Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As more effective therapies have produced longer survival times for human immunodeficiency virus (HIV)-infected patients, new complications of late-stage HIV infection including HIV-related heart disease have emerged. Almost any agent that can cause disseminated infection in patients with acquired immunodeficiency syndrome (AIDS) may involve myocardium, but clinical evidence of cardiac disease is usually overshadowed by manifestations in other organs, primarily the brain and lungs. Cardiac abnormalities are found at autopsy in two-thirds of patients with AIDS, and more than 150 reports of cardiac complications have been published. Cardiac involvement in HIV disease includes pericardial effusion, myocarditis, dilated cardiomyopathy, and/or endocardial involvement at any stage of the disease. This review deals with all the cardiac manifestations of AIDS and serves to highlight two problems and one indication. First of all, there are very few clinical studies. Current knowledge is based almost exclusively on echocardiography and autopsy studies. Observational or clinical trials would be useful. Second, there exists very poor information on the impact of treatment; and epidemiologic and clinicopathologic studies are mandatory for obtaining detailed data concerning the mechanisms of myocardial damage in AIDS. Finally, because cardiac complications are often clinically inapparent or subtle in the initial stages, periodic screening of HIV-positive patients by electrocardiogram and echocardiogram is probably indicated. In addition, AIDS may also provide the opportunity to gain insights into the pathogenesis of little understood cardiac diseases such as lymphocytic myocarditis and dilated cardiomyopathy.
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PMID:Cardiac involvement in acquired immunodeficiency syndrome--a review to push action. The Committee for the Study of Cardiac Involvement in AIDS. 966 54

The first case of Q fever endocarditis that has been diagnosed in Mexico is presented. A 10-year-old girl with discrete subaortic stenosis (SAS) and patent ductus arteriosus (PDA) was seen in December of 1996 with fever, hepatomegaly and splenomegaly. She presented also anemia, leukopenia, hypergammaglobulinemia, positive rheumatoid factor, cryoglobulinemia, antinuclear and anticytoplasmic antibodies (anti-RNA-proteins and anti-DNA). An aortic valve vegetation was seen by echocardiogram. Blood-cultures were negative. Antibody test for Coxiella burnetii was positive. Treatment with doxicyclin was initiated as soon the diagnosis was done. PDA was closed, SAS was liberated and two aortic vegetations were resected. Endocarditis in Q fever occurs when there is predisposing heart disease and/or immunodeficiency. Effective therapy has not yet been established. The diagnosis of Q fever endocarditis is difficult; it should be considered, in case of clinical suspicion of endocarditis with negative blood-cultures.
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PMID:[Coxiella burnetii endocarditis. A report of the first case diagnosed in Mexico]. 981 Mar 69

The DiGeorge syndrome (DGS) is a developmental defect of the third and fourth pharyngeal pouches, which is associated with congenital heart defects, hypoparathyroidism, cell-mediated immunodeficiency, velo-pharyngeal insufficiency and craniofacial dysmorphism. The aetiological factor in a great majority of DGS cases is monosomy for the chromosomal region 22q11. To analyze DGS at the molecular level, a new molecular probe (DGCR680) encompassing the ADU balanced translocation breakpoint was prepared. When 13 Korean patients with DGS-type congenital heart disease were analyzed with this probe, 9 turned out to have a deletion at this locus, and all of them except one exhibited a typical facial dysmorphism associated DGS. Though only 9 independent patients were detected to have a deletion at the locus using the commercial probe N25 (D22S75), which maps at about 160 kb from the ADU breakpoint to the telomeric end, results from fluorescence in situ hybridization revealed a deletion in all cases tested at this locus. Two patients who had a deletion at the locus D22S75 but not at DGCR680 did not exhibit any DGS-type facial abnormalities. This result implies that the 680 bp probe covering the ADU translocation breakpoint might be a candidate for a molecular marker that can distinguish a specific phenotype, such as facial features associated with the DiGeorge syndrome. This study also suggested that systematic approaches with several small DNA probes along the DGCR could help to dissect the complex phenotypes associated with the DiGeorge syndrome, such as cardiac defects, abnormal faces, thymic hypoplasia, cleft palate, and hypocalcemia, etc.
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PMID:Molecular genetic analysis of the DiGeorge syndrome among Korean patients with congenital heart disease. 1010 75

