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 clinical and laboratory findings of 28 patients identified as having late pericardial effusions were examined. Eleven of these patients were asymptomatic; 9 patients had moderate symptoms including fatigue, malaise, weight gain, and dyspnea on exertion, and 8 patients with similar symptoms had evidence of cardiac tamponade. Ten patients underwent right heart catheterization in the intensive care unit; normal hemodynamics were confirmed in 4 and cardiac tamponade in 6 patients. Pericardiocentesis was effective in decompressing cardiac tamponade in 7 of 8 patients. One patient required operative subxiphoid drainage after unsuccessful pericardiocentesis. In addition, 5 patients with moderate clinical symptoms and pericardial effusions, who did not have cardiac tamponade, underwent pericardiocentesis because of a need for chronic anticoagulant therapy. The remaining patients were managed successfully by observation, discontinuation of warfarin when possible, fluid restriction, and diuretic therapy. All but 1 patient was symptomatically improved. A diagnostic and therapeutic schema is presented as an aid to early recognition of this troublesome and potentially lethal complication.
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PMID:Diagnosis and management of postoperative pericardial effusions and late cardiac tamponade following open-heart surgery. 724 42

The end-stage heart failure phenotype is characterized by marked dyspnea on exertion, edema, and overwhelming fatigue, and by a high incidence of sudden death. Patients who display the end-stage phenotype have transitioned from a normal phenotype with myocardial damage at a cellular level. This transition appears to be mediated by events at both the cellular and molecular levels. Until recently, it was generally believed that this transition was irreversible. However, recent clinical trials have demonstrated that the phenotype can be changed with pharmacologic agents. These agents have been demonstrated to improve exercise capability, increase ventricular function, and improve symptoms. Important recent studies have shown that pharmacologic agents can substantially alter the high mortality rates associated with the end-stage heart failure phenotype. As we learn more about the molecular and cellular events that initiate and support the transition from cardiac compensation to decompensation, we will be able to improve our pharmacologic targeting and, we hope, be able to delay the development of the end-stage heart failure phenotype to an even greater degree.
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PMID:Strategies for pharmacologic modulation of the heart failure phenotype. 748 18

Near infrared spectroscopy (NIRS) is a noninvasive technique of monitoring tissue oxygen saturation by detecting changes in tissue absorbance of two wavelengths (850 and 760 nm) reflecting the relative oxygenation of hemoglobin and myoglobin. Aim of the present study was to determine whether changes in skeletal muscle oxygen saturation during incremental exercise detected by NIRS can reflect an impared oxygen delivery and an early onset of anaerobic metabolism in patients with chronic heart failure (CHF). We studied 19 subjects (mean age 43 +/- 16 years). Seven patients had a history of CHF with a diagnosis of ischemic cardiomyopathy (Group A) and 12 were healthy sedentary (Group B). All patients had a history of dyspnea on exertion (NY-HA II), peripheral edema, pulmonary rales and cardiac gallop sounds over the last 6 months. They were in sinus rhythm and stable clinical condition in the last 3 months. They were well matched regarding age, sex and body surface area. All subjects performed an incremental work rate test in a ramp pattern on a upright cycle ergometer until volitional fatigue. Gas exchange was measured breath by breath with a metabolic chart. Muscle oxygenation was determined, transcutaneously, during the exercise test over the vastus lateralis muscle with NIRS. At peak exercise, work rate, VO2, anaerobic threshold (LAT), heart rate and systolic blood pressure were significantly lower in Group A compared to Group B (92 +/- 28 vs 232 +/- 17 watts; 14 +/- 2 vs 21 +/- 2 ml/kg/min; 868 +/- 225 vs 1317 +/- 354 ml/min; 149 +/- 7 vs 172 +/- 18 b/min; 145 +/- 18 vs 195 +/- 21 mm Hg, respectively; p < 0.0001 for all). In both groups, as work rate increased, tissue oxygenation initially either remained constant near resting levels or decreased. In both groups, muscle oxygenation decreased more steeply near the work rate where lactic acidosis (LAT) was detected. However, patients with CHF had an earlier acceleration in muscle deoxygenation compared to the other group, indicating a premature onset of anaerobic metabolism. Moreover, Group A had a flatter increase in both heart rate and systolic blood pressure and a steeper slope of oxygenation profile at all matched workloads compared to normals (Group A: -0.13 +/- 0.03 ml/min; Group B: -0.06 +/- 0.015 ml/min; p < 0.0001). The LAT correlated with the work rate at which the rate of tissue O2 desaturation accelerated (r = 0.94; p < 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Near infrared spectroscopy and changes in skeletal muscle oxygenation during incremental exercise in chronic heart failure: a comparison with healthy subjects. 764 20

