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)

Dyspnea is the medical term for the patient's or subject's complaint of shortness of breath. It encompasses the respiratory discomfort experienced in many different diease states as well as the shortness of breath felt by a normal subject during or after strenuous exercise. Several parameters which have been shown to correlate with the onset or severity of dyspnea are described, including reduced vital capacity, the ratio of minute ventilation to vital capacity, reduced breathing reserve, the work of breathing, and the oxygen cost of breathing. Attempts at quantitation of dyspnea have usually consisted of measuring physiological parameters associated with the sensation, such as the "dyspneic index". The direct measurement of respiratory sensations using modern psycho-physical methods is at an early stage of development. Since the observation that the existence of dyspnea is often unrelated to any disturbance of arterial blood gas composition, it has been generally held that the mechanism of dyspnea is primarily neurophysiological. The neural pathways may conceptually be divided into those which transmit the "dyspnea message" from the respiratory apparatus to integrating centers in the brain, and those concerned with subsequently bringing the sensation to the level of consciousness. It seems likely that there is no single sensing mechanism and neural pathway which will be able to explain dyspnea in the diverse populations of patients and subjects who experience unpleasant respiratory sensations. Three theories concerning mechanisms of dyspnea are briefly described: "length-tension inappropriateness", vagal afferent activity especially from the J-receptors, and the recent concept of diaphragmatic fatigue. Some specific characteristics of the shortness of breath experienced in certain disease states are described, including chronic bronchitis and emphysema, bronchial asthma, pulmonary fibrosis and congestive heart disease.
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PMID:Dyspnea. 50 81

A 42-year-old woman with a known history of paraquat ingestion was admitted to our hospital on the 10th day after ingestion complaining of dyspnea and general fatigue. Steroid therapy and low dose oxygen therapy were administered. She recovered and was discharged on the 190th day after paraquat ingestion. A chest X-ray film on admission disclosed a bilateral ground-glass shadow. As time passed, a reticular shadow with a loss of lung volume leaving a peripherally clear zone appeared on chest X-rays and shrank gradually toward the peri-hilar area during the course. CT of the lung clearly demonstrated progress of the pulmonary fibrosing process. In the early phase of paraquat poisoning, CT revealed diffuse high density areas dominant in the posterior part of the lungs with a subpleural intact area. The high density area was sharply demarcated from the subpleural intact area. As time passed, the high density area shrank toward the central zone, causing bullous changes in the subpleural area. The dominant fibrotic change in the intermediate and central zones seems to be one of the characteristic findings in paraquat induced pulmonary fibrosis.
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PMID:[Observations of the fibrosing process in paraquat lung injury by chest X-ray and CT]. 188 7

10-Edam (10-ethyl-10-deaza-aminopterin), an antifolate derivative, was administered to 14 chemotherapy-naive patients with advanced colorectal carcinoma. The drug was given weekly by intravenous route at an initial dose of 80 mg/m2, with escalation or attenuation according to tolerance. Mucositis was dose limiting and occurred in 11 of 14 patients (78.6%). Removal from the study was required in one patient due to progressive pulmonary fibrosis that was histologically identical to methotrexate-induced lung damage. Toxicity was otherwise mild to moderate and included diarrhea, constipation, abdominal discomfort, anorexia, nausea/vomiting, rash, and fatigue. There were no responses to 10-Edam in this study, 95% confidence interval (0-0.23). Stable disease was achieved in four patients; the remaining 10 patients demonstrated progression within 9 weeks of initiating systemic therapy. 10-Edam employed at this dosage and schedule was not effective as a treatment against advanced colorectal carcinoma.
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PMID:Phase II trial of 10-Edam in patients with advanced colorectal carcinoma. 230 19

