Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of PIE syndrome induced by Saiboku-To (TJ96) is reported. A 56-year-old woman had been treated for intractable bronchial asthma since the age of 42 years. She had a history of PIE syndrome induced by disodium cromoglycate 4 years previously (Jpn. J. Thoracic Disease, 27.1.1989). To reduce the dose of prednisolone for her asthma, administration of TJ96 was started in Dec. 1989. After 5 months of TJ96 treatment, she developed dry cough, fever, and chest pain. Physical findings and laboratory examinations revealed pulmonary infiltrations in the right lung field and severe eosinophilia. Because of suspected drug-induced PIE, TJ96 was stopped and 30 mg/day prednisolone was administered. Her symptoms and laboratory abnormalities subsequently resolved. To confirm the diagnosis of drug-induced PIE syndrome, drug-induced lymphocyte stimulation tests with TJ96 and other drugs were performed. TJ96 significantly induced lymphocyte blastogenesis with a stimulation index of 6.1. Moreover, the supernatant of the incubation mixture of TJ96 and peripheral lymphocytes from the patient showed marked eosinophil chemotactic activity. To our knowledge, there has been no previous report of PIE syndrome induced by TJ96. In addition, this is the first report of the detection of ECF activity in lymphocytes induced by an offending drug in vitro.
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PMID:[A case of pulmonary infiltration with eosinophilia (PIE) syndrome induced by Saiboku-To (TJ96). Detection of ECF activity in lymphocytes stimulated with TJ96]. 140 85

A previously healthy boy presented with cough and diffuse pulmonary interstitial infiltrates. Acute eosinophilic pneumonia was diagnosed by bronchoalveolar lavage in the absence of a demonstrable infectious etiologic agent. Corticosteroid therapy resulted in immediate improvement but was followed by respiratory distress and death from invasive aspergillosis and Pseudomonas cepacia sepsis.
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PMID:Fatal pulmonary aspergillosis presenting as acute eosinophilic pneumonia in a previously healthy child. 188 95

A 46-year-old man presented with progressive dyspnea of acute onset, nonproductive coughing, and a high fever. He had been in his usual good health until symptoms began on the previous day. The chest roentgenogram revealed Kerley A and B lines, perivascular cuffing, hilar haze, and bilateral pleural effusins. Body temperature was 37 degrees C and PaO2 was 42 Torr. All clinical and radiographic signs improved. On the 12th hospital day, dyspnea and diffuse infiltration shadows on the chest roentgenogram suddenly occurred again. Acute eosinophilic pneumonia was strongly suspected because of increasing peripheral eosinophilia, and from the results of histologic examination of a specimen obtained by transbronchial lung biopsy. Without steroid treatment, the patient's condition gradually improved. Most cases of eosinophilic pneumonia have been diagnosed as pulmonary infiltration with eosinophilia (PIE). However, this patient did not have PIE syndrome, but instead was given a diagnosis of acute eosinophilic pneumonia, which was first described in 1990. This case may help establish criteria for the diagnosis and steroid treatment of acute eosinophilic pneumonia.
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PMID:[Remission and relapse of acute eosinophilic pneumonia]. 747 70

An 18-year-old woman presented with coughing, fever, progressive dyspnea, and diffuse infiltrates on the chest X-ray film. Analysis of bronchoalveolar lavage fluid showed 73% eosinophils. Acute eosinophilic pneumonia was diagnosed. Methylprenisolone, 1 g per day was given for three days and her condition improved dramatically. No relapse was observed. Analysis of bronchoalveolar lavage fluid also showed lymphocytosis, abnormally high concentrations of ECP, GM-CSF, IL-5 and sICAM-1, and hypersegmentation of eosinophil nuclei. After steroid treatment almost all these findings returned to normal; only lymphocytosis remained. Precipitating antibodies against four kinds of fungi, including Trichoderma viridae, were noted in the serum, but the environmental provocation test was negative and those fungi were not detected in the environmental culture growth. Comparison of bronchoalveolar lavage findings obtained before and after steroid treatment can provide information on the mechanism of eosinophil accumulation in the lung. This case also draws attention to the relationship between acute and chronic eosinophilic pneumonia.
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PMID:[A case of acute eosinophilic pneumonia: bronchoalveolar lavage findings before and after steroid treatment]. 756

