Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiology was diagnosed by means of clinical, radiographic, electrocardiographic phonocardiographic, angiocardiographic, and pathological findings in 271 or 3,745 cats necropsied from January 1962 to April 1974. The affected cats can be divided into three groups on the basis of the gross and microscopic pathological lesions: 1)endocarditis and myocarditis in 20 young cats; 2)endomyocardial fibrosis and left ventricular hypertrophy in 182 cats; and 3)myocardial degeneration and biventricular dilatation in 69 cats. Of 271 affected cats, thromboembolus was observed in the aorta, and in the carotid, femoral, iliac, renal, pulmonary, and hepatic arteries in 104 instances. The important aspects of cardiomyopathy in cats appears to be the reduced diastolic compliance of the thick left ventricle, resulting in poor fillin. Resistance to ventricular inflow raises the diastolic pressure and causes compensatory left atrial enlargement. A pathogenesis for the onset of clinical signs at any stages as the cause of the heart disease is postulated on the basis of stress causing tachycardia and poor left ventricular filling. Acute left-sided failure with pulmonary edema may be precipitated. Approximately one-fourth of the cats have enlargement of all cardiac chambers, typical of congestive cardiomyopathy. On the basis of the close similarily to cardiomyopathy in man, the cat could serve as a suitable animal model for a conservation of time and effort in the attack against this disorder. There is a need for coordinated research programs for utilizing the multiple avenues of approach such as: epidemiological, clinical, biochemical, pathological, ultrastructural, virological, and immunological.
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PMID:Feline cardiomyopathy. 12 93

Sudden death of pups in the 4- to 6-week age range has recently been occurring in western Canada as a result of severe, primary, nonsuppurative myocarditis. At necropsy, the prominent macroscopic lesion was pulmonary edema, and microscopically, characteristic intranuclear inclusion bodies were found within cardiac myofibers in association with myocarditis. Ultrastructurally, numerous small particles resembling parvoviruses were found within the intranuclear inclusion bodies, which were positive by direct fluorescent antibody test for canine parvovirus. Of three pups inoculated with homogenate from affected myocardium, one developed lesions resembling canine parvoviral enteritis.
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PMID:Sudden death in young dogs with myocarditis caused by parvovirus. 43 48

Myocarditis in 4- to 8-week-old pups from 10 litters was characterized by sudden death. Histopathologic findings included mononuclear cellular infiltration and interstitial fibrosis in the myocardium of the left ventricle. Basophilic intranuclear inclusion bodies were seen in myocardial cells in 4 of 18 pups necropsied, suggesting a viral origin of the disease. Other pathologic changes were variable, but all were attributable to cardiac failure. Of 8 surviving pups examined, 7 had evidence of cardiac failure, including pulmonary edema, cardiomegaly, and cardiac arrhythmias.
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PMID:Myocarditis of probable viral origin in pups of weaning age. 43 49

Experimental Lassa virus infections of squirrel monkeys, guinea-pigs, and the African multimammate rat, Mastomys natalensis, were studied virologically and pathologically. In the monkeys, early viral lymphoreticulotropism, hepatotropism, nephrotropism, and viraemia were noted. At the time of death, viral titres in nearly all target organs were associated with necrotic changes: splenic lymphoid necrosis, renal tubular necrosis, myocarditis, arteritis, and hepatocytic regeneration. In convalescent monkeys, organ titres diminished slowly, and viraemia persisted at 28 days. At this time, renal and splenic regeneration was occurring and a new lesion, choriomeningitis, was present.Guinea-pigs infected with Lassa virus developed respiratory insufficiency with pulmonary oedema, alveolar hyaline membranes, myocarditis, and focal calcification of myocardial fibres and hepatocytes. Dying animals contained Lassa virus in virtually every organ tested, whereas survivors at 56 days were free of virus and had high complement-fixing antibody titres.Infection of neonatal Mastomys did not cause any clinical disease or pathological lesions despite the presence of virus in the blood, lymph nodes, liver, spleen, lung, brain, urine, and throat secretions throughout the 74-day study. Infected adult Mastomys also remained normal but had virus in many organs. In one animal, virus persisted until the termination of the study at 103 days. Several animals developed a mild meningoencephalitis. The pattern of infection and virus shedding in M. natalensis is ideal for maintenance of the virus in nature; together with the epidemiological field data this emphasizes the incidental nature of the exposure and infection of man.
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PMID:Comparative pathology of Lassa virus infection in monkeys, guinea-pigs, and Mastomys natalensis. 82 25

