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 30-year-old female was admitted to our hospital complaining of high fever and fatigue. Laboratory findings showed as follows; WBC 41,500/microliter (40% of blasts), Hb 8.5g/dl, platelets 4.4 x 10(4)/microliter. Cytochemical staining of blasts was positive for peroxidase and non-specific esterase with NaF inhibition. Chromosome analysis showed 46, XX, inv (16p+,q-). AML with eosinophilia was diagnosed. During myelosuppression after remission induction therapy, she developed high fever, and did not respond to transfusions. Marrow smears showed the presence of phagocytic histiocytes consisting of 18% total nuclear cells. A diagnosis of reactive histiocytosis (RH) was made. She recovered spontaneously, but suffered two episode of recurrence during subsequent chemotherapy. Reactive histiocytosis is characterized by proliferation of histiocytes which phagocyte blood cells in immunodeficient cases, e.g. a myelosuppressive state after chemotherapy. RH causes high fever and prolonged myelosuppression. It is considered to be one of the poor prognostic factors in AML during chemotherapy, and spontaneous recovery is rare. In this report, the effect of hydrocortisone on histiocytes derived from patient marrow was also investigated in vitro.
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PMID:[A case with AML (M4EO) accompanied by recurrent reactive histiocytosis which showed spontaneous remission]. 802 88

We identified eight patients (six women and two men) who had pulmonary infiltrates during treatment with minocycline hydrochloride between 1989 and 1992 in French referral centers for drug-induced pulmonary diseases. Clinical files, chest roentgenograms, computed tomographic scans, pulmonary function, and bronchoalveolar lavage data were reviewed. Minocycline treatment was given for acne (n = 4), genital infection (n = 3), and Lyme disease (n = 1). The duration of treatment averaged 13 +/- 5 days (mean +/- SE); the total dose, 2060 +/- 540 mg. Patients presented with dyspnea (n = 8), fever (n = 7), dry cough (n = 5), hemoptysis (n = 1), chest pain (n = 2), fatigue (n = 3), and rash (n = 3). Chest roentgenograms showed bilateral infiltrates in all cases. Pulmonary function was measured in five patients; four had airflow obstruction and two had mild restriction. Blood gas tests demonstrated hypoxemia in seven patients (58 +/- 3 mmHg). Seven patients had blood eosinophilia (1.76 +/- 0.2 x 10(9)/L). Bronchoalveolar lavage (performed in seven patients) showed an increased proportion of eosinophils (0.30 +/- 0.07). The Cd4+/CD8+ ratio was determined in four cases and was low in three. Transbronchial lung biopsy, performed in two patients, showed interstitial pneumonitis in both patients, with marked infiltration by eosinophils in one patient. The outcome was favorable in all patients. Because of severe symptoms, steroid therapy was required in three patients. Rechallenge was not attempted. We conclude that minocycline can induce the syndrome of pulmonary infiltrates and eosinophilia, that presenting symptoms may be severe and may culminate in transient respiratory failure, and that the disease has a favorable prognosis.
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PMID:Minocycline pneumonitis and eosinophilia. A report on eight patients. 803 Dec 12

Chronic eosinophilic pneumonia (CEP) was described by Carrington in 1969. It is twice as common in women as it is in men and is probably most common at middle age. Symptoms usually associated fever, weight loss, fatigue and dyspnoea. Extra-respiratory manifestations are rare but may involve many organs. Classical radiological findings are diffuse alveolar infiltrates, with a peripheral predominance which explains the classic description of a "negative of pulmonary edema". Peripheral blood eosinophilia is present in 90%. The inflammatory syndrome with an eosinophilic alveolitis is constant. Pulmonary function tests show a restrictive pattern with depressed DLCO and hypoxemia. In atypical cases, proof of diagnosis is supported by lung biopsies that show intra alveolar and interstitial accumulation of eosinophils in peripheral air spaces. Areas of bronchiolitis obliterans are also frequently seen. In some atypical forms of chronic eosinophilic pneumonia, other disorders have to be discussed, like bronchiolitis obliterans with an organizing pneumonia or cryptogenetic organizing pneumonia and even tuberculosis. After corticosteroid therapy, the resolution occurs very rapidly but relapses are frequent. Steroid-dependence is seen in 20 to 30% of patients.
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PMID:[Chronic eosinophilic pneumonia or Carrington's disease]. 812 16

