 156 women, mean age 54.4 +/- 9.1 years). Patients with uncontrolled arterial hypertension, hypertrophic cardiomyopathy, severe valve diseases, severe chronic obstructive lung diseases, severe anemia, peripheral atherosclerosis, orthopedic problems, or Parkinson's disease were excluded from the study. The term "important coronary artery disease" (iCAD) covers the following patterns of coronary anatomy: (a) left main stem stenosis > or = 50% with or without disease elsewhere, (b) proximal three-vessel disease, (c) three-vessel disease including the proximal left anterior descending artery (LAD), (d) proximal two-vessel disease including LAD, and (e) two-vessel disease including the proximal LAD. Biostatistical characteristics such as sensitivity, specificity, and predictive values of ETT-201T1 were estimated. Analyzing our results we concluded that: the biostatistical parameters in predicting important CAD in elderly and younger patients by means of exercise test and thallium scintigraphy need to be redefined through more closely scheduled and prospective studies; in elderly coronary patients, the appearance of positive results in both parameters of ETT-201T1 indicates a significant possibility of iCAD existence; in coronary patients younger than 65 years, the appearance of negative results in both parameters of ETT-201T1 almost excludes iCAD, in contrast to elderly patients, who display a significant proportion of iCAD; in elderly coronary patients, the appearance of equivocal results in both tests indicates a significant possibility of the existence of iCAD, in contrast to younger patients.
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PMID:Detection of myocardial ischemia in the elderly versus the young by stress thallium-201 scintigraphy and its relation to important coronary artery disease. 1222 83


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