Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0206061 (interstitial pneumonia)
 6,105 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 48-year-old man who had been a welder for 25 years was admitted to our hospital on February 18, 1990 for investigation of a diffuse bilateral lung shadow that had a ground-glass appearance. On the day of admission, he had been welding copper water supply pipe and used silver brazing with an oxyacetylene torch. After almost 7 hours of work, he had a chill, high fever, and dyspnea. Blood gas analysis revealed severe hypoxemia (PaO2 34.5 Torr, PaCO2 29.4 Torr). The level of copper in serum was slightly higher than normal (174 micrograms/dl). A transbronchial lung biopsy specimen showed lymphocyte infiltration and fibrous changes of the alveolar walls, which seemed to be granulomatous pneumonitis. Steroid therapy was effective against the symptoms, and the radiographic findings also improved. We think this is a rare case of interstitial pneumonitis caused by inhalation of cadmium fumes contained in silver brazing.
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PMID:[A case of interstitial pneumonitis caused by inhalation of cadmium fumes]. 779 56

We recently developed a method of proton magnetic resonance spectroscopy (1H-MRS) to measure the 1H-MR spectra of peripheral blood lymphocytes (PBL) using only 10(7) cells. We investigated the clinical feasibility of this method for evaluating disease activities in sarcoidosis and interstitial pneumonitis. PBL was separated from 10 ml of venous blood by differential centrifugation with Ficoll-Conray. Using a 90 MHz MR spectrometer (EX90, JEOL), the spectrum was obtained with 4000 times accumulation of 1H signals by single 70 degree pulses at 37 degrees C under spinning. Water signal was suppressed with the homo-gated decoupling sequence. The spectra were analyzed with Gaussian curve fitting. The spectra of patients with active disease showed significant increases in peak heights for (CH2)n and CH3 peaks compared with the control. The peak heights decreased after improvement of disease states. The changes in 1H-MR spectra suggested activation of PBL in patients with sarcoidosis and interstitial pneumonitis, since similar changes have been shown for cells activated with mitogens. Our preliminary results indicate that 1H-MRS may be useful to evaluate activation of PBL in sarcoidosis and interstitial pneumonitis.
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PMID:[Proton magnetic resonance spectroscopy (1H-MRS) of peripheral blood lymphocytes in patients with sarcoidosis and interstitial pneumonitis]. 827 56

Tissues from 23 Australian water rats (Hydromys chrysogaster) collected from five localities in central and northern Queensland, Australia, between February 1992 and May 1993, were examined for protozoan parasites and additional pathological changes. We found Klossiella hydromyos in the kidneys, Toxoplasma gondii in the brain and skeletal muscles and Sarcocystis sp. in the somatic musculature. Other pathological findings, including interstitial nephritis, interstitial pneumonia and a tongue abscess, as well as helminth-induced lesions in the lungs, mesenteries, stomach wall and cecal wall were also noted.
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PMID:Protozoan parasites and pathological findings in Hydromys chrysogaster (Muridae: Hydromyinae) from Queensland. 872 76

Nickel is an essential element for at least several animal species. These animal studies associate nickel deprivation with depressed growth, reduced reproductive rates, and alterations of serum lipids and glucose. Although there is substantial evidence of an essential status for nickel in animals, a deficiency state in humans has not been clearly defined. Nickel is a silver-white metal with siderophilic properties that facilitate the formation of nickel-iron alloys. In contrast to the soluble nickel salts (chloride, nitrate, sulfate), metallic nickel, nickel sulfides, and nickel oxides are poorly water-soluble. Nickel carbonyl is a volatile liquid at room temperature that decomposes rapidly into carbon monoxide and nickel. Drinking water and food are the main sources of exposure for the general population with the average American diet containing about 300 micrograms Ni/d. Nickel is highly mobile in soil, particularly in acid soils. There is little evidence that nickel compounds accumulate in the food chain. Nickel is not a cumulative toxin in animals or in humans. Almost all cases of acute nickel toxicity result from exposure to nickel carbonyl. The initial effects involve irritation of the respiratory tract and nonspecific symptoms. Patients with severe poisoning develop intense pulmonary and gastrointestinal toxicity. Diffuse interstitial pneumonitis and cerebral edema are the main cause of death. Sodium diethyldithiocarbamate is an investigational drug used to chelate nickel following exposure to nickel carbonyl. Nickel is a common sensitizing agent with a high prevalence of allergic contact dermatitis. Nickel and nickel compounds are well-recognized carcinogens. However, the identity of the nickel compound or compounds, which cause the increased risk of cancer, remains unclear. Currently, there are little epidemiological data to indicate that exposure to metallic nickel increases the risk of cancer, or that exposure to the carcinogenic forms of nickel causes cancer outside the lung and the nasal cavity.
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PMID:Nickel. 1038 59

