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)

The patient responded to treatment at the first onset of heart failure but gradually became irresponsive to treatment, experiencing fatigue and malaise as the chief complaints and suffering from gradually progressive decrease in exercise capacity and body weight. Dose of DOA gradually increased to maintain well clinical state of the patient. Unusual for heart failure, he had bradycardia as the basal rhythm without showing a tendency for tachycardia. Cardiac catheterization revealed pulmonary hypertension and low cardiac output, however, left ventricular ejection fraction was 37%. There were no notable changes in ultrasonic cardiogram or CTR through the clinical course. Tl-201 myocardial images and pulmonary perfusion images showed gradual worsening corresponding to progressive worsening of clinical state. From these findings, the patient was determined as a candidate for heart transplantation.
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PMID:[Tl-201 myocardial images in a patient with dialated cardiomyopathy, who finally received heart transplantation]. 202 Jan 39

Clinical experience with long-term nifedipine treatment in 23 patients aged between 1 1/12 and 14 8/12 years is reported. The cardiopulmonary diseases comprised primary pulmonary diseases with pulmonary hypertension (n = 4), congenital heart defects with intracardiac shunts and pulmonary hypertension which either were inoperable as a result of an Eisenmenger reaction (n = 7) or presented a high surgical risk (n = 5), or defects in which pulmonary hypertension did not regress despite corrective (n = 1) or palliative surgery (n = 3), and congenital defects without pulmonary hypertension (n = 3). Subjective improvement with an increase in physical performance was clearly observed in 15 cases. Echocardiography and cardiac catheter examinations showed no progression of the pulmonary arterial diseases, except in 1 patient with severe primary pulmonary hypertension and an 11-year observation period with nifedipine treatment during the last 4 years. No complications occurred during the 4 corrective operations. A patient aged 14 8/12 years with the Down syndrome and atrioventricular septal defect developed easily controllable heart failure during 7-day administration of nifedipine without additional cardiotherapy. 4 children initially suffered from flushed face and scalp, in one case with headache; 2 children reported fatigue. Long-term treatment with nifedipine should begin with strict 7-day supervision in hospital and possibly additional digitalization. Success of the treatment was determined by an improved quality of life in patients with primary pulmonary hypertension and inoperable defects, and by a reduced perioperative risk and postoperative regression of pulmonary hypertension in patients with operable defects.
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PMID:Experience with long-term nifedipine therapy in paediatric cardiological patients. 211 16

A 79-year-old woman was admitted with general fatigue. Chest roentgenogram showed diffuse reticular shadows and bilateral pleural effusion. Peripheral blood studies revealed an elevation of platelet count (203.3 X 104/mm3). The case was diagnosed as essential thrombocythemia and treated with ACNU. The platelet count decreased. Bilateral pleural effusions increased gradually and their characteristics changed from bloody exudate to transudate. Biopsy of her pleura and thoracoscopy were carried out without significant results. Later, systemic edema, which suggested right heart failure, developed. The diagnosis of pulmonary hypertension and right heart failure was made by echocardiogram and right cardiac catheterization. Because perfusion scan of the lung revealed some perfusion defects, complication of pulmonary embolism was suspected. Bilateral pleural effusion and pulmonary artery pressure decreased with treatment by nifedipine, furosemide and isosorbide dinitrate. This is the first case report of essential thrombocythemia, pulmonary hypertension, right heart failure and bilateral pleural effusion.
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PMID:[A case of essential thrombocythemia with pulmonary hypertension and bilateral pleural effusions]. 221 92

