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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With changes in the demographics of human immunodeficiency virus (HIV) infection, women and children are becoming the fastest growing group of newly infected patients. With longer survival after HIV infection, more women infected with HIV are becoming pregnant. Pulmonary disease is one of the most common presenting conditions in an AIDS-defining illness. Pneumocystis carini pneumonia and tuberculosis are the most common disorders that herald the onset of AIDS. They are also the most frequently encountered HIV-related pulmonary complications during pregnancy. Others have been rarely reported during pregnancy and include fungal infections (Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitus), bacterial infections (Haemophilus influenzae and Streptococcus pneumoniae along with Pseudomona aeruginosa), viral infections (CMV), opportunistic neoplasms (Kaposi's sarcoma, lymphoma) and miscellaneous conditions peculiar to HIV-infected individuals (nonspecific interstitial pneumonitis, lymphoid interstitial pneumonitis, isolated pulmonary hypertension, and pulmonary edema secondary to cardiac disease or drug abuse). Most of the data regarding the pulmonary complications of HIV infection come from studies in nonpregnant patients. The extent to which pregnancy affects the course of respiratory disease in HIV infection and vice versa is not well documented. Clinical presentation is usually not altered by pregnancy. Except for minor modifications mainly related to potential fetal effects, the diagnostic work-up and management are similar to those in the nonpregnant patient. The most important effect of pregnancy on these conditions remains the delay in diagnosis and treatment. A high index of suspicion should, therefore, be maintained. In addition, most prophylactic measures recommended in nonpregnant HIV-infected individuals also apply to pregnant women.
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PMID:Human immunodeficiency virus (HIV)-related pulmonary complications in pregnancy. 929 23

Increased serum levels of mucin-associated antigen have been previously demonstrated in patients with cystic fibrosis (CF) and interstitial pneumonia, and in lung-transplant recipients. The present study assessed the serum airway mucin levels in patients with acute respiratory distress syndrome (ARDS). An enzyme-linked immunosorbent assay (ELISA) method with a human-airway-mucin-specific monoclonal antibody (17Q2) was used to measure serum mucin levels in normal subjects, chronic smokers, patients with chronic bronchitis and other pulmonary diseases, patients with acute cardiogenic lung edema, and patients with ARDS. The serum mucin levels measured 9.9 +/- 0.8 ng/ml (mean +/- SEM, n = 59) in normal subjects, 12.7 +/- 1.6 ng/ml (n = 29) in chronic smokers, 21.8 +/- 1.9 ng/ml (n = 28) in patients with chronic bronchitis and other pulmonary diseases, 9.0 +/- 3.1 ng/ml (n = 5) in patients with acute cardiogenic lung edema. The serum mucin level was 53.8 +/- 6.6 ng/ml (n = 13) in patients with ARDS (p < 0.05, as compared with the four other groups). Serial measurements of serum mucin levels were obtained in patients with ARDS. Statistical analysis showed an inverse correlation of serial measurements of serum mucin with static respiratory-system compliance (p = 0.021), an inverse correlation of sequential serum mucin levels and log(Pa(O2)/Fl(O2)) (p = 0.016), and a positive correlation of sequential serum mucin levels and lung injury score (LIS) (p = 0.019). Gel-filtration analysis showed that mucin-associated antigens in ARDS sera were polydispersed and smaller than the antigens in normal sera. This study indicates that an increasing amount of degraded mucin occurs in patients with ARDS.
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PMID:Elevated serum levels of mucin-associated antigen in patients with acute respiratory distress syndrome. 937 60

There are frequently respiratory complications with cancer particularly in primary lung carcinoma. Among these are bronchopulmonary infections with or without endobronchial obstruction, carcinomatous lymphangitis, thromboembolic disease and haemorrhagic disease as well. Radiotherapy and chemotherapy may induce various respiratory complications which diagnosis can be of varying shades of difficulty. The classical post radiation pneumonitis occurring exclusively in the field of radiation hardly poses any problem unless it could be masking a recurrence. Certain clinical manifestations address very difficult problems of differential diagnosis by their lack of specificity and by their often unforeseeable character (except for bleomycin fibrosis which is perfectly dose dependent). Moreover patients often have multiple treatments and the identification of the single responsible agent becomes very difficult. We will not discuss here the infectious or secondary haemorrhagic complications of radiotherapy or chemotherapy but rather the anaphylactic manifestations, diffuse interstitial pneumonia with lymphocytic alveolitis or fibrosis, eosinophilic pneumonia, non-cardiogenic pulmonary oedema, bronchiolitis obliterans with organising pneumonia and the rare pulmonary vascular disorders such as pulmonary veno-occlusive disease.
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PMID:[Radiation- and chemically-induced respiratory manifestations]. 948 Apr 78