Four groups of 12 pregnant Wistar rats each were fed with rations containing 0, 0.01, 0.015 and 0.02% of monocrotaline (MCT) from day 6 to 21 of gestation. Liver weights of the dams from the three experimental groups were significantly lower than those from the control group. Serum levels of aspartate aminotransferase; alkaline phosphatase; lactate dehydrogenase; gamma glutamyltransferase, urea and creatinine were significantly higher in dams from MCT 0.02% group. The weights of the placenta, fetuses and fetal lungs of the 0.02% MCT group were significantly lower than those of the control group. A mild to moderate interstitial pneumonia and liver lesions were observed in dams ingesting 0.02% of MCT. These results showed the toxicity of MCT to the females that ingested 0.02% and their fetuses. Because there was no differences on the weight gains and food and water consumption of the dams it is suggested that this toxic effects in the fetuses was caused by the diffusion of MCT through the placenta. No significant differences were observed in the frequency of skeletal and visceral malformation or anomalies between the control and treated groups suggesting that MCT had no teratogenic effect.
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PMID:Fetotoxicity and reproductive effects of monocrotaline in pregnant rats. 1068 74

Aqueous dispersion resin (ADR) is a water-based acrylate copolymer designed to allow a range of ethanol concentrations for hair-spray formulations. A series of inhalation (whole-body) aerosol toxicity studies, including acute, 9-day, and 90-day exposures, was conducted to determine any toxicological effects for ADR. An acute study of ADR was conducted for 4 h with a 14-day observation period. The maximum ADR aerosol concentration was 1.07 (+/- 0.04) mg/L with a mass medium aerodynamic diameter (MMAD) value of 1.46 microm and a geometric mean (sigma(g)) of 1.42. No deaths or exposure-related lesions were observed. Thus, the LC50 value was greater than 1.07 mg/L. For the 9-day study, each group contained 10 animals/sex and was exposed for 2 h/day. The mean exposure concentrations (+/- standard deviation) were 244 (+/- 39.6), 543 (+/- 71.9), and 843 (+/- 186.2) mg/m(3) for the 250-, 500-, and 1000-mg/m(3) groups, respectively. The mean MMADs were 2.83, 2.90, and 4.09 microm for the 250-, 500-, and 1000-mg/m(3) groups, respectively, with sigma(g) values ranging from 3.15 to 6.22. Unkempt fur and alopecia in the males and females from the 1000-mg/m(3) group at sacrifice were the only exposure-related clinical signs observed. Increased lung weights in the 500- and 1000-mg/m(3) exposure groups were found. Histopathological effects, such as alveolar histiocytosis and interstitial pneumonitis, were also noted in these two exposure groups. For the 90-day study, 10 animals per sex were included in each group with a 6-wk recovery group of 5 female rats/group. Exposures were conducted for 2 h/day. The mean exposure concentrations were 30.4 (+/- 2.3), 102 (+/- 11.6), and 308 (+/- 19. 3) mg/m(3) with mean MMADs of 3.09, 2.64, and 2.67 microm and sigma(g) values ranging from 3.54 to 3.90 for exposure concentrations of 30, 100, and 300 mg/m(3), respectively. The only findings at the 90-day sacrifice were increased lung weights for the males and females in the 300-mg/m(3) group and males in the 100-mg/m(3) group. For the 6-wk recovery sacrifice of the females, the lung weights for the 300- and 100-mg/m(3) groups were increased. Histopathological effects at the 90-day sacrifice included alveolar histiocytosis and lymphadenitis in the mediastinal lymph nodes in the 100- and 300-mg/m(3) exposure groups for males and females, while alveolar histiocytosis, intraalveolar cellular debris, lymphadenitis in the mediastinal lymph nodes, and/or interstitial pneumonitis were noted in these 2 exposure groups of the females after the 6-wk recovery period. Animals exposed for 90 days to 100 and 300 mg/m(3) for 2 h had increased lung weights. However, no effects were observed in the 30-mg/m(3) exposure group. Thus, under the conditions of the present 90-day study, a no-observable-effect level (NOEL) was found to be 30 mg/m(3).
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PMID:Inhalation toxicity studies of aqueous dispersion resin. 1071 31

