Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-year-old man underwent cardiac transplantation for long-standing severe dilated cardiomyopathy. Postoperative complications included primary cytomegalovirus (CMV) infection with several episodes of moderate acute rejection and severe pneumonia. Six months after transplantation, an endomyocardial biopsy specimen revealed focal necrotizing myocarditis with intranuclear inclusions consistent with CMV. The patient subsequently developed fulminant pneumonia and died 7 months after transplantation. Postmortem examination revealed that the cause of death was acute necrotizing bronchopneumonia due to Staphylococcus aureus, with underlying CMV pneumonitis. The transplanted heart had left ventricular hypertrophy with multiple organizing myocardial infarcts, moderate coronary atherosclerosis, and organizing thrombi of the left atrium. Characteristic inclusions of CMV were identified, predominantly within endothelial cells, in the left coronary artery, left ventricular endocardium, and myocardium. With in situ hybridization, the presence of CMV was verified in the inclusions, as well as in many fibroblasts without inclusions. In situ hybridization is warranted in myocardial biopsy specimens when suspicious inclusions or infiltrates are present, to confirm CMV infection, so that appropriate therapy can be initiated.
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PMID:Cytomegalovirus endomyocarditis in a transplanted heart. A case report with in situ hybridization. 185 May 89

123 patients with small cell lung cancer (SCLC) presented to the National Cancer Center Hospital (Tokyo) between 1978 and 1986. 22 of 71 patients with limited stage disease (LD) and none of 52 patients with extensive disease (ED) survived for 3 years. 15 of the 22 three year survivors had significant late complications. All patients received chemotherapy and either thoracic irradiation, resection or both. No prophylactic cranial irradiation was given. 4 patients developed cardiac failure, 2 with a dilated cardiomyopathy, despite the fact that no patient received over 420 mg/m2 of doxorubicin. 12 patients of the 17 who received thoracic irradiation developed radiation pneumonitis and 3 required hospitalisation for severe haemoptysis (2) or cavity formation (1). 1 patient who received nimustine developed a fatal myelodysplastic syndrome and 2 additional patients developed second primary tumours in the oesophagus (1) and stomach (1). Mild peripheral neuropathy (WHO grade 1) was persistent in 3 patients and asymptomatic azotemia (WHO grade 1) in 7. Despite advances in the treatment of SCLC there are very few asymptomatic long-term survivors.
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PMID:Late toxicities and complications in three-year survivors of small cell lung cancer. 185 18

Amiodarone pneumonitis is a serious complication that may lead to fatal lung fibrosis. In an attempt to diagnose this condition as early as possible, the technetium-99m-labelled diethylene triamine penta-acetic acid (99mTc-DTPA) aerosol washout rates of 10 non-smoking normal volunteers (group 1), 10 non-smoking patients on a long-term amiodarone regimen with dilated cardiomyopathy but no congestive heart failure (group II) and 10 patients with amiodarone pneumonitis (group III) were compared. Spirometric measurements, as percentage predicted, were higher in group I than in group III (P less than 0.05). The global mean effective half-lives of 99mTc-DTPA aerosol for both lungs together in minutes were 65 +/- 14, 55 +/- 16 and 27 +/- 4 for groups I, II and III, respectively. Group III values were significantly lower than those of groups I and II (P less than 0.05). Our results demonstrated that amiodarone pneumonitis alters the alveolar-capillary membrane permeability to hydrophilic molecules. The pulmonary clearance of 99mTc-DTPA aerosol is a useful test in the differentiation of patients on a long-term amiodarone regimen without side effects from patients with amiodarone pneumonitis. The test is rapid, easy to perform and has the potential for playing an important role in deciding which patients should discontinue therapy.
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PMID:Pulmonary clearance of technetium 99m diethylene triamine penta-acetic acid aerosol in patients with amiodarone pneumonitis. 228 6

Eight children with human immunodeficiency virus (HIV) infection had symptomatic cardiac dysfunction. The median age was 1.4 years (range 0.2 to 7.9 years). All had hepatosplenomegaly, fever, pneumonia with tachypnea, and tachycardia ascribed to infection and anemia. An S3 gallop was present in six of eight. All had normal creatine phosphokinase values. Chest x-rays did not aid in the diagnosis of cardiac dysfunction. ECG showed flattened T waves in five of eight with left ventricular hypertrophy, right ventricular hypertrophy, or both in seven of eight. Results of echocardiography showed decreased left ventricular function in all eight, despite anemia, with dilated left ventricular myopathy in six, concentric left ventricular wall thickening in two of eight, an enlarged right ventricle in two, and pericardial fluid in three. Medical therapy improved cardiac function in all. All patients subsequently died of noncardiac causes. Results of autopsies on four of eight patients showed focal myocarditis in two (with cytomegalovirus inclusions in one) and dilated cardiomyopathy in two others. We conclude: (1) Preexistent hepatosplenomegaly, fever, infection, and anemia result in physical findings that mimic findings of heart failure, thereby masking the occurrence of cardiac dysfunction; (2) an S3 gallop may indicate the presence of impaired heart function when other clinical signs are masked; (3) confirmation of cardiac compromise may be accomplished by noninvasive evaluation with echocardiography and (4) medical therapy can improve cardiac dysfunction in HIV-infected children.
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PMID:Symptomatic cardiac dysfunction in children with human immunodeficiency virus infection. 252 16