A 16-year-Old boy was admitted with acute onset of fever, cough, and dyspnea. Chest radiography showed diffuse infiltrated shadow and right pleural effusion. BALF revealed a high level of eosinophils (56.8%), and TBLB specimen showed infiltration of inflammatory cells, chiefly eosinophils. Symptoms and radiographic findings resolved spontaneously within a few days after admission. Acute eosinophilic pneumonia was diagnosed as in the case reported by Allen et al. However, the present patient had a high IgE level and history of atopic allergic rhinitis. In more than one third of previously reported cases in Japan, there was a history of atopy, unlike in Allen's report.
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PMID:[A case of acute eosinophilic pneumonia with acute onset of dyspnea]. 769 71

A 16-year-old male, an industrial high school student working at an ironworks, without a dust mask, began to complain of dry cough and fever several hours after inhalation of stainless steel dusts including 0.1% nickel. A chest X-ray film revealed ground glass shadows, patchy shadows and Kerley B lines in the right lung fields. A high resolution chest CT scan showed fusing panlobular densities, thickening of bronchial walls and thickening of interlobular septa. Blood cells counts revealed leucocytosis with eosinophilia. Arterial blood gas analysis revealed hypoxemia. A bronchoalveolar lavage fluid specimen showed a marked increase in the total cell count and in eosinophils. A transbronchial biopsy specimen showed eosinophilic and lymphocytic infiltration in the alveolar septa. Steroid therapy with methylpredonisolne (250 mg x three days) resulted in clinical remission. As we suspected nickel-induced eosinophilic pneumonia, an inhalation provocation test with 0.5% nickel sulfate solution was carried out with the patient's informed consent. Six hours after inhalation he developed a dry cough and fever with leucocytosis and A-aDo2 widening. The positive results of the inhalation provocation test provided a definite diagnosis of nickel induced eosinophilic pneumonia. A review of the world literature revealed three case reports of nickel induced PIE syndrome, all of whom were clinically diagnosed without biopsy however. We believe that this is the first case diagnosed by transbronchial biopsy-proven tissue eosinophilia and a positive nickel inhalation provocation test.
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PMID:[A case of eosinophilic pneumonia caused by inhalation of nickel dusts]. 808 5

A 18-year-old woman presented to our hospital complaining of an acute onset of progressive dyspnea with nonproductive cough and high fever. The patient was in her usual good health until the previous day, when she started to develop symptoms 8 hours after taking aspirin for a headache. The chest roentgenogram revealed Kerley's lines (A and B), perivascular cuffing and hilar haze with bilateral pleural effusions. Body temperature was 38 degrees C and PaO2 was 48 torr. Infectious diseases and extrinsic allergic alveolitis were excluded. The lymphocyte stimulating test was negative for aspirin. Acute eosinophilic pneumonia was strongly suggested by bronchoalveolar lavage showing a marked increase in eosinophils without peripheral eosinophilia. By the seventh hospital day all clinical and radiographic signs were improved without steroid therapy. Most cases of acute eosinophilic pneumonia reported previously showed diffuse infiltrative shadows on the chest roentgenogram. The present case had interesting radiographic findings which suggested interstitial pulmonary edema.
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PMID:[A case of acute eosinophilic pneumonia with Kerley's lines (A and B) on chest X-ray]. 823 Aug 83