We reported a case of Addison's disease, caused by adrenal tuberculosis. The patient was female, seventy four years old. She complained cough and body weight loss. She complained cough from June, 1989, but her home doctor didn't take care of her symptoms. September 1989, she felt appetite loss, and easy fatigue, so her home doctor suspected her disease as pulmonary tuberculosis, so he introduced our hospital, and she admitted. When she admitted, her chest roentogenogram revealed bIII2. Sputum smear examinations were negative. Laboratory data on admission, we observed slightly eosinophilia, severe iron deficiency anemia, and accenturation of blood sedimentation rate. Immediately after admission, she complained nausea, vomiting, coldness, and powerless. On 25 days after admission, she lost her senses suddenly, and her blood pressure fell 5 days after, she fell in shock state, too. We found out her blood sugar data was 29. After blood examinations, we found out that ACTH was high, cortisole, 17-KS, 17-OHCS were low. So we thought she got acute hypoadrenocorticism. We found her abdominal CT revealed calcification in her right adrenal gland. We diagnosed her disease as Addison's disease caused by adrenal tuberculosis so we began to give prednisolone, 7.5 mg per day. After giving, her state made better. We thought her disease as Addison's disease caused by adrenal tuberculosis, revealed acute hypoadrenocorticism.
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PMID:[A case of Addison's disease caused by adrenal tuberculosis, and revealed acute hypoadrenocorticism]. 826 25

Eosinophilia-myalgia syndrome (EMS) is a multisystem illness of uncertain pathogenesis that occurred in an epidemic related to the ingestion of contaminated L-tryptophan. To investigate the role of immune dysfunction in EMS we prospectively measured a serologic index of T-cell activation, the soluble interleukin-2 receptor (sIL-2R), in 7 patients followed into the late stages of the illness. As a group, EMS patients had significantly elevated sIL-2R levels throughout the study. Five patients suffered chronic symptoms of myalgia, arthralgia, muscle cramps, fatigue, or subjective memory impairment and all had persistently elevated sIL-2R levels. Two patients had near-resolution of EMS and normal sIL-2R levels. We conclude that chronic symptoms are common in EMS and are associated with persistent T-cell activation as measured by serum sIL-2R levels. These findings suggest that immunosuppressive treatment may be beneficial in EMS.
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PMID:Chronic immune activation in the eosinophilia-myalgia syndrome. 793 35

Cisplatin, mitomycin C and 5-fluorouracil were given a 55-year-old woman for an unresectable gastric cancer, and successful radical gastrectomy was performed. Postoperative adjuvant immunochemotherapy using UFT and PSK was continued for about 4 years and 4 months. Pancytopenia was observed at 5 years after the treatment and then marked leucocytosis was noted. She also showed complications of general fatigue, appetite loss etc. A secondary acute leukemia associated with eosinophilia was diagnosed by peripheral blood examinations, showing WBC, 122,400: blast, 37.5 % and eosinophil, 41%. Results also showed atypia and pseudo-Pelger nuclear abnormality of eosinophil, high positive stain of cell myelogenic cell surface marker, many numeral and structural abnormalities of chromosomal analysis, etc. From the above results, it was suggested that the leukemia might be induced by previously performed chemotherapy. The patient died about 2 months following its onset.
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PMID:[A case of secondary leukemia induced by chemotherapy with a CDDP-based regimen for gastric cancer 5 years following radical resection]. 842 78