Between December, 1967 and August, 1988, 147 heart transplants (64 orthotopic, 68 heterotopic procedures; 15 heart-and-lung replacements) were performed on 128 patients. In the majority of the recipients, dilated cardiomyopathy or end-stage ischaemic heart disease was diagnosed. From 1985 to the present, 70 transplants (45 orthotopic, 11 heterotopic and 14 heart-lung) took place. Seventeen of these patients (mean age 46.6 years) suffered from end-stage disabling (NYHA IV) coronary artery disease; in each case the angiogram verified severe stenosis or occlusion of the three main coronary artery systems. Their histories revealed a total of 22 previous myocardial infarctions; 8 patients needed a total of 9 surgical revascularization procedures. The left ventricular ejection fraction (LVEF) ranged from 9% to 24% (mean 15.3%). Before transplantation three patients required intraaortic balloon pump (IABP) support. Fourteen of the 17 patients are at present still alive with post operative periods ranging from 8 weeks to 3.5 years (the actuarial 90-days and 1-year-survival rates being respectively 91.7% and 81.5%). Twelve of the patients are in NYHA class I; 2 are in class II. Three late deaths occurred: one from pneumocystic carinii/cytomegalovirus pneumonia, a second from atypical pneumonia and a third from chronic graft rejection. Radionuclide ventricular studies demonstrated postoperative left ventricular ejection fractions ranging from 54%-81% (mean 71%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart transplantation--the treatment of choice for patients with end-stage ischaemic heart disease. 264 61

A 65 year old man developed atrial arrhythmias secondary to a congestive cardiomyopathy which were resistant to quinidine and disopyramide. Amiodarone controlled the paroxysmal atrial tachycardia but 4 months after starting the drug he developed increasing dyspnoea and radiological changes highly suggestive of metastatic lung disease. Lung biopsy showed change of drug-induced pneumonitis and 4 months after stopping amiodarone his symptoms resolved and the chest X-ray had cleared. Amiodarone may cause pulmonary toxicity mimicking metastatic lung disease.
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PMID:Amiodarone-induced pulmonary toxicity mimicking metastatic lung disease. 367 Dec 75

A 75-year-old woman with acute respiratory failure due to pneumonia superimposed on bronchospastic chronic obstructive pulmonary disease and dilated cardiomyopathy developed multifocal and unifocal atrial tachycardia. Arrhythmia recurrence appeared to be dependent on reaching a critical but "nontoxic" serum theophylline concentration in the presence of high normal levels of digoxin. The arrhythmias responded to a decrease in serum theophylline concentration or to the administration of verapamil. The precipitation of the atrial arrhythmias by theophylline in the presence of digitalis, both of which may increase intracellular calcium and a dramatic response to verapamil, which inhibits calcium uptake and release, suggests that these arrhythmias may represent an example of "triggered activity" in man.
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PMID:Atrial arrhythmias exacerbated by theophylline. Response to verapamil and evidence for triggered activity in man. 406 86

A 53-year-old man with dilated cardiomyopathy underwent left ventriculoplasty (Batista procedure), a new surgical procedure, which reduces ventricular volume to improve left ventricular function. Left ventricular ejection fraction increased from 19.7% to 43.7%. Unfortunately, he died of pneumonia 12 days after surgery. This is the first such procedure in a human in Japan.
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PMID:[New surgical procedure for patients with dilated heart and end-stage cardiac failure (Batista procedure)]. 912 Jul 93