Extrinsic allergic alveolitis often occures as bird fancier's lung or is caused by occupational treatment with antigenic materials. In housing environments antigens of allergic alveolitis are also found, especially mould fungi. lf a source of antigens is absent in the anamnesis and the clinical picture as well as the clinical findings are ambiguous, the diagnosis of extrinsic allergic alveolits is delayed or unobtained. The following example shows that in spite of a detailed allergic anamnesis the source of antigens may remain occult and only an inspection of the dwelling rooms leads to an elucidation. - A sixty-one year old non-smoking women was twice admitted to hospital with a temperature of more than 39 degrees C, intense dyspnea on exertion and a strong dry cough under the persumed diagnosis pneumonia. The laboratory values showed nonspecific signs of inflammation, the blood gas analysis was changed to a heavy hypoxemia (pO subset2 49.2 mmHg) and in the chest x-ray there were seen miliary and partly reticular alterations. The chest computed tomography showed extensive densities in both upper and lower parts of the lungs and the pulmonary function test corresponded with a low-grade to middle-grade restriction (VC subsetin = 67%, TLC = 69%). A high dose of corticosteroids produced an improvement of the radiological findings and of the pulmonary function. Also the specialized diagnostic in a hospital for pulmonary diseases yielded no new knowledge, and an interstitial pneumonia was diagnosed. Only the new formation of an acute pneumonic clinical picture on the day of returning to the patients own habitation suggested a noxious substance in the domestic environment. The inspection of the rooms finally showed the source of antigen to be from a condensation water soaked, moulded tapestry on the embrasure of a small unopenable window in the bedroom just on the head of the bed. The nutritive mediums left in the rooms furnished evidence of the mould-species Penicillium, Cladosporium and Botrytis, in the bedroom however mostly Penicillium. The RAST of specific IgG proved a positive result of all three mould species (Penicillium sp. 1 : 100, Cladosporium sp. 1 : 200 and Botrytis sp. 1 : 200). The diagnosis of an extrinsic allergic alveolitis caused by mould was confirmed by a controlled re-exposure test, which promptly gave rise to a relapse and forced the patient to change habitation with the result of no further ailments. - Characteristic for the extrinsic allergic alveolitis in the described case is the inefficiency of antibiotic therapy, the immediate recovery by corticosteroids and furthermore the outbreak of relapses caused by re-exposure. If the source of antigens is unclear, the inspection of the habitation by an experienced allergologist may lead to success.
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PMID:Extrinsic allergic alveolitis in domestic environments (Domestic allergic alveolitis) caused by mouldy tapestry 1075 68