Hypersensitivity pneumonitis (extrinsic allergic alveolitis) represents a spectrum of granulomatous, interstitial, and alveolar-filling lung disorders of which farmer's lung is a classic example. A major source of offending antigens in these diseases are thermophilic actinomycetes growing in moldy vegetable matter especially Micropolyspora faeni, and members of the Thermoactinomyces genus. Acutely, hypersensitivity pneumonitis presents as cough, dyspnea and fever, with crepitant rales, leucocytosis, diffuse interstitial and alveolar pulmonary infiltrates and a restrictive-type pulmonary functional deficit. Symptoms usually begin 4 to 6 hr after exposure to large quantities of causative organic dust. Chronically, these diseases may present with the gradual onset of cough, dyspnea on exertion, fatigue, anorexia, and weight loss which may progress to pulmonary fibrosis or severe pulmonary insufficiency. While early ideas on the pathogenesis of hypersensitivity pneumonitis support the role of Type III immune complex hypersensitivity, more recent evidence attests to the important and integral role of Type IV or delayed-type hypersensitivity. It is the purpose of this review, therefore, to describe those immune mechanisms relevant to the pathogenesis of hypersensitivity pneumonitis and stress the importance of "local" pulmonary immune responsiveness.
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PMID:Immunology of hypersensitivity pneumonitis. 676 Oct 66

A pediatric patient is reported who experienced fatal progressive pulmonary fibrosis as a complication of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) therapy. The patient received a cumulative dosage of 1.29 g (1.72 g/m2) over a two-year period as adjuvant therapy for a medulloblastoma. Two and one-half years after cessation of therapy, cough, tachypnea and fatigue were noted. Progressive pulmonary insufficiency developed. Pulmonary pathologic findings included interstitial fibrosis and alveolar dysplasia. Other cases of BCNU pulmonary toxicity are cited from the medical literature.
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PMID:Pulmonary fibrosis: a complication of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) therapy. 727 34

Well-recognised complications are pulmonary fibrosis, cor pulmonale, glaucoma, cataract and nephrocalcinosis causing failure of lungs, heart, vision and kidneys. Less well-recognised is the post-sarcoidosis chronic fatigue syndrome. The afflicted join sarcoidosis patients' associations because of their profound symptoms of myalgia, fatigue, sleep reversal and low-spiritedness. The symptoms are out of proportion to the lack of physical signs and the absence of objective evidence of sarcoidosis. Management includes unremitting sympathy and replenishment of essential neurochemicals.
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PMID:Complications of sarcoidosis. Chronic fatigue syndrome. 817 98

Except for benign pleural effusion, asbestos-related pulmonary complications, including asbestosis, malignant mesothelioma and bronchogenic carcinoma, usually occur more than 20 years after exposure. Pleural plaques and pleural thickening serve as markers for asbestos exposure, but they are not associated with an increased risk of malignancy. Clinical criteria for the diagnosis of asbestosis include a reliable history of asbestos exposure, an appropriate interval between exposure and disease detection, radiographic evidence of pulmonary fibrosis, decreased vital capacity and diffusing capacity, and bilateral posterior inspiratory crackles. A lung biopsy is indicated only to rule out other causes of interstitial lung disease. A history of dyspnea, pleuritic chest pain, fatigue, weight loss and pleural effusion in a former asbestos worker is suggestive of mesothelioma. Cigarette smoking greatly increases the risk of lung cancer in asbestos workers.
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PMID:Pulmonary complications of asbestos exposure. 804 65

Over 100 cases of disorders closely resembling classic autoimmune diseases have been reported among patients who were injected or implanted with a diverse group of chemicals including paraffins, vegetable oils or silicone. Most cases have occurred in silicone breast implant recipients, especially those who received their prostheses 2-10 years prior to onset of symptoms. A high proportion of patients exhibit classic signs and symptoms of Sjogren's syndrome or scleroderma. Affected patients typically experience some combination of fatigue, myalgia, joint pain, sicca syndrome (dry eyes and mouth), synovitis, rash, alopecia, muscular weakness or lymphadenopathy, and autoantibody formation. Less commonly, patients may have the CREST syndrome (calcinosis, Raynaud's phenomena, esophageal hypomotility, sclerodactyly and telangiectasias), hypertension, pulmonary fibrosis, or central nervous system pathology.
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PMID:Silicone-reactive disorder: a new autoimmune disease caused by immunostimulation and superantigens. 828 1