Fifty-four children from the Jerusalem area were studied prospectively following scorpion envenoming. Their ages ranged from 11 months to 10 years. Severe symptoms (convulsions, brain oedema, shock, respiratory distress and myocarditis) were encountered in 19. Respiratory distress was the main feature in 17 of the children, in two cases owing to pulmonary oedema and in a third because of adult respiratory distress syndrome and myocarditis; mechanical ventilation was required in three cases. The severity of the symptoms and signs was not related to sex, age, weight, interval between scorpion sting and admission or to the type of offending scorpion; it was most likely dependent upon the susceptibility of the individual and/or the dose of venom injected by the scorpion. Intravenous antivenom quickly reversed the symptoms, and no side-effects were seen in the patients studied. The two patients who died had not received the antivenom intravenously. We recommend that specific antivenom should be given intravenously in all children who show significant symptoms. Furthermore, a longer period of observation is necessary following scorpion sting in this age group.
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PMID:Scorpion sting in children in the Jerusalem area: a review of 54 cases. 171 20

Cocaine-related cardiovascular events escalated during the 1980s as cocaine became purer, cheaper, and easier to obtain. Cocaine abuse is a risk factor for myocardial ischemia and/or infarction, cardiac arrhythmias, pulmonary edema, ruptured aortic aneurysm, cerebral infarction, infective endocarditis, vascular thrombosis, myocarditis, and dilated cardiomyopathy. As medical and social complications of cocaine have become evident, and with the growing negative image of cocaine, the number of first-time users has begun to decline. Cocaine abuse is seen on all levels of our society and has emerged as an issue of significant medical and public health importance. All routes and forms of cocaine abuse are potentially cardiotoxic and can be lethal. Fatal cardiac complications can occur in a first-time user. All physicians should be alert for cocaine abuse when confronted with unexplained cardiac symptoms. Cocaine is the newest and sometimes unrecognized risk factor for cardiovascular disease in young individuals otherwise free of cardiovascular risk factors.
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PMID:Cocaine: the newest risk factor for cardiovascular disease. 181 Jun 80

To assess whether steroid therapy influenced the clinical course of myocarditis in a pediatric population, findings in 13 consecutive infants and children (8 female, 5 male) with biopsy-proved myocarditis were reviewed. The mean age was 5.7 +/- 4.8 years (range 1.1 to 14.8). Congestive heart failure was present in all as were ST-T wave changes, cardiomegaly and pulmonary edema on chest roentgenogram. Echocardiography demonstrated pericardial effusion in five patients and mitral regurgitation in eight. Mean left ventricular ejection fraction was 34 +/- 12%. Prednisone was administered to all patients; one patient also received azathioprine. There was one death. All survivors showed clinical improvement with normalization of ECG changes, heart size and systolic function. No significant side effects occurred. Repeat myocardial biopsy in eight patients demonstrated improvement in all eight and elimination of the inflammatory infiltrate in six. Immunosuppressive therapy in this pediatric population appeared useful in improving the clinical course and cardiac function in acute myocarditis with no adverse side effects.
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PMID:Immunosuppressive therapy in the management of acute myocarditis in children: a clinical trial. 199 4

The records of 188 consecutive patients admitted for acute opiate intoxication were analyzed retrospectively to evaluate the morbidity and mortality of opiates. The most frequently used of these drugs were heroin (127 cases) and methadone (41 cases). In 79 cases the opiate was associated with another psychodepressant, usually benzodiazepines, alcohol or barbiturates. Forty-seven percent of the patients were admitted in deep coma, with respiratory arrest in almost every case. The complications observed in 49 patients were: aspiration of gastric contents (n = 24), rhabdomyolysis (n = 22), often associated with myocarditis (n = 13), pulmonary edema (n = 16), convulsions (n = 10), left ventricular dysfunction (n = 5) and lesions of the peripheral nervous system (n = 4). All patients survived, except one who died of cardiac arrest before admission. It is concluded that acute opiate intoxication treated in hospital has an excellent prognosis for life provided no cardiac arrest occurs prior to admission. One quarter of the patients require prolonged stay in an intensive care unit because of complications. The other patients, even when deeply comatose on admission, spend less than 1 day in hospital owing to the specific antagonist available.
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PMID:[Hospital morbidity and mortality of acute opiate intoxication]. 214 23

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state.
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PMID:Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted. 266 11


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