Eight patients who became ill while taking tryptophan had myalgia, fatigue, rash, fever, edema, alopecia, arthralgias, diminished joint motion, skin tightening, muscle cramping, and distal paresthesias. Three had shortness of breath, and one had pulmonary hypertension. Laboratory abnormalities included peripheral eosinophilia, leukocytosis, thrombocytosis, raised erythrocyte sedimentation rate, and elevated serum levels of aldolase, lactate dehydrogenase, and liver enzymes. Of 4 chest radiographs, 3 were abnormal. Of 5 skin and muscle biopsies, 4 showed sclerosis or mixed inflammatory cell infiltration of the dermis, subcutis, and fascia. Eosinophils were often present, but vasculitis was absent. Muscle inflammation was minimal. We conclude that the "eosinophilia-myalgia syndrome" is related to the ingestion of tryptophan and that abnormalities in the secretion of lymphokines may be important in its pathogenesis.
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PMID:Tryptophan-induced eosinophilia-myalgia syndrome. 221 1

Haemodynamic studies at rest and during exercise together with radionuclide ventriculography, pulmonary function and clinical well-being assessment were evaluated in ten patients with COPD and secondary pulmonary hypertension (mean PAP 25 mm Hg), before and after 6 months therapy with pirbuterol 20 mg thrice daily. Despite the continued pharmacological action of pirbuterol on the heart and systemic circulation during peak pirbuterol levels at 6 months, no significant effect on the pulmonary circulation was observed. Seven patients reported an improvement in the level of fatigue, the partial pressure of carbon dioxide fell significantly (6.5 +/- 0.9 to 6.1 +/- 0.9 kPa: P less than 0.01) and there was a slight bronchodilator effect [forced expiratory volume in 1s (FEV1) 0.60 +/- 0.18 to 0.71 +/- 0.2 1s-1: P less than 0.02] after 6 months. The drug was generally well tolerated but three patients with pre-existing biliary tract disease developed obstructive jaundice.
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PMID:Long term haemodynamic, pulmonary function and symptomatic effects of pirbuterol in COPD. 251 10

A clinical syndrome identical to the chronic mountain sickness of the Andes occurs commonly in Lhasa, Tibet. It affects, almost exclusively, the immigrant Han population and develops after an average of 15 years' residence at high altitude. The early symptoms are attributable to polycythaemia--headache, dizziness, loss of memory and fatigue being prominent. In the later stages of the disease, dyspnoea and peripheral oedema develop. Haemodynamic investigations show pulmonary hypertension with a normal cardiac output and dilatation of the right ventricle in the long-established case. Respiratory gas studies provide evidence of alveolar underventilation and ventilation: perfusion inhomogeneity. Both clinical and investigatory data suggest that the earlier stages of the disease are dominated by polycythaemia, while cardiopulmonary involvement increases with the duration of the disease. The disease is rare in women and uncommon in Tibetans. Cigarette smoking appears to be a contributory factor.
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PMID:Chronic mountain sickness in Tibet. 251 94

Pulmonary hypertension occurs frequently in patients with chronic lung disease and contributes to morbidity and mortality. The most common symptoms are dyspnea, fatigue, chest pain, and syncope; sudden death can occur. Signs of pulmonary hypertension include prominent a-waves in the jugular venous pulse, a prominent P2 and murmur of tricuspid regurgitation. Introduced in 1964, cardiac catheterization is still required for the clinical assessment. Many patients reveal a vasoconstrictive component in their lung vessels that is potentially reversible therapeutically. Accurate noninvasive diagnostic methods and an understanding of the mechanisms causing pulmonary hypertension are necessary, as is appropriate therapy based upon the results.
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PMID:[Pulmonary hypertension. Clinical picture and therapy]. 266 41