The aim of this study was to determine whether it is feasible to reduce the overall treatment time from 7 to 4 weeks in patients with non-small cell lung cancer (NSCLC) receiving radiotherapy with cisplatin. This follows an EORTC phase III randomised trial (08844) in which cisplatin given before each radiation dose resulted in improved local control and survival, but which had a relatively long treatment period of 7 weeks [Schaake-Koning et al., N Engl J Med 1992, 326, 524-530]. 38 patients with confirmed NSCLC (2 stage I, 1 stage II, 18 stage IIIA, 17 stage IIIB) received a total tumour dose of 55 Gy/20 fractions/26 days, from January 1992 to March 1994. Daily fractions of 2 Gy (5 times/week) were given to the macroscopic tumour and the non-involved adjacent lymph node areas. During the same session, a dose of 0.75 Gy was given to the macroscopic tumour (simultaneous boost). Cisplatin 6 mg/m2 was administered 1-2 h before each fraction, in an escalating total dose, during week 1 in 3 patients, during weeks 1 and 2 in 6 patients, during weeks 1, 2 and 3 in 5 patients and during the whole treatment in 24 patients. 38 patients were evaluable for acute side-effects (WHO). Maximal therapy-related toxicity (WHO) was grade 3 (nausea/vomiting in 2 patients, oesophagitis in 3 patients, dyspnoea in 3 patients, cough in 1 patient). Late side-effects were evaluated in 34 patients. There was grade 2 oesophagitis in 2 patients; grade 3 toxicity in 8 patients (tiredness in 3 patients, dyspnoea in 3 patients, oesophagitis in 2 patients); grade 4 toxicity in 4 patients (dyspnoea in 3 patients, cough in 1 patient). Pulmonary fibrosis grade 3 occurred in 4 and grade 4 in 6 patients. One patient developed a severe (grade 3) radiation pneumonitis. The low incidence of acute and late side-effects with this treatment, combining daily administration of 6 mg cisplatin with radical radiotherapy using a simultaneous boost technique, indicates that escalation of the radiation dose seems feasible.
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PMID:Feasibility of escalating daily doses of cisplatin in combination with accelerated radiotherapy in non-small cell lung cancer. 886 92

Postoperative radiotherapy (RT) forms an intrinsic part of breast conservation therapy, substantially reducing the risk of breast relapse. It is given 4-6 weeks postoperatively using medial and lateral beams to achieve a near homogeneous dose to the breast while minimising the dose to adjacent structures. Typically, a dose of 40 Gy in 15 daily fractions over three weeks or 50 Gy in 25 fractions over five weeks is given, with a boost of 10 Gy using low energy electrons or superficial X-rays. RT is delivered to the chest wall after mastectomy in patients with large tumours (> 5 cm), close surgical margins, or significant axillary node involvement and may result in an additional 10% survival benefit. Early complications of RT include tiredness, skin erythema and moist desquamation. Late reactions, breast fibrosis, telangiectases and peau d'orange are reduced if more treatment fractions are given. Lung irradiation is minimised by careful treatment planning and < 1% of patients experience radiation pneumonitis or pulmonary fibrosis. Patients with locally advanced breast cancer may be offered a combination of systemic therapy, endocrine, chemotherapy and radical RT. Preoperative systemic and radiation therapy reduces the mastectomy rate but at present does not improve survival. Those who are unfit for radical treatment and have large ulcerating or fixed cancers are offered either endocrine or cytotoxic therapy, depending upon the oestrogen receptor status, followed by RT, which is unlikely to cure but may achieve local control for a variable duration. RT forms part of the multidisciplinary approach to palliative treatment for metastatic disease. Bone metastases occur in 75% of women with metastatic disease and RT provides effective pain relief and reducing risk of pathological fractures. Patients with brain metastases need high-dose steroids followed by cranial RT.
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PMID:Radiotherapy for early and advanced breast cancer. 1177 Mar 58


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