The development of highly sensitive molecular biological methods such as in-situ hybridization and polymerase chain reaction (PCR) made it possible to detect viral/bacterial nucleic acid in human endomyocardial biopsies. However, only a few investigations addressed the problem of latent persistence of viral and bacterial genome and the detection of the corresponding proteins, which could have important consequences for the clinical course of the disease. The purpose of this study was to determine whether protein of various viruses (adenovirus, enterovirus, cytomegalovirus, influenza A and B virus, herpes simplex virus 1 and 2) and bacteria (chlamydia pneumonia) can be detected in endomyocardial biopsies of patients with myocarditis and dilated cardiomyopathy with and without inflammation by use of an immunofluorescence assay and to compare the frequency of its detection with the results of PCR, immunohistology and serology. Thirty-nine patients with myocarditis and dilated cardiomyopathy with and without inflammation were examined by a direct immunofluorescence assay using the endomyocardial biopsy as antigen. Each of the samples was additionally studied by immunohistological methods and PCR for the detection of infiltrating cells and the genome of cardiotropic viruses or bacteria. Fourteen of patients were considered to have myocarditis (group 1), 9 dilated cardiomyopathy with inflammation (group 2), 10 dilated cardiomyopathy (group 3), 6 to have no myocarditis or dilated cardiomyopathy (group 4). Using a direct immunofluorescence assay we could show only that 1 patient without histological myocarditis or dilated cardiomyopathy (group 4) was positive for influenza B and chlamydia pneumonia antigens in the endomyocardial biopsy. In addition we have determined influenza B-specific antibodies, such as IgG (marginal titer) and IgA (high titer) and chlamydia pneumonia-specific antibodies, such as IgG (marginal titer) in serum of this patient. A second patient with dilated cardiomyopathy was found to be positive for protein of chlamydia pneumonia, who was shown to have chlamydia pneumonia-specific antibodies, such as IgG (high titer) in serum. There was no correlation with PCR results, but good correlation with influenza B and chlamydia pneumonia-specific antibodies in sera of these patients. In this investigation we have determined viral/bacterial-specific antibodies using serological methods and proteins of these agents using immunoflourescence. Despite the detection of virus or bacteria-specific antibodies in the sera and detection of viral and/or bacterial protein in the biopsies of some of the patients viral and/or bacterial genome was not found in the biopsy. This may be explained by the focal character of myocarditis and sampling error, because for technical reasons we use different biopsies for immunohistochemical and molecular biological investigations.
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PMID:Detection of viral and bacterial protein in endomyocardial biopsies of patients with inflammatory heart muscle disease? 1090 44

The clinical picture of myocarditis/myopericarditis is of importance in differential diagnosis, especially in younger patients with suspected myocardial infarction. Myocarditis/myopericarditis commonly presents with chest pain, and the diagnosis is usually established on clinical grounds. However, endomyocardial biopsy is necessary to confirm the diagnosis. We evaluated the characteristics of acute myocarditis over the years 1980-1998 in 54 patients of the Department of Medicine of the University Hospital, Zurich. Two to 6 patients per year were hospitalised with this diagnosis. In most cases the diagnosis was established by a combination of criteria, such as a preceding infection of the upper respiratory tract, thoracic pain, ST segment elevations in different precordial leads followed by T wave inversions, arrhythmias, elevation of cardiac enzymes, reversible hypokinesia by echocardiography and normal coronary arteries. At least 3 of 5 criteria were requested. In a first step we analysed retrospectively all patients with acute myocarditis/myopericarditis in the years 1980-1993. Among 30 cases of acute myocarditis/myopericarditis the following causes could be identified: one influenza B, one Toxoplasma gondii infection, 2 Epstein-Barr infections and one bacterial myocarditis with gram-negative rods. The aetiology of the other 25 cases remained unknown. The majority of myocarditis/myopericarditis healed without complications. One patient with Epstein-Barr myocarditis and one with Toxoplasma gondii infection died. Two patients developed dilated cardiomyopathy. In a second phase we analysed prospectively all cases with acute myocarditis/myopericarditis over the period 1994-1998: 24 patients with acute myocarditis/myopericarditis were hospitalised. At that time coronary angiography and endomyocardial biopsies were performed more frequently. We found 2 patients with giant cell myocarditis and 2 with Toxoplasma gondii infection and HIV, all of whom died. In addition, there were 2 patients with eosinophilic myocarditis, one with Lyme carditis, one with Epstein-Barr myocarditis, one with myopericarditis after Campylobacter enteritis and one histologically proven myocarditis after pneumonia with Haemophilus influenzae. The aetiology of the remaining 13 cases with myocarditis/myopericarditis could not be established. Three patients with probable viral myocarditis developed cardiogenic shock requiring intraaortic balloon pump, and fully recovered. The patient with Lyme carditis manifested with total atrioventricular block and was treated with a temporary pacemaker. One patient with lymphocytic myocarditis required heart transplantation because of terminal heart failure and one female patient with histologically proven diffuse lympho-monocytic myocarditis died of cardiogenic shock. All the other cases healed without complications. Serologies are of little diagnostic value and should be restricted to serologies with therapeutic implications. We believe that the apparent increase in myocarditis/myopericarditis in recent years is a result of better diagnostic tools, such as more specific cardiac enzyme tests, coronary angiography and endomyocardial biopsies. In most cases the therapy remains symptomatic. In elected, severe cases steroids and other immunosuppressive drugs are sometimes used.
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PMID:[Diagnosis and course of myocarditis: a survey in the medical clinics of Zurich University Hospital 1980 to 1998]. 1102 70


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