Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Orthostatic hypotension is very common in the elderly. It increases morbidity and is an independant predictor of all cause mortality. It is defined as a fall in systolic blood pressure greater than 20 mm Hg or a fall in diastolic blood pressure greater than 10 mm Hg within 3 minutes of standing. Symptoms include light headedness, weakness, blurred vision, fatigue and lethargy and falls. Most patients have orthostatic hypotension due to non neurogenic causes. Drugs like antihypertensives and tricyclic antidepressants are very common causes of orthostatic hypotension. Diagnosis is based on the history and a thorough clinical examination. Based on the history and physical examination, further testing of the heart, kidneys and autonomic nervous system may be required in selected patients. Non pharmacological methods like slow position change, increased fluid and sodium intake, compression stockings and elevation of head of the bed are the key to management of orthostatic hypotension. After these methods, pharmacological treatment with fludrocortisone and midodrine should be tried. Other drugs like desmopresin acetate, xamoterol, erythropoetin and ocreotide can be used as second line agents in selected patients.
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PMID:A clinical, physiology and pharmacology evaluation of orthostatic hypotension in the elderly. 1630 60

Chronic heart failure is a common problem in old age. Dyspnoea and fatigue are the most common symptoms and should alert the clinician to the likely diagnosis. When there is a clinical suspicion of heart failure, further assessment is required to confirm the aetiology. In older patients, heart failure with normal systolic function is frequently encountered. However, patients with left ventricular systolic dysfunction usually have a poorer prognosis, and most treatments have been evaluated in these patients. Useful investigations include the 12-lead electrocardiogram, chest radiology and echocardiography. A blood test for B-type natriuretic peptide is being increasingly used as a 'rule out' test for heart failure. There are several treatment options. Initially, patients should be treated with a diuretic and ACE inhibitor, provided there are no contraindications. beta-Blocker therapy is also first-line therapy once a patients' haemodynamic status has been stabilized. Additional treatments include spironolactone, angiotensin antagonists and digoxin. Patient factors and tolerability may limit the number of treatment options. Treatment regimes are most effective when delivered using a multidisciplinary approach.
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PMID:The diagnosis and management of chronic heart failure in the older patient. 1649 10

The Adacolumn is an adsorptive-type extracorporeal device, which is filled with cellulose diacetate beads that selectively adsorb granulocytes and monocytes. Patients with severe persistent asthma experience highly variable continuous symptoms and severe exacerbations in spite of medication based on inhaled glucocorticosteroids. Granulocyte and monocyte adsorption apheresis using extracorporeal circulation through the Adacolumn was performed in nine patients with severe persistent asthma. The extracorporeal circulation through the Adacolumn was performed once a week for 5 weeks. We were able to perform this therapy without any severe adverse effects in all patients, although one patient complained of general fatigue just after the circulations. In six of the nine patients, the increase in peak expiratory flow (PEF) was more than 50 mL/min. The average increase in morning PEF was 23.3% while that in the evening PEF was 26.4% after the therapy. This therapy was not harmful for patients with severe persistent asthma. A placebo-controlled study will be desired to evaluate the efficacy of this nonpharmacological strategy accurately.
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PMID:Safety and efficacy of extracorporeal granulocyte and monocyte adsorption apheresis in patients with severe persistent bronchial asthma. 1650 41

Despite its frequency and high functional impact, very little is known about effective strategies for managing cognitive impairment in multiple sclerosis (MS). Disease-modifying drugs, such as beta-interferons and glatiramer acetate, may prevent or reduce the progression of cognitive dysfunction by containing the development of new cerebral lesions. To date, clinical trials have provided inconsistent results, with neuropsychological effects documented only in one trial. Moreover, pilot studies have tested symptomatic therapies for fatigue, a frequent symptom in MS, which may share a common physiopathological substrate with cognitive dysfunction. Small trials with amantadine, pemoline, 4-aminopyridine and 3-4 aminopyridine have provided mainly negative results. Acetylcholinesterase inhibitors (AChEI) used to treat Alzheimer's disease (AD)-such as donepezil, rivastigmine, and galantamine-have recently been tested in other cognitive disorders, including MS. The majority of pilot trials with AchEI in MS have provided promising results, and the donepezil study recently published by Krupp et al. represents a major development in this field. As for non-pharmacological interventions based on cognitive rehabilitation, few studies have used an experimental approach and, in general, results have been disappointingly negative. Further research is clearly needed in this area.
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PMID:Are there protective treatments for cognitive decline in MS? 1664 49