Genes of an influenza A (H5N1) virus from a human in Hong Kong isolated in May 1997 were sequenced and found to be all avian-like (K. Subbarao et al., Science 279:393-395, 1998). Gene sequences of this human isolate were compared to those of a highly pathogenic chicken H5N1 influenza virus isolated from Hong Kong in April 1997. Sequence comparisons of all eight RNA segments from the two viruses show greater than 99% sequence identity between them. However, neither isolate's gene sequence was closely (>95% sequence identity) related to any other gene sequences found in the GenBank database. Phylogenetic analysis demonstrated that the nucleotide sequences of at least four of the eight RNA segments clustered with Eurasian origin avian influenza viruses. The hemagglutinin gene phylogenetic analysis also included the sequences from an additional three human and two chicken H5N1 virus isolates from Hong Kong, and the isolates separated into two closely related groups. However, no single amino acid change separated the chicken origin and human origin isolates, but they all contained multiple basic amino acids at the hemagglutinin cleavage site, which is associated with a highly pathogenic phenotype in poultry. In experimental intravenous inoculation studies with chickens, all seven viruses were highly pathogenic, killing most birds within 24 h. All infected chickens had virtually identical pathologic lesions, including moderate to severe diffuse edema and interstitial pneumonitis. Viral nucleoprotein was most frequently demonstrated in vascular endothelium, macrophages, heterophils, and cardiac myocytes. Asphyxiation from pulmonary edema and generalized cardiovascular collapse were the most likely pathogenic mechanisms responsible for illness and death. In summary, a small number of changes in hemagglutinin gene sequences defined two closely related subgroups, with both subgroups having human and chicken members, among the seven viruses examined from Hong Kong, and all seven viruses were highly pathogenic in chickens and caused similar lesions in experimental inoculations.
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PMID:Comparisons of highly virulent H5N1 influenza A viruses isolated from humans and chickens from Hong Kong. 965 15

A 45-year-old Japanese woman presented with a high fever, a nonproductive coughing, and severe dyspnea, and was admitted to another hospital. During the week prior to hospitalization, she had been given Shosaikoto for treatment of liver dysfunction of unknown etiology. Mycoplasma pneumonitis was initially suspected, so she was treated with antibiotics (clindamycin and minocycline) and received oxygen therapy. Pulmonary insufficiency worsened rapidly, and she was transferred to our hospital. On admission, a chest roentgenogram revealed bilateral alveolar infiltrates predominantly in the medial lung fields. Furosemide and high-dose methylprednisolone were immediately administered, but hypoxemia increased. When the PaO2 was 55.7 Torr while the patient breathed 100% oxygen, mechanical ventilation with positive end-expiratory pressure (PEEP) was started. Arterial blood-gas values improved dramatically, and the chest roentgenogram became clear. Our diagnosis of noncardiogenic pulmonary edema is based on the chest-roentgenographic findings, infiltration of inflammatory cells as seen in two lung-biopsy specimens and bronchoalveolar lavage fluid, the lack of findings of heart failure on physical examination and electrocardiography, and the good clinical response to PEEP. A positive lymphocyte stimulation test in response to Shosaikoto implicated this non-traditional herbal medicine as an etiologic factor in the non-cardiogenic pulmonary edema. Shosaikoto has been identified as the cause of interstitial pneumonia or eosinophilic pneumonia, but pulmonary edema associated with Shosaikoto has not been previously described. This case suggests that methylprednisolone treatment may be insufficient for Shosaikoto-induced pulmonary edema, and that mechanical ventilation with PEEP is very effective.
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PMID:[Pulmonary edema associated with the Chinese medicine shosaikoto]. 986 80

A number of drugs used to treat systemic autoimmune diseases can cause respiratory complications. These include bronchospasm, noncardiac pulmonary edema, interstitial pneumonitis and fibrosis, hypersensitivity, and numerous other disorders. Additionally, some of these drugs increase the risk of infections, particularly with opportunistic organisms. This article reviews the clinical presentation and mechanism of toxicity of drug related pulmonary complications.
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PMID:Pulmonary toxicity of drugs used to treat systemic autoimmune diseases. 991 66

