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 66-year-old woman was admitted to our hospital because of high fever, general fatigue, hypoxemia and liver dysfunction. Chest radiographs showed diffuse interstitial shadows in both lungs. We suspected drug-induced pneumonitis because of her history of drug administration for upper respiratory infection. Her symptoms and findings were markedly decreased by discontinuation of the drugs. Transbronchial lung biopsy specimens showed infiltration of eosinophils and lymphocytes to the alveolar septa, granuloma with Langhans' giant cells, and Masson bodies in a manner suggestive of hypersensitivity pneumonitis. Drug lymphocyte stimulation tests were negative except for loxoprofen. There was no recurrence of systemic or respiratory symptoms during overnight stays at home. On the basis of these findings, we arrived at a diagnosis of drug-induced pneumonitis caused by loxoprofen.
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PMID:[A case of loxoprofen-induced pneumonitis pathologically resembling hypersensitivity pneumonitis]. 1197 66

In January 2001, three machinists at an automobile brake manufacturing facility in Ohio (plant A) were hospitalized with respiratory illness characterized by dyspnea, cough, fatigue, weight loss, hypoxia, and pulmonary infiltrates. Hypersensitivity pneumonitis (HP) was diagnosed in all three workers. In March 2001, additional employees began seeking medical attention for respiratory and systemic symptoms. In May 2001, union and management representatives requested assistance from CDC's National Institute for Occupational Safety and Health (NIOSH) in determining the cause of the illnesses and preventing further illness in employees. This report describes two case reports and the preliminary results of the ongoing investigation, which found that exposure to aerosolized nontuberculous mycobacteria (NTM) might be contributing to the observed respiratory illnesses in this manufacturing facility. Clinicians and public health professionals should be alert to the variable presentation of occupational respiratory disease that might occur in workers in the machining industry.
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PMID:Respiratory illness in workers exposed to metalworking fluid contaminated with nontuberculous mycobacteria--Ohio, 2001. 1200 86

Hypersensitivity pneumonitis (HP) represents a group of lung disorders caused by the inhalation of a wide variety of organic particles by susceptible individuals. HP occurs mainly in nonsmokers, but smoking may promote an insidious and chronic disease. The prevalence of HP is difficult to estimate accurately since several antigens can produce the disease, but the range spans infancy to old age. Regardless of the causative antigen or its environmental setting, the clinical manifestations are essentially the same. Three different clinical presentations have been recognized: acute, subacute, and chronic. In the acute form, patients show flu-like symptomatology, followed by dyspnea and dry cough. Symptoms subside a few hours or days later. The subacute and chronic forms result from recurrent low-level antigen exposure and are characterized by progressive dyspnea and dry cough. Other constitutional symptoms such as fatigue, anorexia, and weight loss can be apparent. Fever may occur in the subacute form. Importantly, chronic HP may evolve insidiously or may result from repeated acute/subacute episodes. Recurrent acute, subacute, and chronic HP may progress to irreversible lung fibrosis or provoke emphysematous changes.HP can be difficult to identify, and precise diagnosis requires a history of exposure and a constellation of clinical, imaging, laboratory, bronchoalveolar lavage and pathologic findings. General laboratory tests show an increase of acute phase reactants. Specific precipitating antibodies, when present, are evidence of antigen exposure, and are a hallmark for diagnosis. Chest radiograph usually reveals widespread ground-glass attenuation, and nodular or reticulonodular shadowing. High-resolution CT features include diffuse or patchy ground-glass opacities with small poorly defined nodules and air trapping. Pulmonary function tests are characterized by a predominantly restrictive ventilatory defect with loss of lung volume and hypoxemia at rest that worsens with exercise. Bronchoalveolar lavage reveals a significant increase in lymphocytes, mostly over 40%. In the acute form there is also an increase in neutrophils. Antigen-induced lymphocyte proliferation, and environmental or laboratory-controlled inhalation challenge, may be used for diagnostic purposes and can help to establish a diagnosis of insidious forms of HP. In subacute or chronic cases, lung biopsy may be necessary. Typical findings include bronchiolitis, lymphocytic alveolitis, and loosely formed granulomas, although occasionally other morphologic patterns such as nonspecific interstitial pneumonia may exist. Treatment focuses on avoiding further exposure to the offending antigen(s). Corticosteroids are recommended in subacute and chronic forms. The usual regimen consists of initial high doses of systemic corticosteroid (e.g. prednisone 0.5-1.0 mg/kg/day), followed by gradual tapering.
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PMID:Hypersensitivity pneumonitis : a broader perspective. 1669 87

