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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immunoglobulin class and subclass of cytophilic antibodies have been studied using peripheral leucocytes from twenty-two patients with allergic bronchopulmonary aspergillosis, aspergilloma and cryptogenic pulmonary eosinophilia. In patients with allergic bronchopulmonary aspergillosis, significantly increased histamine liberation occurred following challenge of their leucocytes with antisera to IgE, IgG2, IgG3 and IgG4 as well as with Aspergillus fumigatus antigen. The results were considerably modified if the patient was receiving corticosteroids at the time of the test. The presence of IgG2-specific antibody to A. fumigatus in the serum of one patient, capable of sensitizing donor leucocytes, was demonstrated in passive sensitization experiments. In two patients with uncomplicated aspergillomas no evidence of cytophilic antibody to any class was found although large amounts of precipitating IgG antibody was present in the serum. Two patients with aspergilloma and systemic symptoms of weight loss and fatigue (which have been interpreted by others as 'hypersensitivity' responses) had increased amounts of cytophilic antibody similar to those with allergic bronchopulmonary aspergillosis. Six patients with cryptogenic pulmonary eosinophilia were also studied. No evidence of specific antibody to A. fumigatus was found but, as a group, significantly increased histamine liberation using antisera to IgG2 was demonstrated. Individual patients also showed evidence of other classes of cytophilic antibody, one having IgE, three IgG3 and two IgG4. The relationship between heat-stable short-term sensitizing antibody (IgG STS) inducing immediate skin responses and the pattern of cytophilic antibodies found in our patients with bronchopulmonary aspergillosis having dual (immediate and late reactions) is discussed. Clinically these tests are of diagnostic value and they may be helpful in assessing symptomatic patients with aspergillomas for corticosteroid treatment.
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PMID:Cytophilic antibodies in bronchopulmonary aspergilloma and cryptogenic pulmonary eosinophilia. 6 46

We report a 47-year-old man diagnosed as angio-immunoblastic lymphadenopathy with dysproteinemia (AILD) with fibrosis of the bone marrow, lymph node, liver and spleen, and proliferation of epithelioid cells in lymph node. He was admitted to a hospital in May, 1980 because of general fatigue, cough, fever and systemic lymphadenopathy. The diagnosis of AILD was based on a biopsy of right cervical lymph node. His symptoms were improved but recurred with the addition of icterus and progressive pancytopenia with decrement of prednisolone. He was referred to our hospital in July, 1980 and his physical examination revealed generalized lymphadenopathy, icterus and hepatosplenomegaly. Hemogram showed pancytopenia, and needle biopsy of the bone marrow disclosed fibrosis. Sections from the lymph node showed AILD with proliferation of epithelioid cells. Administration of 60 mg/day of prednisolone improved the fever, lymphadenopathy and hepatosplenomegaly. However he died suddenly of acute respiratory failure on July 30. Autopsy showed fibrosis of bone marrow, lymph node, liver and spleen with infiltration of abnormal lymphocytes, and pulmonary aspergillosis.
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PMID:[Angio-immunoblastic lymphadenopathy with fibrosis of bone marrow, lymph node, liver and spleen, and proliferation of epithelioid cells in lymph nodes]. 221 92

Unclear pulmonary infiltrates with eosinophilia, a problem of differential diagnosis. HISTORY AND ADMISSION FINDINGS: A 60-year-old woman was admitted for the diagnosis of pulmonary infiltrates. A year before she had been exposed to tuberculosis when working as a doctor in Manila, the Philippines. Ten days before admission she had spent 10 days in Sao Paulo, Brazil. On admission she complained of fatigue, dry cough and nocturnal sweating. Her body temperature was 37.8; C. At auscultation of the chest fine rales were heard with diminished percussion sounds over both lungs. INVESTIGATIONS: The chest radiogram showed bilateral apical infiltrates. Blood count indicated normal white and red cells, but platelets were raised to 606 x 10 9/l. The differential blood count revealed an eosinophilia of 30%, ESR was raised at 91 mm/h and C-reactive protein increased to 103 mg/l. Angiotensin-converting enzyme, IgG, IgA, IgM, IgE, C3 and C4, paraproteins, antinuclear antibodies and double-strand DNA antibodies were all within normal limits. There was no direct or indirect evidence of tuberculosis and no parasites were found in sputum, stool, urine and blood. DIAGNOSIS, TREATMENT AND COURSE: After bronchoscopy with bronchial biopsy had failed to establish a diagnosis, an open lung biopsy with partial lung resection was performed. This revealed histologically an eosinophilic pneumonia with intra-alveolar protein precipitation and multinucleated giant cells, as well as interstitial fibroblast proliferation without demonstrable mincroorganisms. Under cortisone administration there was striking improvement of symptoms within a few days, and C-reactive proteins fell to 3 mg/l, ESR to 25 mm/h and the eosino-philia to 2%. CONCLUSION: Eosinophilic pneumonia should be included in the differential diagnosis of unclear pulmonary infiltrations with eosinophilia, once parasitological and malignant diseases, tuberculosis and allergic pulmonary aspergillosis have been excluded.
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PMID:[Unclear pulmonary infiltrates with eosinophilia, a problem of differential diagnosis] 1275 Oct 17

