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)

A rare side effect of minocycline is acute eosinophilic pneumonia. In the literature only ten cases have been reported. We report two cases of minocycline which induced (eosinophilic) alveolitis. A high fever, dry cough, dyspnoea and fatigue are the main features of the clinical picture. Peripheral blood eosinophilia and elevated total IgE content were seen in one patient. Bronchoalveolar lavage in this patient revealed eosinophilia. Transbronchial lung biopsies showed infiltration with eosinophilic granulocytes in both patients. Airway macrophages contained brown-black pigment granules. In the acute stage an important decrease in diffusion capacity was observed. The pulmonary and systemic symptoms promptly cleared up after discontinuation of minocycline. Provocation with minocycline was positive, because both patients noticed the same symptoms within one day.
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PMID:[Minocycline as a cause of acute eosinophilic pneumonia]. 153 40

Autopsy or surgical specimens from six patients with primary cardiac angiosarcoma seen at the Mayo Clinic (all in men) between 1939 and 1988 were studied (patients' ages, 31 to 80 years; mean 50 years). The symptoms were nonspecific and included dyspnea and thoracoabdominal pain in six; anorexia in five; fatigue, hemoptysis, or orthopnea in four; nausea and vomiting, fever, or weight loss in three; and night sweats in two. Cardiomegaly was present in five, and a pericardial effusion or density, a mass adjacent to the heart, or nonspecific ST-T wave changes were present in three. All six neoplasms arose from the right atrium and exhibited epicardial or endocardial extension; three produced obstructive intracavitary right atrial masses. Pulmonary metastatic lesions were noted in five patients. The cardiac neoplasm was diagnosed by computed tomography or magnetic resonance imaging in the three most recent patients, and surgical resection was performed in two of them. Mean survival was 6 months after presentation. Causes of death were pulmonary hemorrhage in three, thoracic metastasis in two, and hemopericardium in one. The diagnosis of primary cardiac angiosarcoma was established at operation in two patients and at autopsy in four. Despite diagnosis by noninvasive imaging procedures and aggressive early surgical intervention, survival was less than 6 months. Thus optimal therapy is unclear.
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PMID:Primary cardiac angiosarcoma: a clinicopathologic study of six cases. 154 8

Tricuspid valvular insufficiency caused by blunt thoracic trauma may be clinically silent and imprecise. Diagnosis is often done by cardiac catheterization and two-dimensional echocardiography (2-DE); the latter may show abnormalities of the tricuspid leaflet motion. The surgical technique for its correction is still controversial. We report here the case of an eighteen year old man who was involved in a high-speed motorcycle accident. Seven months later, due to dyspnoea and fatigue, 2D-E examination revealed cardiac enlargement and severe tricuspid regurgitation. Surgery was indicated in order to repair valve incompetence. Reinsertion of the chordae tendineae at the anterolateral papillary muscle and annuloplasty was performed and ten months postoperatively, he is in good clinical condition and 2D-E control shows a trivial residual tricuspid insufficiency.
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PMID:Traumatic tricuspid regurgitation. 157 90

To evaluate the frequency of the causes of exercise limitation in patients with chronic pulmonary disease and to assess the relationship between the resting pulmonary functional parameters and the degree of exercise dyspnea, we reviewed the data from 88 consecutive stable patients with chronic lung disease (62 COPD, 16 interstitial lung disease [ILD]). In each patient, the intensity of dyspnea was measured by a Borg scale (BS) during an incremental symptom-limited exercise test. COPD patients stopped exercise due to fatigue (46%), dyspnea (36%), cardiac limitation (12%), and peripheral circulatory limitation (6%). ILD patients stopped exercise due to dyspnea (62%), fatigue (25%), and cardiac limitation (12%). In all patients, dyspnea severity increased linearly with exercise intensity as measured as VO2, VE, and VE/MVV. The severity of dyspnea expressed as the slope of the relationship between BS and VE/MVV (DBS/D[VE/MVV]) showed in COPD a significant inverse correlation with VC, FEV1, MIP, and a positive correlation with PaCO2 and VE/MVV at rest. In ILD, DBS/D(VE/MVV) showed a significant inverse correlation with VC, FEV1, TLC, and PaO2 and a positive correlation with VE/MVV at rest. The predicting power of all equations was very low.
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PMID:Dyspnea on exercise. Pathophysiologic mechanisms. 157 44

The factors that contribute to the symptoms of breathlessness and fatigue, and that limit exercise capacity in patients with chronic heart failure are poorly understood. Recent evidence suggests that the major mechanism is not related to central hemodynamics but to a reduction of skeletal muscle mass and diminished blood flow to skeletal muscle on exercise.
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PMID:Blood flow and skeletal muscle in patients with heart failure. 157 60

