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)

Thirty-eight workers from a factory producing nickel-cadmium and other types of batteries came to us for medical evaluation. They included 21 women and 17 men (seniority 2-20 years, age range 31-63 years), and represented a self-selected subset of 700-900 ever-employed and 200+ recently or currently employed workers in the factory. Thirty-four worked on the nickel-cadmium assembly line. Symptoms and signs included: headache in 34; weakness, fatigue and lassitude in 26; dizziness in 16; pruritus and skin eruptions in 37; gingivitis, teeth loss and caries in 34; nasal congestion, nosebleeds and anosmia in 30; cough, phlegm production, wheezing and shortness of breath in 26; "asthma" in 14; bone pain in 18; urinary frequency, beta 2 microglobulinuria and kidney stones in 17; and sterility or multiple abortions (33) in 8 of 21 women. One additional patient had died from an "amyotrophic lateral sclerosis-like syndrome", while CT scans in six workers revealed brain atrophy. One other worker had leukemia, and two had died from cancer (lung and pancreas). Those who had worked for more than 10 years had more symptoms and signs than shorter-term employees, especially neurological illness, bone pain and urinary tract problems, including beta 2 microglobulinuria. Past blood and urinary cadmium levels were in the range of 1.6-8.7 micrograms/dl and 8-306 micrograms/l, respectively. Our findings indicated that: a) health risks for workers were not confined to the nickel-cadmium assembly line or to older workers, b) hazardous exposures still existed and illness appeared in new workers after a clean-up and intervention program, and c) exposures involved increased risks for renal disease and cancers. Finally, there is a need to control exposures and determine health risks in the full cohort of those ever employed, in the workers' children, and in the surrounding environment (air, ground, water) due to the dumping of waste from the plant.
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PMID:Medical findings in nickel-cadmium battery workers. 142 13

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

A case report of an urban family who experienced excessive exposure to organophosphate and carbamate pesticides is presented. All three family members developed symptoms that were compatible with cholinesterase inhibition: headache, lightheadedness, wheezing, shortness of breath, nausea, and fatigue. Serial measurement of red blood cell and serum cholinesterases soon after exposure and during subsequent months confirmed the diagnosis of pesticide poisoning. This report demonstrates that the misapplication of pesticides commonly used in residences in urban areas can cause acute pesticide poisoning and demonstrates the usefulness of repeated measurements of cholinesterase during the post-exposure period in establishing the correct diagnosis.
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PMID:Poisoning of an urban family due to misapplication of household organophosphate and carbamate pesticides. 158 78

Seventeen patients with malignant carcinoid tumour, ten of whom had the malignant carcinoid syndrome, were treated with recombinant alpha-2b interferon by subcutaneous injection (3 MU per dose) three times per week for a median of 12 weeks (range 4-48). No objective tumour responses were observed; however, there was a greater than 50% reduction in 24-hour urinary 5-hydroxyindolacetic acid (5-HIAA) excretion in four of ten patients (40%) with elevated pretreatment levels. Five of ten patients (50%) with flushing, five of seven patients (71%) with diarrhoea and both patients with wheezing experienced relief of symptoms. Three of four patients (75%) with weight loss as their only problem experienced weight gain. Responses occurred within the first eight weeks of treatment, but were generally of short duration. Toxicity occurred in all patients, and consisted mainly of fever, chills, anorexia, fatigue and weight loss. Four patients ceased therapy due to toxic reactions. Although interferon has activity against carcinoid tumours, its benefits are short-lived and toxicity limits its use with increasing dose. Patients with carcinoid syndrome appear to achieve the best therapeutic response, and it is likely that low doses (9-20 million IU weekly) are as effective as higher doses (36-72 million IU weekly).
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PMID:Recombinant alpha-2b interferon in patients with malignant carcinoid tumour. 172 59

The purpose of this study was to compare psychologic and physiologic variables during intense dyspnea to those at times of no or low dyspnea in people with asthma. Thirty-six adults ranging from 19 to 76 years old were tested when they first came to the emergency department in acute dyspnea and again when they had no or low dyspnea just prior to discharge. Clinical signs found to be higher during high dyspnea than low dyspnea were respiratory rate, pulse, wheezing, and accessory muscle use. Peak expiratory flow rates and oxygen saturation were significantly lower, while anxiety, depression, somatization, and hostility were higher during times of high dyspnea. The panic/fear, fatigue, dyspnea, hyperventilation/hypocapnia, congestion, and rapid breathing subscales of the Asthma Symptom Checklist were also higher during high dyspnea compared to low dyspnea.
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PMID:Psychologic and physiologic aspects of acute dyspnea in asthmatics. 185 43

During autumn- and winter epidemics respiratory syncytial (RS) virus accounts for the majority of respiratory infections in infants and young children. In case of an acute lower respiratory tract infection, RS virus can induce serious symptoms. These are age-dependent. The most important symptoms in babies and toddlers are dyspnea, wheezing, cyanosis and apneas. In the case of respiratory insufficiency or fatigue, as well as recurrent apneas, mechanical ventilation is required. Diagnosis can be made using a direct immunofluorescence technique with monoclonal antibodies. To control the risk of nosocomial RS virus infections, isolation precautions are necessary. The overall mortality is low (less than 1%), but may be strikingly higher in children at risk: babies less than one month of age, preterm babies, infants with congenital heart- or pre-existent respiratory diseases, and those with severe immunodeficiency syndromes. In these subgroups therapy with ribavirin (Virazole) may be beneficial, although until now there is no strong evidence for the effectiveness of this antiviral agent. The majority of the children will have recurrent symptoms of dyspnea and wheezing over the subsequent years following the RS virus infection. In acute lower respiratory RS virus infection, there may be IgE mediated hypersensitivity reactions to viral agents, with release of chemical mediators of airway obstruction. The pathophysiological mechanisms might be comparable to those in patients with asthma.
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PMID:[Once more a discussion of the RSV affair]. 218 Jan 18