Urapidil is a postsynaptic alpha 1-adrenoceptor antagonist with a pharmacodynamic profile similar to prazosin. Unlike prazosin, however, urapidil also has some central activity which may explain the apparent improved tolerability of urapidil, including the absence of first-dose syncope. In clinical trials urapidil therapy resulted in significant reductions in blood pressure in patients with mild to severe essential hypertension, with little influence on heart rate. It is an effective antihypertensive when administered as monotherapy or in combination with beta-blockers and thiazide diuretics. In the few patients with cardiac dysfunction who have been studied to date, urapidil has improved myocardial oxygen consumption, systemic vascular resistance, left ventricular function, cardiac output and pulmonary capillary wedge pressure; however, further study is needed to assess the full therapeutic potential of urapidil in these patients. Urapidil has also been used successfully in the treatment of hypertensive emergencies, including eclampsia and pre-eclampsia, hypertensive crisis and hypertension occurring during general and cardiac surgery, rapidly lowering blood pressure without altering heart rate. Urapidil does not affect lipid or glucose metabolism, nor does it impair renal function. In addition, urapidil may be beneficial to patients with pulmonary hypertension, in whom it dilates pulmonary vascular beds to a greater extent than systemic vasculature, although therapeutic trials have not examined this effect. The most common adverse effects associated with urapidil therapy are dizziness, nausea, headache, fatigue and palpitations; however, these tend to be mild and transient and usually do not require discontinuation of treatment. Thus, urapidil offers a useful alternative to currently available drugs for the treatment of mild to severe hypertension, either as monotherapy or in combination with other antihypertensive drugs.
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PMID:Urapidil. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the treatment of hypertension. 269 46

Elevation of pulmonary arterial pressure may be secondary to many diseases of the lungs, chest wall, and heart. From a pathophysiologic viewpoint, pulmonary hypertension is secondary to vascular obstruction, vasoactivity, increased circulation, and passive forces. Clinically, the entities that result in secondary pulmonary hypertension present with a picture that identifies the primary disease. Patients with primary pulmonary hypertension may be difficult to identify. Pulmonary hypertension may present early with dyspnea and fatigue, while syncope and hemoptysis are late symptoms. In many instances, pulmonary hypertension can be diagnosed utilizing physical examination and noninvasive tests. Eventually, right heart catheterization is necessary to confirm the diagnosis and to monitor trials of therapy with vasodilators. Treatment may be specific (closure of a septal defect, thromboendarterectomy) or generic (vasodilators). These have been used recently for both secondary and primary pulmonary hypertension in an effort to reduce pulmonary vascular resistance, thereby decreasing right ventricular afterload and improving cardiac output and oxygen delivery. The success of these treatments has not been demonstrated.
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PMID:Pulmonary hypertension: etiology and clinical evaluation. 333 61

Calcium-channel antagonists may provide an effective approach to the treatment of pulmonary hypertensive disorders. Biochemical evidence suggests that pulmonary vasoconstriction results from the transmembrane flux of calcium into vascular smooth muscle; accordingly, the pulmonary pressor responses in experimental hypoxic pulmonary hypertension can be attenuated by verapamil and nifedipine. In patients with chronic obstructive lung disease, nifedipine decreases pulmonary artery pressures and pulmonary vascular resistance in proportion to the severity of hypoxemia before treatment. However, little pulmonary vasodilator effect is seen when hypoxemia is corrected by inhalation of oxygen, and systemic arterial oxygen desaturation can occur after nifedipine in patients breathing room air; most importantly, long-term studies in patients with chronic lung disease are lacking. In selected patients with primary pulmonary hypertension and other obliterative diseases of the pulmonary vasculature, nifedipine produces short- and long-term hemodynamic improvement at rest and during exercise, and these benefits are frequently paralleled by amelioration of dyspnea and fatigue. However, in patients in whom right ventricular function has been severely compromised by chronic pressure overload, both verapamil and nifedipine may exert notable depressant effects on right ventricular performance, despite the decrease in right ventricular afterload that would be expected to accompany a decrease in pulmonary vascular resistance. These negative inotropic actions may result in serious deleterious clinical reactions. Although calcium-channel antagonists represent a promising approach to the management of patients with pulmonary hypertension, the long-term efficacy and safety of these drugs in this disorder remain to be established.
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PMID:Therapeutic application of calcium-channel antagonists for pulmonary hypertension. 388 14


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