Multiple compensatory mechanisms operate to preserve exercise tolerance in patients with left ventricular failure. Exercise capacity of most patients with chronic heart failure is limited by dyspnea or fatigue, or both. Maximal stress testing with direct assessment of peak O2 uptake is an essential measurement in planning exercise conditioning programs, which are now attracting patients with chronic heart failure. The biochemical and histologic patterns of skeletal muscle changes seen in chronic heart failure patients are consistent with the effects of long-term exercise deconditioning in normal subjects. Recent studies have suggested beneficial effects of training in subjects with moderate or even severe left ventricular dysfunction by showing increased exercise tolerance or peak O2 consumption, anaerobic threshold, peak leg blood flow, peak central arteriovenous oxygen difference and decreased lactate accumulation. However, a number of questions remain unanswered. Exercise training for the treatment of chronic heart failure should be determined on an individual basis and used with caution.
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PMID:Physical training in patients with congestive heart failure. 157 63

Tropical pulmonary eosinophilia is one of the many PIE syndromes [pulmonary infiltrates with eosinophilia (of the peripheral blood)]. It is caused by immunologic hyperresponsiveness to the filarial parasites Wuchereria bancrofti or Brugia malayi. Its clinical presentation includes nocturnal cough, dyspnea, wheezing, fever, weight loss, fatigue, interstitial mottling on chest radiograph, predominantly restrictive but also obstructive lung function abnormalities, and peripheral blood eosinophilia of more than 3000 per microliter. It can be distinguished from other PIE syndromes by the patient's history of residence in the tropics, by the presence of extraordinarily high levels of both serum IgE and antifilarial antibodies, and by the dramatic clinical improvement after treatment with the antifilarial drug diethylcarbamazine. Recent studies indicate that the compromised lung diffusion capacity of patients with acute tropical pulmonary eosinophilia is a function of the degree of the eosinophilic alveolitis present and that, despite a 3-week course of diethylcarbamazine, low-grade alveolitis persists in almost half of such patients; this persistent alveolitis is likely to be the cause of the progressive interstitial fibrosis seen in many untreated or inadequately treated patients with tropical pulmonary eosinophilia.
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PMID:Tropical pulmonary eosinophilia. 158 May 99

Allergic alveolitis due to bird antigens was diagnosed in a 12-year-old boy. He suffered from cough, dyspnea, easy fatigue, anorexia, and severe weight loss. The diagnosis was verified by a gradual improvement when he was removed from the birds, exacerbation upon re-exposure, and the demonstration of serum precipitating antibodies against bird antigens. The patient recovered completely after a short course of oral prednisolone, treatment with inhaled nebulized budesonide for 3 months, and removal of the birds from his home.
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PMID:Allergic alveolitis in a 12-year-old boy: treatment with budesonide nebulizing solution. 161 53

Health status of 7 men was examined in order to study the effect of duty work cycle of 3-d stay at the altitude of 2,000 m and one-day holiday at 600 m for a period of 6 months from May to October. Their usual works were desk work and road patrol. Total hemoglobin concentration in blood increased significantly after work at high altitude, which was considered to be a compensatory response to the hypoxic state. Subjective symptoms were obtained by a self-administered questionnaire before (April), during (June and October) and after (November) work at high altitude. Fatigue was observed in three out of the seven subjects in June, which subsequently disappeared in October. Dyspnea was observed also in June in three of the subjects, which disappeared in two, persisted in one, and newly appeared in another subject in November. In contrast, a tendency of favorable effects of the work environment on nausea and lumbago was observed. Blood pressure and pulse rate were measured for 24 h. The mean systolic blood pressure during 24 h decreased in two of five subjects in October and November, and the mean values during the working hours decreased in two in October from 145 to 131 mmHg and from 147 to 129 mmHg, respectively. The blood pressure measured at health examination correlated well with the mean blood pressure during 24 h and working hours. The mean pulse rate during 24 h and working hours increased in one in June, October and November. These results indicate that adaptive responses to low barometric pressure environment developed during a work period of 5 months at high altitude.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of seasonal and intermittent work at high altitude on health status]. 161 5

The timing of valve replacement in patients with mitral valve disease, severe resting pulmonary hypertension, and severe symptoms is usually straightforward. However, this may not be true for patients with mild to moderate resting pulmonary pressures and symptoms that are difficult to evaluate. The measurement of hemodynamic parameters with exercise has been useful during cardiac catheterization. The purpose of this study was to evaluate the hemodynamic significance of dyspnea provoked by exercise in patients with mitral valve disease using exercise Doppler echocardiography. Nineteen tests were done in 17 patients (two patients had repeat studies 1 year after the first test). Dyspnea developed in patients during exercise in 11 tests, and the others were limited by fatigue (and angina in one patient). There was a significantly greater increment in pulmonary artery systolic pressure during exercise in the patients who developed dyspnea (24 mm Hg) than in those who did not (15 mm Hg, p = 0.04). The two groups exercised to approximately the same heart rate and blood pressure, but the dyspneic patients had a significantly shorter exercise capacity (p = 0.04). Furthermore, clinical decision making was affected by the test results in 84% (only three tests did not affect patient management) and included a decision to proceed to invasive testing and surgery in seven patients, and a decision to treat the patient medically in nine. In conclusion, exercise Doppler echocardiography is a useful adjunct in the diagnosis and treatment of patients with mitral valve disease and an aid to clinical decision making.
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PMID:Exercise Doppler echocardiography as an aid to clinical decision making in mitral valve disease. 162 12


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