The purpose of the present study was to evaluate the effectiveness of fish oil in preventing tissue pathologies associated with monocrotaline (MCT) toxicity. Twenty-four weanling rats were randomly assigned to one of two groups: (1) 12 to a group fed a diet containing 15% (w/w) corn oil (control) and (2) 12 to a group fed a diet containing fish oil (13%) and corn oil (2%) as the source of fat. Rats were fed for 4 weeks prior to MCT treatment. Six rats in each group were subcutaneously injected with MCT and six injected with its vehicle (water) and all were continued on their respective diets. All rats were sacrificed 3 weeks after injection. In rats receiving MCT, we observed severe interstitial pneumonia, septal fibrosis, vasculitis with virtual obliteration of the lumen of the small arteries and arterioles, right ventricular hypertrophy (RVH), and hepatomegaly and hepatocyte vacuole formation. Dietary fish oil significantly reduced septal fibrosis and development of pneumonia. There was a slight, but statistically insignificant decrease in vasculitis and fish oil did not prevent RVH (pulmonary hypertension). In addition, fish oil effectively protected the MCT-treated rats from development of hepatocyte vacuoles (steatosis), hepatic inflammation and vasculitis, increased presence of fibroblasts and collagen deposition in the centrilobular and, to a lesser extent, in the periportal spaces. These results suggest that lung parenchymal inflammation can be attenuated without altering the course of development of pulmonary hypertension in the MCT model. These results also indicate that fish oil protects against inflammation and fibrosis in the lung and liver, and against hepatocyte vacuole formation in MCT-treated rats.
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PMID:Dietary fish oil protects against lung and liver inflammation and fibrosis in monocrotaline treated rats. 1204 31

Bronchiolitis obliterans combined organizing pneumonia (BOOP), now called organizing pneumonia, is a multi-etiologic disease. It can present as a solitary lesion, or as multinodular or diffuse interstitial lung disease. It is speculated if solitary BOOP may evolve into inflammatory pseudotumor of the lung. BOOP can be seen after non-resolving infectious bronchopneumonia as well as acute interstitial pneumonia with diffuse alveolar damage. BOOP can be the early morphologic pattern in toxic inhalation, especially water-soluble substances, but also in drug induced lung disease. BOOP can be the late stage of extrinsic allergic alveolitis, but also a morphologic sequel of collagen vascular disease. Even Wegener's granulomatosis can be preceded by a BOOP pattern. In many cases a careful analysis of BOOP, including changes of the pneumocytes, macrophages, myofibroblasts and endothelial cells, can establish the correct etiologic diagnosis. For example virus-induced pneumocyte proliferation can be seen months after the onset of interstitial pneumonia, and can be found within BOOP. A small percentage of BOOP, however, has to be labeled as idiopathic, which is important too, because of different modalities of therapy. Idiopathic BOOP also is different with respect to prognosis. In the overview different BOOP etiologies will be discussed, and the etiologic background will be analyzed. The pathogenesis will be discussed with respect to the understanding of the causing mechanisms. The role of bronchoalveolar lavage and the optimal tissue sample for establishing the diagnosis will be discussed and demonstrated by examples. A part of the presentation will deal with the differential diagnosis, such as usual interstitial pneumonia, non-specific interstitial pneumonia, constrictive, and respiratory bronchiolitis combined interstitial lung disease.
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PMID:Bronchiolitis obliterans. Organizing pneumonia. 1264 57

Polymyositis, dermatopolymyositis, and inclusion body myositis imply chronic inflammation of skeletal muscles. Pulmonary complications include aspiration pneumonia, interstitial pneumonitis, or respiratory muscle myositis. This study aims at better describing their impact on respiratory muscle. Twenty-three consecutive patients (12 PM, 5 DM, 6 IBM) were studied (static inspiratory and expiratory pressures; diaphragm function in terms of the mouth and transdiaphragmatic pressure responses to bilateral phrenic stimulation). Pulmonary parenchymatous abnormalities were mild (6 cases) or absent. The mouth pressure produced by phrenic stimulation was 6.83+/-3.01 cm H2O, with 18 patients (78%) diagnosed with diaphragm weakness (<10 cm H2O) and lower values in DM (4.35+/-1.48 cm H2O) than in IBM and in PM (P<0.05). Diaphragm weakness is frequent and probably overlooked in inflammatory myopathies. Further studies are needed to delineate the clinical relevance of these results.
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PMID:Diaphragmatic dysfunction in patients with idiopathic inflammatory myopathies. 1563 18


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