We report on the distress associated with physical symptoms in 761 male hypertensive patients enrolled in a clinical trial of the effects of captopril, methyldopa or propranolol on quality of life. Educational level at entry into the trial showed a negative association with a series of physical symptom distress items among patients not previously treated with antihypertensive medications but no association with symptoms among the previously treated. Over the 24 weeks of therapy captopril as monotherapy was associated with no change from baseline in distress in all symptoms examined. In contrast, distress increased in the methyldopa treated patients for dry mouth and blurred vision. Propranolol treated patients had increased "trouble getting breath," bradycardia, shortness of breath or wheezing, and blurred vision. Between group comparisons revealed significant differences favorably comparing captopril to both methyldopa and propranolol in regard to fatigue, and blurred vision, as well as to methyldopa alone for dry mouth and "feeling worn out." There were significant differences as well between captopril and propranolol with patients on propranolol worsening in bradycardia. Other comparisons of patients on propranolol and methyldopa monotherapy showed propranolol patients worsening in bradycardia and loss of taste, but methyldopa patients reported more dry mouth and feeling worn out than those on propranolol. The addition of hydrochlorothiazide to therapy worsened total physical symptom distress scores for methyldopa and propranolol patients. This study confirms the value of methods which assess the degree of distress associated with symptoms commonly reported by hypertensive patients receiving antihypertensive medications. This approach can be useful in establishing a treatment regimen least likely to cause distress and can be of value in preserving quality of life, preventing noncompliance, and withdrawal from treatment.
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PMID:Self-reported side effects from antihypertensive drugs. A clinical trial. Quality of Life Research Group. 240 65

One hundred forty-five male welders from a West Coast shipyard were studied cross-sectionally and across a Monday work shift by pulmonary function tests and a questionnaire. Ten years of welding was associated with chronic bronchitis in 23.3% of nonsmokers compared to 3.3% in male controls, shortness of breath in 31.5% of nonsmokers compared to 1.5% in controls, and chest pain or heaviness in 38.4% compared to 4.4% in controls. Men who welded aluminum but had never smoked had more frequent wheezing, chest tightness, phlegm, feverishness and fatigue than those welding mild (black) or stainless steel. There were no significant cross-shift effects from welding exposure on measurements of pulmonary function. Although baseline expiratory flows were reduced slightly when compared to Caucasian-predicted values, ethnic specific comparisons for the largest subgroup showed only that FEF25-75 was reduced to 92.9 percentage of predicted values. Diffusing capacities for carbon monoxide were significantly reduced as compared to referents. The pulmonary function values of 25 current smokers were indistinguishable from the 41 who had never smoked, which probably reflects their low consumption of cigarettes.
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PMID:Respiratory symptoms and functional impairment from acute (cross-shift) exposure to welding gases and fumes. 281 87

Rare upper airway lesions may be mistaken for asthma. A 16-year-old Hispanic male athlete presented to our allergy clinic with a 4-month history of wheezing and snoring with hoarseness and progressive fatigue on exertion or during sleep. His mother taped periods of harsh stridor and sleep apnea. There was no family history of vocal cord abnormalities. A year before the onset of symptoms, he suffered injury to his oral cavity with a loss of consciousness during a wrestling match. He denied dysphagia or dysphonia. He failed to respond to bronchodilators, cromolyn, or prednisone therapy during 4 weeks. On referral to our clinic, his physical examination and tape recording were characterized by harsh inspiratory stridor. His pulmonary function tests were significant for peak flow depressed out of proportion to FEV1 with reduced FVC, no response to bronchodilator, and flattened inspiratory loop unresponsive to cough or panting. Fluoroscopy and endoscopy of the upper airway was consistent with "marked bilateral limitation of vocal cord abduction." Sleep study demonstrated desaturation with CO2s in the 60s during sleep. He was started on continuous positive airway pressure, 10 cm at night, with no desaturation or sleep disturbance on follow-up.
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PMID:Bilateral abductor paresis masquerading as asthma. 337 24

To determine if spirometric changes reflect early high-altitude pulmonary edema (HAPE) formation, we measured the FVC, FEV1, and FEF25-75 serially during the short-term period following simulated altitude exposure (4,400 m) in eight male subjects, four with a history of HAPE and four control subjects who had never experienced HAPE. Three of the four HAPE-susceptible subjects developed acute mountain sickness (AMS), based on their positive Environmental Symptom Questionnaire (AMS-C) scores. Clinical signs and symptoms of mild pulmonary edema developed in two of the three subjects with AMS after 4 h of exposure, which prompted their removal from the chamber. Their spirometry showed small decreases in FVC and greater decreases in FEV1 and FEF25-75 after arrival at high altitude in the presence of rales or wheezing on clinical examination and normal chest radiographs. One of the two subjects had desaturation (59 percent) and tachycardia during mild exercise, and excessive fatigue and inability to complete the exercise protocol developed in the other at 4 h. The six other subjects had minimal changes in spirometry and did not develop signs of lung edema. Further, we measured each subject's ventilatory response to hypoxia (HVR) prior to decompression to determine whether the HVR would predict the development of altitude illness in susceptible subjects. In contrast to anticipated results, high ventilatory responses to acute hypoxia, supported by increased ventilation during exposure to high altitude, occurred in the two subjects in whom symptoms of HAPE developed. The results confirm that HAPE can occur in susceptible individuals despite the presence of a normal or high ventilatory response to hypoxia.
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PMID:Pulmonary function and hypoxic ventilatory response in subjects susceptible to high-altitude pulmonary edema. 841 62


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