Deficiencies of mitochondrial enzymes cause a number of severe neurologic syndromes in pediatric patients. Isolated myopathy secondary to enzymatic deficiency only rarely has been recognized and reported in adults. Three normal-appearing patients with unexplained dyspnea on exertion, tachycardia, and fatigue were studied with progressive incremental and constant load exercise testing with hemodynamic and gas exchange measurements. Subsequently, muscle biopsies were performed and enzymatic profiles determined. Exercise testing suggested altered cellular energy metabolism. Oxygen transport and gas exchange at rest and with exercise were normal. During exercise, ventilation increased excessively for the work performed, but it was appropriate for carbon dioxide production. Cardiac outputs increased significantly (196 to 305%), heart rates reached maximum levels, and lactic acid levels increased (385 to 833%) during exercise at 25 W. Muscle morphology was normal, but mitochondrial enzyme assays demonstrated one or more deficiencies in all three patients. Mitochondrial enzymatic deficiency can be a cause of unexplained exercise symptomatology and limitation in adults. Our experience would suggest the incidence of the disorder may be greater than that previously recognized or expected. Symptoms of exercise limitation associated with dyspnea, tachycardia, or muscle fatigue should alert the clinician to a possible abnormality in cellular energy metabolism.
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PMID:Mitochondrial enzyme deficiency causing exercise limitation in normal-appearing adults. 784 54

A 26-year-old male who had been diagnosed as pulmonary tuberculosis three years ago with an antituberculous chemotherapy of only two months, complained of tiredness, exertional dyspnea and fever since a month ago. Bloody sputum, bloody stool and hematuria have developed three days before admission. Petechiae over the body trunk and lower extremities were observed on admission. Peripheral blood examination revealed lymphocytopenia (672/microliters), low hemoglobin content (6.2 g/dl), thrombocytopenia (3,000/microliters), elevated FDP (36.2 micrograms/ml) and D-dimer (25.0 micrograms/ml) values. Chest radiograph showed a massive pleural effusion in the right hemithorax, bilateral pulmonary infiltrates and a cavity on CT scan. Together with positive acid-fast bacilli in sputum, diagnoses of relapsed pulmonary tuberculosis, tuberculous pleurisy associated with DIC (disseminated intravascular coagulation) were made. Left hydronephrosis which was presumed to be a consequence of infundibulum stenosis due to renal tuberculosis, was detected by abdominal ultrasonography. Treatment with antituberculous drugs and protease inhibitors were started with thoracic tube drainage. DIC condition was improved by the 20th hospital day and sputum culture turned to be negative after the 4th week, however, fever up to 38 degrees C continued until the end of the 7th week and a D-dimer which is a representative marker for secondary fibrinolysis, continuously showed a high level up to the 10th week of hospitalization. The patient was uneventful during the three months follow up period after discharge. DIC is a well known complication of sepsis including miliary tuberculosis, whereas it is rarely associated with cavitary tuberculosis and no case of prolonged elevation of D-dimer have been reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of pulmonary, pleural, and renal tuberculosis associated with DIC and a prolonged increase in D-dimer]. 804 Oct 60

Exertional intolerance is a major clinical problem in ambulatory patients with chronic heart failure and is associated with both muscle fatigue and dyspnea. The increased muscle fatigability is most likely caused by a combination of muscle underperfusion and muscle deconditioning; patients frequently exhibit skeletal muscle atrophy, altered muscle metabolism and reduced mitochondrial-based enzyme levels, consistent with deconditioning. The muscle underperfusion is largely due to impaired arteriolar vasodilation within exercising muscle. Exertional dyspnea appears to be due to increased respiratory muscle work mediated by excessive ventilation and decreased lung compliance. Both excessive carbon dioxide production, secondary to increased muscle lactate release, and increased lung dead space contribute to the excessive ventilation. Decreased lung compliance is caused by chronic pulmonary congestion and fibrosis. Optimal management of exercise intolerance in patients with heart failure requires an understanding of the role of these multiple potential contributors to exertional fatigue and dyspnea.
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PMID:Factors contributing to the exercise limitation of heart failure. 837 1