Acute eosinophilic pneumonia is characterized by acute respiratory insufficiency, hypoxemia, fever, diffuse radiographic infiltrates, and eosinophilia in bronchoalveolar lavage fluid (BALF) or lung biopsies in the absence of infection, atopy, or asthma. A rapid response to corticosteroids is characteristic. We reviewed our experience with nine cases of acute lung disease with histologic features of acute and organizing diffuse alveolar damage and prominent interstitial and alveolar eosinophils in order to determine whether this pathology was characteristic of acute eosinophilic pneumonia. The mean age of the patients (four men and five women) was 53 yr (range: 33 to 71 yr). They presented with 2 to 21 d of dyspnea, cough, myalgias, and fever. All were hypoxic and had bilateral infiltrates on chest radiographs. Peripheral blood eosinophilia was present in four of eight patients (peripheral blood count unavailable for one patient). All patients were treated with high-dose corticosteroids with a mean time to symptomatic and radiographic improvement of 4 d. Seven of the nine patients enrolled in the study are alive without relapse; one patient has a mild deficit in diffusing capacity, and one patient died of a myocardial infarct while improving on therapy. The presence of eosinophils in cases of acute respiratory insufficiency due to diffuse alveolar damage (DAD) should suggest the diagnostic possibility of acute eosinophilic pneumonia. Acute eosinophilic pneumonia should be distinguished from other causes of DAD because of important differences in natural history.
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PMID:Acute eosinophilic pneumonia: histopathologic findings in nine patients. 900 28

Ascariasis and hookworm (ancylostomiasis) remain the most common intestinal nematodes in the world with significant economic, social, and medical impact. An understanding of the transmission and pathogenesis of ascariasis and hookworm are necessary to recognize their clinical manifestations and to manage the pulmonary sequelae of infection. Transmission occurs predominantly in the tropics and rural areas where there is suboptimal sanitation, personal hygiene, and education regarding these parasites. Ascariasis generally occurs through hand-to-mouth ingestion of agricultural products or food contaminated with parasite eggs. Hookworm is transmitted through larval penetration of the skin. Larval pulmonary migration generally is asymptomatic. However, symptomatic pulmonary disease may occur with fever, cough, chest pain, hemoptysis, dyspnea, and wheezing due to (1) Loffler's syndrome, (2) the effects of larval tissue migration, (3) airway reactivity or bronchospasm, (4) infectious bacterial complications from parasitic migration and associated aspiration, and rarely (5) chronic eosinophilic pneumonia, transdiaphragmatic penetration, or symptoms of upper airway obstruction. Clinical evaluation shows pulmonary opacities on chest radiograph, peripheral blood eosinophilia, and larvae in respiratory or gastric secretions. Symptomatic treatment may be necessary with bronchodilators and systemic steroids or antibiotics for bacterial complications. The drug of choice is mebendazole (Vermox) 100 mg twice a day for 3 days. Alternatives include a single dose of pyrantel pamoate (Antiminth) 11 mg/kg (maximum dose, 1 g) or albendazole (Zentel) 400 mg orally once. Invermectin (Mectizan) is available through the World Health Organization, and, in the United States, through the manufacturer on a compassionate-use basis. Ivermectin is as effective as currently available drugs against Ascaris but shows only partial efficacy against hookworms, which infest humans. Preventive measures, improvement of sanitary facilities, education, and school screening may be important in the endemic areas to control these parasitic infections.
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PMID:Ascariasis and hookworm. 919 78

A 46-year-old man had had an occasional dry cough in the early morning since about the age of 20, but had received no treatment. He had been taking an antirheumatic drug for 2 years for rheumatoid arthritis. The patient complained of fever and dry coughing that began in the middle of November 1995, and he was treated for acute bronchitis. His condition did not improve, and he was admitted to the hospital in early December. Wheezing and rhonchi were heard in both lung fields. His white blood cell count was 19,000/mm3, and the eosinophil percent age was 48%. A chest CT scan revealed macular lesions with an increased density in both lung fields, and markedly swollen mediastinal and hilar lymph nodes. Analysis of alveolar lavage fluid revealed an increased number of cells (total) and eosinophilia (37%), and examination of a transbronchial lung biopsy specimen indicated infiltration with eosinophils and lymphocytes. Our diagnosis was eosinophilic pneumonia. The patient's condition improved soon after the start of pulse therapy with steroids. Bilateral swelling of mediastinal and hilar lymph nodes is rare in patients who have pulmonary in filtration with eosinophilia (the PIE syndrome).
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PMID:[Bilateral hilar and mediastinal lymphadenopathy accomporying pulmonary infiltration with eosinophilia]. 921 72


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