The authors retrospectively examined their experience with amlodipine in the treatment of hypertension in 32 pediatric-aged patients, ranging in age from 4 to 26 years, with blood pressure (BP) readings greater than the 90th percentile for age. Amlodipine was used as the sole therapy in 9 patients and with other antihypertensive therapy in 23 patients. Additional antihypertensive drugs used in combination with amlodipine included beta-adrenergic antagonists, ACE inhibitors, and diuretics. The starting dose of amlodipine was 0.13+/-0.09 mg/kg/d. The dose was increased in 20 of 32 patients to 0.23+/-0.13 mg/kg/d. Amlodipine was administered once daily to 26 patients and twice daily to 6 patients. After therapy with amlodipine was initiated, the systolic BP decreased from 141+/-15 to 132+/-9 mm Hg (P=0.01) and the diastolic BP decreased from 84+/-16 to 77+/-8 mmHg (P=0,03). There were a total of 2145 follow-up BP readings. The follow-up systolic BP was lower than the initial BP prior to starting amlodipine 59% of the time and the diastolic BP was lower than the initial BP 61% of the time. The follow-up systolic BP was lower than the 90th percentile predicted for age 33% of the time after starting amlodipine and the diastolic BF was lower than the 90th percentile for age 52% of the time. Adverse effects were noted in 4 of the 32 patients (12.5%). These included fatigue (n=2), dizziness (n=1), and ankle edema (n=1). Amlodipine therapy was discontinued in only 1 patient (the patient with ankle edema). Given its efficacy, the low incidence of adverse effects, and availability as a suspension, amlodipine is an effective agent for the treatment of hypertension in the pediatric-aged patient.
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PMID:Preliminary experience with amlodipine in the pediatric population. 1677 60

There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress. Nuclear factor kappa beta (NFkappabeta) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators. In order to examine the role of NFkappabeta in the pathophysiology of CFS, this study examines the production of NFkappabeta p50 in unstimulated, 10 ng/mL TNF-alpha (tumor necrosis factor alpha) and 50 ng/mL PMA (phorbolmyristate acetate) stimulated peripheral blood lymphocytes of 18 unmedicated patients with CFS and 18 age-sex matched controls. The unstimulated (F=19.4, df=1/34, p=0.0002), TNF-alpha-(F=14.0, df=1/34, p=0.0009) and PMA-(F=7.9, df=1/34, p=0.008) stimulated production of NFkappabeta were significantly higher in CFS patients than in controls. There were significant and positive correlations between the production of NFkappabeta and the severity of illness as measured with the FibroFatigue scale and with symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection. The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NFkappabeta. The results suggest that the symptoms of CFS, such as fatigue, muscular tension, depressive symptoms and the feeling of infection reflect a genuine inflammatory response in those patients. It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids.
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PMID:Not in the mind of neurasthenic lazybones but in the cell nucleus: patients with chronic fatigue syndrome have increased production of nuclear factor kappa beta. 1769 79

Young adult male Wistar rats were treated, by gavage, with 80 or 320 mg/kg Pb2+ (lead acetate), 0.4 or 1.6 mg/kg Hg2+ (mercuric chloride) or both by combining the lower doses. For combination with alcohol, ethanol was added to the rats' drinking water in 5 v/v %. After 12 weeks of treatment, electrophysiological recording was made from the somatosensory cortex in urethane anaesthesia. Evoked potentials obtained by stimulation of the whiskers were recorded. Both metals, and alcohol alone, increased significantly the latency of the evoked response. Alcohol seemed to abolish the effect of Pb, but not of Hg. Fatigue, calculated form the response amplitude, was increased by Pb and Hg treatment and this effect of Hg was reduced by ethanol. Evoked activity and its dynamic characteristics were sensitive to the complex neurotoxic effect induced in the rats and can provide a basis for developing functional markers.
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PMID:Subchronic heavy metal and alcohol treatment in rats: changes in the somatosensory evoked cortical activity. 1789 83