Atrial septal defect (ASD) is one of the most common congenital cardiac anomalies found in the adult population. Although usually asymptomatic in childhood, ASD will be symptomatic in approximately 75 percent of adults. The most common symptoms include fatigue, dyspnea on exertion, and palpitations. However, the presentation of ASD can be protean. We present four patients with secundum ASD with unusual clinical manifestations. Patient 1 had moderately severe mitral regurgitation. Patient 2 had pulmonary edema with generalized left ventricular impairment. Patient 3 had chest pain typical of angina pectoris. Patient 4 had right-to-left shunt following an orthopedic surgical procedure. These patients had chest radiographs and electrocardiograms typical of secundum ASD, but their presentations were uncommon. In three of four of these patients, dramatic resolution of symptoms followed surgical repair of their ASD.
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PMID:Unusual clinical presentations of secundum atrial septal defect. 840 69

A 60-year-old man with pneumoconiosis complained of general fatigue, exertional dyspnea, and anorexia. The patient had severe anemia, and laboratory examination revealed autoimmune hemolytic anemia with positive direct and indirect Coombs tests. After corticosteroid therapy, the anemia resolved markedly, and the antinuclear antibody test became negative. However, the silicotic shadow on chest X-ray film showed no remarkable change. The autoimmune hemolytic anemia in this case was probably due to an immunological disturbance caused by silicosis.
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PMID:[Silicosis associated with autoimmune hemolytic anemia]. 858 25

A 68-year-old white woman was referred to us by her rheumatologist for possible participation in a clinical study of photopheresis for scleroderma. In February 1993, she noticed edema of her distal phalanges, Raynaud's phenomenon in both hands, flu-like symptoms, fatigue, intermittent diarrhea, abdominal pain, tearing in both eyes, dyspnea on exertion, dysphagia, and odynophagia. Bilateral silicone-gel breast implants had been placed 12 years before; 2 months before her present evaluation, they were removed and found to be ruptured. Physical examination revealed edema, limited to the fingers and hands bilaterally, and slight induration of the skin on the dorsum of both hands and distal forearms. The remainder of the physical examination was normal. According to our study protocol, a skin biopsy specimen from the dorsum of the right hand was taken, but all other laboratory investigations were refused. Histopathologic examination revealed multiple clear spaces of varying sizes in the dermis and multinucleated macrophages containing small refractile particles, characteristic of silicone granuloma (Figs. 1 and 2); however, the specimen showed no evidence of scleroderma. X-ray energy dispersive analysis by scanning electron-microscopy confirmed the presence of elemental silicon in the small refractile particles. The patient did not receive any treatment after her diagnosis and shortly thereafter, she was lost to follow-up.
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PMID:Silicone granuloma in acral skin in a patient with silicone-gel breast implants and systemic sclerosis. 883 27

Primary pulmonary hypertension (PPH), an often fatal disease, is characterized by elevated pulmonary artery pressures in the absence of a secondary cause. Endovascular occlusion in the smallest pulmonary arteries occurs by proliferation of cells and matrix, with thrombus and vasospasm. Diagnosis is often delayed because the initial symptoms of fatigue and dyspnea on exertion are nonspecific and definitive diagnosis requires invasive procedures. The average life expectancy after diagnosis is two to three years with death usually due to progressive right heart failure. The aetiology of the disease is unknown. Although most cases appear to be sporadic, approximately 6% of cases recorded in the NIH Primary Pulmonary Hypertension Registry are inherited in an autosomal dominant manner with reduced penetrance. Following a genome-wide search using a set of highly polymorphic short tandem repeat (STR) markers and 19 affected individuals from six families, initial evidence for linkage was obtained with two chromosome 2q markers. We subsequently genotyped patients and all available family members for 19 additional markers spanning approximately 40 centiMorgans (cM) on the long arm of chromosome 2. We obtained a maximum two-point lod score of 6.97 at theta = 0 with the marker D2S389; multipoint linkage analysis yielded a maximum lod score of 7.86 with the marker D2S311. Haplotype analysis established a minimum candidate interval of approximately 25 cM.
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PMID:Localization of the gene for familial primary pulmonary hypertension to chromosome 2q31-32. 905 41


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