A girl aged 2.5 years with "covert toxocariasis" was treated with low-dose diethylcarbamazine because of supposed noticeable disseminated Toxocara canis infection without ocular or visceral manifestations. There was marked blood and bone marrow eosinophilia, significant increased Toxocara canis antibody (ELISA) and immunoglobulins E, G and M, leucocytosis and an increased sedimentation rate. She had no geophagia, but often sucked small stones, probably contaminated with faeces from puppies. Symptoms were fever, inactivity, weakness, tiredness and loss of appetite. She was followed clinically and with blood samples throughout a period of three years and four months.
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PMID:"Covert toxocariasis" in a child treated with low-dose diethylcarbamazine. 845 8

The similarity of eosinophilia-myalgia syndrome (EMS) and toxic-oil syndrome (TOS) to systemic sclerosis and diffuse fasciitis with eosinophilia (DFE) highlights the potential for environmental agents to induce autoimmune disease. Further, a candidate etiologic agent for EMS, 3-(phenylamino)alanine, is chemically similar to the aniline derivative identified in samples of oil implicated in TOS, 3-(N-phenylamino)-1,2-propanediol, suggesting pathogenic overlap. The late-stage manifestations of EMS and TOS are muscle cramping, arthralgia, severe fatigue, and cognitive impairment. This review focuses on the divergent and parallel findings in EMS, TOS, and DFE. The formation of the Environmentally Associated Connective Tissue Disease Study Group within the American College of Rheumatology will provide a forum for the development of registries to study suspected toxin-induced disorders.
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PMID:Eosinophilia-myalgia syndrome, toxic-oil syndrome, and diffuse fasciitis with eosinophilia. 857 79

In December 1989, a 72-year-old woman was hospitalized with atelectasis in the left lower lobe. The atelectasis resolved after bronchoscopic removal of impacted mucous plugs. Histopathological examination showed pulmonary mycosis. Microscopy suggested that a species of Aspergillus was responsible, but no definite diagnosis was made. After treatment with flucytosine and nebulized amphotericin, the patient's condition improved and she was discharged. In the middle of August 1994, she visited a local hospital complaining of fatigue. Eosinophilia (22%) was detected, and a few days later she visited that hospital again due to sudden dyspnea. A chest X-ray examination showed an abnormal shadow, and she was referred to our hospital. Atelectasis was seen in the left upper lobe. This finding, together with eosinophilia, suggested recurrence of pulmonary mycosis, and therefore bronchoscopy was performed. White mucous plugs obstructing the left upper lobe were observed and were bronchoscopically removed. Microscopical examination of the mucous plugs showed marked eosinophil infiltration and hyphae. Cultures of specimens obtained during bronchoscopy showed Schizophyllum commune, and allergic bronchopulmonary mycosis due to this microorganism was diagnosed. Identification of this microorganism as a cause of deep-seated pulmonary mycosis is very rare.
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PMID:[Allergic bronchopulmonary mycosis caused by Schizophyllum commune]. 881 Jul 63

Acute eosinophilia-myalgia syndrome (EMS) due to contaminated L-tryptophan (LT) exposure is an inflammatory microangiopathy of the dermis, fascia, and muscle. Select individuals evolve from acute EMS to have persistence of myalgia, fatigue, cramps, and skin changes for years. Many develop memory dysfunction and confusion. The objective of this study is to delineate the pathology in individuals with chronic EMS. Seventeen patients with ongoing symptoms representing chronic EMS are studied by skin, fascia, and muscle biopsies four to five years after exposure to contaminated LT and initial onset of EMS. All have microvascular disease. Most have lymphocytic inflammatory infiltrates. Several have dermal sclerosis. The findings indicate that persistent microvascular disease is present in chronic EMS. The pathologic changes are similar to those of acute EMS but with notable differences. Tissue eosinophil infiltration is rare in the chronic state as compared to acute EMS. The persistence of endothelial pathology indicates continuing microvascular dysfunction.
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PMID:Persistent microvasculopathy in chronic eosinophilia-myalgia syndrome. 890 89


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