Deaths from infectious diseases have declined markedly in the United States during the 20th century. This decline contributed to a sharp drop in infant and child mortality and to the 29.2-year increase in life expectancy. In 1900, 30.4% of all deaths occurred among children aged <5 years; in 1997, that percentage was only 1.4%. In 1900, the three leading causes of death were pneumonia, tuberculosis (TB), and diarrhea and enteritis, which (together with diphtheria) caused one third of all deaths. Of these deaths, 40% were among children aged <5 years. In 1997, heart disease and cancers accounted for 54.7% of all deaths, with 4.5% attributable to pneumonia, influenza, and human immunodeficiency virus (HIV) infection. Despite this overall progress, one of the most devastating epidemics in human history occurred during the 20th century: the 1918 influenza pandemic that resulted in 20 million deaths, including 500,000 in the United States, in <1 year-more than have died in as short a time during any war or famine in the world. HIV infection, first recognized in 1981, has caused a pandemic that is still in progress, affecting 33 million people and causing an estimated 13.9 million deaths. These episodes illustrate the volatility of infectious disease death rates and the unpredictability of disease emergence.
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PMID:Control of infectious diseases. 1045 35

The authors report a case and treatment of multiple brain abscesses located in the cerebrum and cerebellum combined with subdural empyema. In conjunction with the case report, the authors review the literature on the pathogenesis of brain abscesses and discuss therapeutic strategies concerning the topic. In the case presented, the primary infection persisted in the lung causing subclinical bronchitis. The hemoculture showed evidence of Streptococcus mitis infection. Although the etiological role of this bacterium in meningitis is known, it rarely causes bacterial meningitis without underlying predisposing factors. In their case, the patient was free of the most common predisposing factors such as congenital heart disease or immunodeficiency. Following the 2 month period of latency, a rapid onset of the symptoms of intracranial inflammation could be observed: fever, headache, meningeal symptoms, focal neurological symptoms and coma. They were not able to identify any bacteria in the cerebrospinal fluid; the Streptocossus mitis could be cultivated only from the haemoculture. The cytological analysis of the cerebrospinal fluid showed typical signs of bacterial infection and the cranial Computed Tomography revealed multiple cerebral abscesses. Neurosurgical intervention was not recommended because of the number, localization and size of the focal lesions. The therapy consisted of intravenous administration of 24 x 10(6) IU/die Penicillin and 4 g/die ceftriaxon. For supportive therapy, Mannitol B, 3 mg/die clonazepam and 300 mg/die phenytoin were administered. Corticosteroids were not used during the course of therapy. Two years later the 55 year old female is symptom free and doing well.
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PMID:[Non-invasive management of multiple brain abscesses. Case report and review of the literature]. 1053 93

RSV is the most important respiratory pathogen in infants and young children. About 1% of primary RSV infections result in hospitalization. The virus is spread by large droplets of secretions or contact with contaminated secretions. Infants infected with RSV may demonstrate poor feeding, rhinorrhea, apnea, lethargy, wheezing, and respiratory distress. Diagnosis may be made by clinical signs and symptoms (especially those observed during epidemics), by chest radiographs showing hyperinflation, or by rapid antigen detection with immunofluorescence of nasopharyngeal aspirates. Risk factors for severe disease accompanied by complications include chronic heart disease, chronic lung disease, immunodeficiency, HIV, and prematurity. Immunity is incomplete and of short duration, and reinfection is common. Treatment remains supportive and consists of oxygen administration, hydration, and diligent monitoring. Use of corticosteroids, bronchodilators, antibiotics, and ribavirin is controversial and is dependent largely on physician preference. Use of ribavirin should be reserved for patients who have severe underlying conditions associated with increased mortality rates. Intravenous RSV Ig has been replaced by palivizumab, which is generally recommended for infants at high risk for severe RSV, including those with a history of prematurity and those with chronic lung disease.
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PMID:RSV infection in infants and young children. What's new in diagnosis, treatment, and prevention? 1060 68