We describe 18 nonimmunocompromised patients with chronic pulmonary aspergillosis. Duration of the disease ranged from several months to >12 years. All 18 patients had prior pulmonary disease. Weight loss, chronic cough (often with hemoptysis and shortness of breath), fatigue, and chest pain were the most common symptoms. All 18 patients had cavities, usually multiple and in 1 or both upper lobes of the lung, that expanded over time, with or without intraluminal fungal balls. All had detectable Aspergillus precipitins and inflammatory markers. Elevated levels of total immunoglobulin E were seen in 78% of patients and of Aspergillus-specific immunoglobulin E in 64%. Directed lung biopsies showed chronic inflammation, necrosis, or granulomas without hyphal invasion. Antifungal therapy with itraconazole resulted in 71% of patients improved or stabilized, with relapse common. Interferon-gamma treatment was useful in 3 patients. In azole nonresponders, modest responses to intravenous amphotericin B (80%) followed by itraconazole were seen. Surgery removed disease but postoperative pleural aspergillosis was inevitable. Indicators of good long-term medical outcomes were mild symptoms, thin-walled quiescent cavities, residual pleural fibrosis, and normal inflammatory markers.
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PMID:Chronic cavitary and fibrosing pulmonary and pleural aspergillosis: case series, proposed nomenclature change, and review. 1297 54

The exposure to Aspergillus organisms/spores is likely common, but disease caused by tissue invasion with these fungi is uncommon and occurs primarily in the setting of immunosuppression. We report a case of rapidly advancing invasive endomyocardial aspergillosis secondary to prolonged usage of multiple broad-spectrum antibiotics in a nonimmunocompromised host. A 36-year-old cotton textile worker presented to our institution with a 3-month history of weight loss and fatigue. He reported receiving prolonged use of multiple broad-spectrum antibiotic treatment. The echocardiogram demonstrated multiple endomyocardial vegetations and a mass in the left atrium. Myocardial biopsy specimen revealed an invasive endomyocardial aspergillosis. The patient was investigated for immune deficiency including HIV, and this workup was negative. Treatment was started with amphotericin B and heparin for presumed left atrial thrombus. The patient died because of a rupture of mycotic aneurysm that resulted in cerebral hemorrhage. This case illustrates the risk of an invasive fungal infection in a nonimmunocompromised host who is a prolonged user of antibiotics in the setting of environmental exposure of opportunistic invasive fungal infections.
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PMID:Rapidly advancing invasive endomyocardial aspergillosis. 1568 58

The rate of pulmonary nontuberculous mycobacteriosis (NTM) in the total pulmonary mycobacteriosis has been continuously increasing. While M. avium complex is the most common cause of NTM, there are a few case reports of pulmonary infection due to M. szulgai. We described two cases of pulmonary NTM caused by M. szulgai. A 75-year-old male was admitted to our hospital because of dyspnea on effort, and productive cough. A chest X-ray showed an infiltrative shadow with cavity in the right upper lobe. A sputum smear for mycobacteria was positive, and a culture grew M. szulgai which was identified by DNA-DNA hybridization. He was treated with isoniazid, rifampicin, and ethambutol. His symptoms and CT and X-ray findings improved, and his sputum smear and culture converted to negative for mycobacteria. Second case was a 73-year-old male who had previously been diagnosed as MAC and pulmonary aspergillosis, and had been treated with antituberculous and antifungal drugs. He was readmitted to our hospital, because of general fatigue and hemoptysis. A chest X-ray revealed a consolidation with bronchiectasis and cavity in the both upper lung fields. A sptum smear for mycobacteria was positive, and a grown culture was identified as M. szulgai. He was treated with rifampicin, ethambutol and kanamycin based on the results of susceptibility testing. After 3 months of this treatment his sputum smear and culture converted to negative for mycobacteria, and his symptoms, and CT and X-ray findings improved.
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PMID:[Two cases of Mycobacterium szulgai pulmonary disease in the elderly]. 1608 51