Exposure to fungi, particularly in water damaged indoor environments, has been thought to exacerbate a number of adverse health effects, ranging from subjective symptoms such as fatigue, cognitive difficulties or memory loss to more definable diseases such as allergy, asthma and hypersensitivity pneumonitis. Understanding the role of fungal exposure in these environments has been limited by methodological difficulties in enumerating and identifying various fungal components in environmental samples. Consequently, data on personal exposure and sensitization to fungal allergens are mainly based on the assessment of a few select and easily identifiable species. The contribution of other airborne spores, hyphae and fungal fragments to exposure and allergic sensitization are poorly characterized. There is increased interest in the role of aerosolized fungal fragments following reports that the combination of hyphal fragments and spore counts improved the association with asthma severity. These fragments are particles derived from any intracellular or extracellular fungal structure and are categorized as either submicron particles or larger fungal fragments. In vitro studies have shown that submicron particles of several fungal species are aerosolized in much higher concentrations (300-500 times) than spores, and that respiratory deposition models suggest that such fragments of Stachybotrys chartarum may be deposited in 230-250 fold higher numbers than spores. The practical implications of these models are yet to be clarified for human exposure assessments and clinical disease. We have developed innovative immunodetection techniques to determine the extent to which larger fungal fragments, including hyphae and fractured conidia, function as aeroallergen sources. These techniques were based on the Halogen Immunoassay (HIA), an immunostaining technique that detects antigens associated with individual airborne particles >1 microm, with human serum immunoglobulin E (IgE). Our studies demonstrated that the numbers of total airborne hyphae were often significantly higher in concentration than conidia of individual allergenic genera. Approximately 25% of all hyphal fragments expressed detectable allergen and the resultant localization of IgE immunostaining was heterogeneous among the hyphae. Furthermore, conidia of ten genera that were previously uncharacterized could be identified as sources of allergens. These findings highlight the contribution of larger fungal fragments as aeroallergen sources and present a new paradigm of fungal exposure. Direct evidence of the associations between fungal fragments and building-related disease is lacking and in order to gain a better understanding, it will be necessary to develop diagnostic reagents and detection methods, particularly for submicron particles. Assays using monoclonal antibodies enable the measurement of individual antigens but interpretation can be confounded by cross-reactivity between fungal species. The recent development of species-specific monoclonal antibodies, used in combination with a fluorescent-confocal HIA technique should, for the first time, enable the speciation of morphologically indiscernible fungal fragments. The application of this novel method will help to characterize the contribution of fungal fragments to adverse health effects due to fungi and provide patient-specific exposure and sensitization profiles.
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PMID:Airborne fungal fragments and allergenicity. 1705 Apr 46

A 49-year-old woman was admitted with cough, general fatigue, and dyspnea on effort. Her hobby was the Japanese traditional handicraft of lacquer-carving. She sometimes used smut spores of Ustilago esculenta, pronounced as "Makomozumi"on lacquer ware. The chest radiographs showed diffuse ground-glass opacities and small centrilobular nodules. Bronchoalveolar lavage yielded a marked number of lymphocytes as well as total cell counts and a low CD4 +/CD8 + ratio. The transbronchial lung biopsy specimen revealed lymphocytic alveolitis and non-necrotizing epithelioid cell granulomas. The results of provocation test by Makomozumi were positive. Serum tests of the specific antibody against extracted soluble antigens of smut spores were positive. The peripheral lymphocyte proliferation test, performed with Mokomozumi antigens was also positive. The final diagnosis was hypersensitivity pneumonitis induced by smut spores of fungus Ustilago esculenta.
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PMID:[A case of hypersensitivity pneumonitis caused by smut spores of Ustilago esculenta]. 1749 14

A 42-year-old female non-smoking onion and potato sorter developed work-related shortness of breath, cough, fatigue and flu-like symptoms. The diagnosis of hypersensitivity pneumonitis was based on patchy infiltrates in both lungs on high resolution computed tomography and lymphocytosis of 71% in a bronchoalveolar lavage sample with a CD4/CD8 ratio of 0.4. Exposure cessation and initial corticosteroid therapy resulted in complete recovery. IgG antibodies to Penicillium species and Fusarium solani cultivated from samples from the patient's workplace were detected in the patient's serum and cross-reactivity was demonstrated within Penicillium species, but also between Penicillium species and Aspergillus fumigatus. We conclude that occupational hypersensitivity pneumonitis due to molds may develop in onion and potato sorters.
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PMID:Occupational hypersensitivity pneumonitis due to molds in an onion and potato sorter. 1816 26