The time course of intensive care for severe respiratory syncytial virus (RSV) lower respiratory tract illness may be predicted by the severity of gas exchange during the first 48 h of mechanical ventilation. To test this hypothesis, two studies were undertaken in RSV-positive mechanically ventilated patients who did not have chronic lung disease, congenital heart disease or immunodeficiency. First, a retrospective criteria-generating review of 45 infants was carried out. In these infants, more severe lower airway disease, as demonstrated by four-quadrant consolidation on chest X-ray, was associated with 'best' alveolar arterial oxygen gradients (AaDO2, torr) and mean airway pressure (MAP, cm H2O) values as follows: first 24h, AaDO2 > 400 and MAP > 10 (positive and negative predictive values 100% and 97%, respectively); second 24 h, AaDO2 > or = 300 and MAP > 10 (positive and negative predictive values 91% and 100%, respectively). The second study, a prospective, hypothesis-testing, analysis of length-of-stay in 44 infants stratified according to the above AaDO2 and MAP criteria demonstrated that the duration of intensive care was longer in the severe group: median (interquartile range in days) 17 (15-39) vs 7 (4-8) (p < 0.01). We suggest that, in mechanically ventilated infants with RSV, the time course of intensive care is predictable based on early clinical features and respiratory parameters. Therefore reports on the effectiveness of special therapies using intensive care stay as a measure of outcome should be interpreted with respect to these observations before drawing conclusions about efficacy.
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PMID:Time course of severe respiratory syncytial virus infection in mechanically ventilated infants. 1097 23

Respiratory syncytial virus (RSV) infection, which primarily manifests as bronchiolitis or pneumonia, is the leading cause of lower respiratory tract infection in infants and young children. It is associated with more than 100,000 pediatric hospitalizations each year in the United States. Infants who were premature; have chronic lung disease, congenital heart disease, or immunodeficiency disorders; or have underlying metabolic or neuromuscular disorders are at increased risk for especially severe RSV disease. Treatment of children hospitalized with RSV disease is primarily supportive, with administration of supplemental oxygen and fluid replacement therapy. Bronchodilators may benefit at least a subset of such patients. Antiviral therapy with aerosolized ribavirin is available for high-risk, severely ill patients. Handwashing, cleaning of environmental surfaces, and cohorting in hospital settings may decrease RSV transmission. In children born premature and younger than 1 year of age, and in patients with bronchopulmonary dysplasia younger than 2 years of age, passive protection against severe RSV disease may be achieved through monthly injections of anti-RSV antibody (palivizumab) during winter months. No vaccine is available to provide active immunity against RSV, but live attenuated and subunit cloned surface protein vaccines are in development.
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PMID:Respiratory Syncytial Virus: Update on Infection, Treatment, and Prevention. 1138 54

In recent years, a spectrum of metabolic and morphologic alterations has emerged among patients infected with human immunodeficiency virus (HIV) receiving antiretroviral treatment. Changes observed include insulin resistance, dyslipidemia, abdominal and dorsocervical fat accumulation, and fat depletion in the extremities and in the face. The health consequences of these changes are not well understood but may include increased risk for diabetes, heart disease, and stroke. Therefore, clinicians that treat patients with HIV need current, practical information on management strategies and interventions for patients with manifestations of HIV-associated lipodystrophy. Literature is reviewed on the health consequences of insulin resistance, dyslipidemia, and alterations in body fat distribution in non-HIV populations to gain perspective on how such abnormalities might affect HIV-infected patients. We also suggest treatments and strategies to manage metabolic and morphologic changes in patients with HIV.
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PMID:Clinical evaluation and management of metabolic and morphologic abnormalities associated with human immunodeficiency virus. 1174 Jul 15

Reviews and studies published before the introduction of highly active antiretroviral therapy (HAART) regimens have tracked the incidence and course of human immunodeficiency virus (HIV) infection in relation to cardiac illness in both children and adults. HAART regimens have significantly modified the course of HIV disease, with longer survival rates and improvement of life quality in HIV+ subjects expected. However, early data raised concerns about HAART's being associated with an increase in both peripheral and coronary arterial diseases. A variety of potential etiologies have been postulated in HIV-related heart disease, including myocardial infection with HIV itself, opportunistic infections, viral infections, autoimmune response to viral infection, drug-related cardiotoxicity, nutritional deficiencies, and prolonged immunosuppression. In this review article we discuss HIV-associated cardiovascular complications, focusing on pathogenetic mechanisms that may play a role in diagnosis, management, and therapy of these complications.
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PMID:Pathogenesis of HIV-associated cardiomyopathy. 1176 96


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