A 74-year-old woman was treated with steroid and cyclosporine A for hypersensitivity pneumonia. To examine the causes of general fatigue and increased levels of beta-D glucan in serum, she was admitted to our hospital. Chest computed tomography (CT) scan revealed nodular opacity with a well-defined margin in the right S1. 67Ga scintigraphy image showed high uptake in the left thigh and CT showed circularly enhanced lesions in the thigh. An ultrasonography-guided needle aspiration and biopsy of the muscle abscess allowed isolation of Aspergillus fumigatus and evidence of necrotic tissues around the granuloma formation. We therefore diagnosed invasive aspergillosis. Because of the poor response to initial therapy with micafungin and itraconazole for 4 weeks, we treated her with voliconazole (VCZ). Spectacular regression of lung lesions and muscle abscesses was rapidly achieved. Furthermore, the high level of beta-D glucan in serum decreased gradually. This case suggests that administration of VCZ can be recommended for deep seated mycoses.
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PMID:[Successful treatment by voliconazole for pulmonary and adductor magnus muscle aspergillosis induced by immunosuppressive therapy for hypersensitivity pneumonia]. 1708 45

This is a case of vocal cord aspergillosis in a 36-year-old woman whose chief complaint was progressive hoarseness and vocal fatigue of one month duration. These symptoms followed the use of systemic administration of penicillin, cefotaxime natrium and dexamethasone to treat her rhinitis and asthma. Fiberoptic laryngoscopy revealed whitish plaques involving both vocal cords. Microscopic examination of KOH preparations and histopathology studies of tissue revealed dichotomously branching, hyaline, septate hyphae. Morphological and molecular biological identification of the fungal growth in cultures inoculated with clinical specimens from the patient indicated that the etiologic agent was Aspergillus fumigatus. The patient was cured with oral itraconazole without any side effects.
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PMID:Primary vocal cord aspergillosis caused by Aspergillus fumigatus and molecular identification of the isolate. 1863 95

A 67-year-old woman with systemic lupus erythematosus (SLE) was admitted to our hospital because of lupus nephritis. Methylprednisolone minipulse therapy dramatically reduced her proteinuria; however; she then complained of general fatigue with low-grade fever. Radiological and culture studies revealed no infectious focus, but she was treated with meropenem and micafungin, considering her immunosuppressive state. Cytomegalovirus antigenemia was later determined and ganciclovir was added. She became afebrile, but complained of nausea and headache, and disorientation, without meningeal signs. Because a brain computed tomography (CT) scan showed no abnormality, we initially suspected some kind of drug interaction. Despite the discontinuation of all drugs, however, she still suffered from disturbance of consciousness. A lumbar puncture revealed yeast cells stained by India ink. A diagnosis of cryptococcal meningitis was confirmed. Though fluconazole and meropenem were administered, the patient died. Autopsy findings revealed disseminated cryptococcosis concomitant with pulmonary aspergillosis. Micafungin is a recently approved echinocandin-class antifungal agent that is now widely used in Japan because of its minimal toxicity and broadspectrum activity. However, such echinocandins have limited activity against a number of fungi. Indeed, breakthrough trichosporonosis is becoming a significant problem in patients with hematological malignancies who are receiving echinocandins. To the best of our knowledge, breakthrough cryptococcosis, as seen in our patient, has not been reported previously in patients who were receiving micafungin as an empiric antifungal therapy. This case highlights that cryptococcosis should be kept in mind as a possible breakthrough infection during the administration of echinocandins, especially in patients with cellular immunodeficiency.
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PMID:Breakthrough cryptococcosis in a patient with systemic lupus erythematosus (SLE) receiving micafungin. 1870 36

The aim of the present study is to define the characteristics of the clinical and histopathological features of chronic necrotizing pulmonary aspergillosis (CNPA) cases with severe hemoptysis. We conducted a histological study of three patients clinically diagnosed as having CNPA who had hemoptysis for 5 years. A tuberculosis sequelae was found as the underlying disorder in all three cases. All patients had fever, general fatigue, and hemoptysis, and their chest computed tomographic images revealed fungus balls, cavity wall thickening, consolidation surrounding the cavity, and satellite foci. All had been treated with anti-fungal drugs and corticosteroids. However, all patients died from respiratory failure due to massive hemoptysis. Histopathological examination revealed that the cavity wall consisted of three layers comprised of necrotic, granulation, and fibrous tissue layers. Aspergilli were found in both the fungus ball and necrotic tissue comprising the inner layer of the cavity. In addition, most of the vessels were incompletely occluded with thrombosis and were necrotic, as well as showing local invasion of Aspergilli. Surgical intervention should be considered as a prior procedure for CNPA patients, because vessels at the cavity wall, whether occluded completely or incompletely, are usually necrotic and/or show local invasion of Aspergilli.
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PMID:Pathophysiological study of chronic necrotizing pulmonary aspergillosis. 1905 Mar 52


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