There is virtually no information in the literature about the exposure levels needed to induce hypersensitivity pneumonitis (HP) by diisocyanates. The present study reports a case of occupational HP due to diisocyanates after low-level exposure. A 53-yr-old female never-smoker developed progressive shortness of breath on exertion, cough, fatigue and flu-like symptoms shortly after she began work as a secretary of a car body repair shop. A diagnosis of HP was made 2 yrs later, based on a restrictive ventilatory defect, a reticulonodular and discrete ground-glass pattern on high-resolution computed tomography, lymphocytosis in bronchoalveolar lavage and specific immunoglobulin G antibodies to diisocyanate human serum albumin conjugates in the patient's serum. The diagnosis was confirmed by recovery after exposure cessation and deterioration after re-exposure. Ambient monitoring revealed air concentrations of different diisocyanate monomers below the detection limit in both the patient's work station and in front of the paint spray booths, with the exception of one measurement that showed 4,4-methylenediphenyl diisocyanate concentrations of 3 microg x m(-3) in front of one booth (corresponding to a total reactive isocyanate group concentration of 1 microg x m(-3)). The present authors conclude that concentrations of diisocyanates far below current exposure limits may induce hypersensitivity pneumonitis in susceptible subjects.
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PMID:Sub-acute occupational hypersensitivity pneumonitis due to low-level exposure to diisocyanates in a secretary. 1875 5

Moulds are responsible for diseases in humans through the three pathogenetic mechanisms of infection, allergy, and toxicity. Fungal infection is especially a risk factor for immunodeficient patients, but it occurs in immunocompetent patients as well. Fungal allergy is manifested as bronchial asthma, hypersensitivity pneumonitis, allergic bronchopulmonary aspergillosis, or allergic fungal sinusitis. Mycotoxicosis is almost exclusively the result of ingestion of mould-contaminated foodstuffs. In each case there is specificity for the etiologic mould. There is controversy regarding the ability of indoor airborne mould spores to cause human disease through non-specific toxicity via the inhalation route. Pulmonary mycotoxicosis is an established, although rare, occupational disease of farmers who inhale enormous quantities of mycotoxins, endotoxins, and other toxic chemicals from contaminated silage. Other conditions attributed to indoor airborne mycotoxin are unproven. These include infantile pulmonary hemosiderosis, epistaxis, 'toxic encephalopathy', immune dysregulation and a variety of subjective complaints without objective signs of pathology such as fatigue, headache, dyspnea, gastrointestinal distress, neuromuscular and skeletal complaints, etc. Non-specific irritation from moulds via the inhalation route is also a controversial subject that remains unproven. Published studies alleging an epidemiologic causal relationship are unconvincing.
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PMID:Sick Building Syndrome: is mould the cause? 1925 24

To date, there is little information in the literature that hypersensitivity pneumonitis due to birds may occur without direct contact to birds. A 62-yr-old pensioner developed mild flu-like symptoms, fatigue and polyuria several hours after each meeting with his new female partner, either in hotels or his apartment. After divorcing from her ex-husband, who was a canary fancier, the female had moved into a bungalow approximately 6 months earlier. When the couple met for the first time at the bungalow, the patient's symptoms worsened and he developed shortness of breath. The patient had never entered the bird house or the married couple's house. Hypersensitivity pneumonitis was demonstrated by chest radiography, computed tomography, a restrictive ventilatory defect, decreased diffusion capacity and hypoxaemia after physical exercise. Sensitisation to canaries was shown by immunoassays. Canary antigens were detected by a polyclonal immunoassay at different locations of the married couple's house and the female's bungalow, where no birds had ever been kept. In conclusion, hypersensitivity pneumonitis should be recognised as a further consort disease, i.e. a disease that can be transmitted by partners.
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PMID:Consort hypersensitivity pneumonitis. 1940 57

A 51-year-old man presented with fever and fatigue after 3.5 months of antituberculosis therapy. High-resolution computed tomography of his chest revealed new ground-glass opacities and poorly defined centrilobular nodules. He had undergone catechin inhalation for 1 month. We diagnosed hypersensitivity pneumonitis (HP) based on the clinical course, bronchoscopy and a challenge test. Cases of HP due to inhalation of extracted catechin powder are rare. Although it has many known positive attributes, it is necessary to be aware that catechin can cause HP.
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PMID:Hypersensitivity pneumonitis associated with inhalation of catechin-rich green tea extracts. 2145 52


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