A 62-year-old man presented with fatigue, pallor and mild weight loss. Laboratory studies showed Hb 7.6 g/dl, Hct 21.8%, WBC 108x10(9)/1, PLT 143x10(9)/1. At morphological examination, circulating cells appeared as 60% blasts and 40% lymphocytes, with smudge cells. A bone marrow aspirate showed infiltration by blasts (50%) and lymphocytes (40%); alpha-naphtyl-acetate esterase was positive in 90% of blasts, while myeloperoxidase was positive in 10%. The immunologic phenotype of blasts was characterized by the co-expression of CD13, CD33, CD14, CD4, CD15, CD64, CD117, HLA-DR, CD11b. Lymphocytes were characterized by a B-CLL immunophenotype: CD19+, CD5+, CD23+, CD20+(dim), FMC7+(dim), K light chain+(dim). Karyotype was normal and PCR assays for AML-ETO, CBFbeta-MYH11, PML-RARalpha, BCR-ABL and bcl-1/JH translocation were negative. Coexistence of CLL and AML with monoblastic features was diagnosed. Simultaneous appearance of CLL and AML has rarely been described and represents a peculiar biological phenomenon.
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PMID:Association of B-chronic lymphocytic leukemia and acute myeloid leukemia. 1798 6

Disease progression and advancing disability will supervene in the majority of multiple sclerosis patients who are followed over the long-term. This process can begin insidiously from the onset of the disease (primary progression) or after one or more clinical flares (secondary progression). The factors which lead to progression of disability are incompletely understood. The progressive forms of multiple sclerosis have been remarkably resistant to treatment. The legacy of heroic immunosuppression as a treatment for the disease progression has been modest indeed although there is some recent enthusiasm for immunosuppression with agents like mitoxantrone. In the last decade, the treatment of relapsing forms of multiple sclerosis has been revitalised by the interferons and glatiramer acetate. The robust treatment effect on the magnetic resonance imaging burden of the disease and the modest treatment effect in the suppression of clinical attacks have raised hopes that these agents might stall the disease in its progressive phase. Recent clinical trials with the interferons are indeed showing promise for modest clinical efficacy in patients selected for treatment on the basis of chronic progression. Given the weakness of the current treatment, the essence of disease management remains the handling of the complications of the disease. The management of bladder disturbances, spasticity, pain, depression, emotional lability, paroxysmal disorders, fatigue and heat intolerance, tremor and sexual dysfunction is reviewed.
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PMID:Treatment of secondary progressive multiple sclerosis: current recommendations and future prospects. 1803 Nov 81

This paper reports on the development of a novel electrochemical assay for Zn(2+) in human sweat, which involves the use of disposable screen-printed carbon electrodes (SPCEs). Initially, SPCEs were used in conjunction with cyclic voltammetry to study the redox characteristics of Zn(2+) in a selection of supporting electrolytes. The best defined cathodic and anodic peaks were obtained with 0.1 M NaCl/0.1 M acetate buffer pH 6.0. The anodic peak was sharp and symmetrical which is typical for the oxidation of a thin metal film on the electrode surface. This behaviour was exploited in the development of a differential pulse anodic stripping voltammetric (DPASV) assay for zinc. It was shown that a deposition potential of -1.6 V versus Ag/AgCl and deposition time of 60 s with stirring (10 s equilibration) produced a well-defined stripping peak with E(pa) = -1.2 V versus Ag/AgCl. Using these conditions, the calibration plot was linear over the range 1x10(-8) to 5x10(-6) M Zn(2+). The precision was examined by carrying out six replicate measurements at a concentration of 2x10(-6) M; the coefficient of variation was calculated to be 5.6%. The method was applied to the determination of the analyte in sweat from 10 human volunteers. The concentrations were between 0.39 and 1.56 microg/mL, which agrees well with previously reported values. This simple, low-cost sensitive assay should have application in biomedical studies and for stress and fatigue in sports studies.
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PMID:Development of an anodic stripping voltammetric assay, using a disposable mercury-free screen-printed carbon electrode, for the determination of zinc in human sweat. 1858 5


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