Unusual clinical and pathological observations in the field in goats and sheep suffering from Strongyloides papillosus infection prompted experimental work on this parasite. Goats were infected percutaneously with either single or multiple, low or high levels of S. papillosus. Young goats up to 12 months of age were found to be the most susceptible. Some animals, however, showed substantial resistance to infective doses. Clinical signs included transient diarrhoea, misshapen, elongated faecal pellets terminally, dehydration, anorexia, cachexia, gnashing of teeth, foaming at the mouth, anaemia and nervous signs such as ataxia, a wide-based stance, stupor and nystagmus. A 'pushing syndrome' was seen in 22% of the animals. The pathological changes are described and included enteritis, status spongiosus in the brain, hepatosis leading to rupture of the liver, nephrosis, pulmonary oedema, interstitial pneumonia and pneumonia. About 6% of the goats died acutely from fatal hepatic rupture. The development of an acquired immunity was determined. The immunity elicited an allergic skin reaction at the application site of larvae or injection sites of larval metabolites. This immunity, however, could be breached by large doses of larvae. The most profound clinicopathological changes induced by the parasites were an anaemia (most pronounced in the young goats) and hypophosphataemia. Trace element analyses provided evidence of Cu, Mn and possibly Se deficiencies in some goats.
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PMID:Experimental studies with Stronglyloides papillosus in goats. 1063 9

Carbamate insecticides are commonly used agricultural insecticides. The major cause of morbidity and mortality in acute carbamate poisoning is respiratory failure associated with pulmonary edema. Although carbamate poisoning is well recognized in the clinical literature, the findings of high resolution CT (HRCT) with carbamate have not been reported. We report the radiographic and HRCT findings of a patient with acute carbamate poisoning who had pathologically proven interstitial pneumonitis after resolution of initial pulmonary edema.
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PMID:Carbamate poisoning: high resolution CT and pathologic findings. 1066 58

Various drugs are associated with adverse respiratory disorders (ARDs) ranging in severity from mild, moderate to severe and even fatal. Cardioselective and nonselective beta-blockers, calcium antagonists and dipyridamole can induce asthma. ACE inhibitors are mainly associated with cough. Amiodarone is related to a form of interstitial pneumonitis (IP) which can be fatal, tocainidine and flecainidine to a form of IP, and hydrochlorothiazide to a form of IP and pulmonary oedema. Antiasthmatic drugs can be associated with a paradoxical bronchospasm, while leukotriene antagonists are linked to the development of Churg-Strauss syndrome. Nonsteroidal anti-inflammatory drugs including aspirin (acetylsalicylic acid) may induce asthma. Gold is mainly related to IP, penicillamine to IP, systemic lupus erythematosus, bronchiolitis obliterans, and Goodpasture's syndrome. Acute respiratory reactions to nitrofurantoin include dyspnoea, cough, IP, and pleural effusion while IP and fibrosis are common in chronic reactions. Other antibacterials mainly evoke pneumonitis, pulmonary infiltrates and eosinophilia, and bronchiolitis obliterans. ARDs are similar for most categories of cytotoxic agents, with chronic pneumonitis and fibrosis being the most common. Noncardiogenic pulmonary oedema occurs as the most common respiratory complication in opioid agonist addiction. Psychotropic drugs such as phenothiazides, butyrophenones and tricyclic antidepressants can also induce pulmonary oedema. Oral contraceptives may produce asthma exacerbation, while long term use and/or high doses of postmenopausal hormone replacement therapy increase the risk of asthma. Bromocriptine is mainly associated with pleural effusion, while methysergide is usually associated with pleural effusion and fibrosis. Some anorectic agents have been linked to the development of primary pulmonary hypertension. The possibility of the occurrence of ARDs should be taken into account in each individual patient. Although in most cases the adverse effects are unpredictable, they can be reduced to a minimum or prevented if some drugs are avoided or stopped in time.
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PMID:Drug-induced respiratory disorders: incidence, prevention and management. 1094 76

Cobalt alone and in combination with tungsten carbide known as hard metal is capable of causing lung damage. This may vary from development of pulmonary oedema to asthma and fibrosing alveolitis. We report a case of giant cell interstitial pneumonitis caused by exposure to cobalt dust which was not identified as the etiological agent initially and hence led to progression of the disease. The patient subsequently improved following cessation of exposure and treatment with oral corticosteriods, thereby stressing the importance of occupational history in all cases of interstitial pulmonary fibrosis.
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PMID:Giant cell pneumonitis induced by cobalt. 1137 May 7


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