Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of right-sided endocarditis due to Salmonella typhi is described involving a native tricuspid valve in a child who was human immunodeficiency virus negative with no evidence of intravenous drug addiction. The patient had classic features of typhoid and tricuspid regurgitation without clinical evidence of bacterial endocarditis. Transthoracic echocardiography confirmed the tricuspid regurgitation. However, transesophageal echocardiography was necessary to demonstrate the vegetations affecting the tricuspid valve leaflets that made possible the diagnosis of endocarditis. The infection was cured with intravenous ceftriaxone and oral amoxicillin.
Pediatr Cardiol
PMID:Right-sided endocarditis due to Salmonella typhi. 932 94

We evaluated left ventricular function by echocardiography in a prospective study that included 98 consecutive human immunodeficiency virus (HIV)-infected patients and 40 HIV-seronegative normal controls. When compared with controls, HIV patients showed increased isovolumic relaxation time (101+/-18 ms versus 71+/-10 ms; p<0.0001) and left ventricular diastolic diameters (51+/-6 mm versus 47+/-3 mm; p<0.0005), and decreased fractional shortening (31+/-6% versus 37+/-2%; p<0.0001). Diastolic dysfunction was the most frequent finding (63% of the patients). We found depressed ejection fraction in 31 (32%) patients. Only 8 (8%) patients had symptomatic congestive heart failure. Left ventricular dysfunction was not attributable to intravenous drug abuse or to therapy. It was less severe in earlier stages of the infection (fractional shortening: acquired immunodeficiency syndrome=30%+/-6%, asymptomatic HIV-seropositives 34%+/-5%; p<0.005) and in HIV-2-infected patients. Patients with opportunistic infections (all aetiologies mixed) had more frequent congestive heart failure than those without infections (16% of the patients with versus 4% of the patients without infections; p<0.05). The fact that even asymptomatic HIV-seropositives had signs of left ventricular dysfunction (fractional shortening: asymptomatic HIV-seropositives=34%+/-5%; controls=37%+/-2%; p<0.05) favours the hypothesis of the HIV being one of the causes of these abnormalities.
Int J Cardiol 1998 Jan 05
PMID:Left ventricular dysfunction in human immunodeficiency virus (HIV)-infected patients. 948 43

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.
Clin Cardiol 1998 Jul
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.
Arch Inst Cardiol Mex
PMID:[Coxiella burnetii endocarditis. A report of the first case diagnosed in Mexico]. 981 Mar 69

Recent reports have suggested a possible association between HIV-1 infection and "idiopathic" pulmonary hypertension (PH), but the pathogenetic role of the viral agent has not been fully defined yet. We report the cases of two white males positive for human immunodeficiency virus type 1 (HIV-1) who presented with clinical and hemodynamic diagnosis of pulmonary hypertension. They were heterosexual, non-hemophiliac, heroin abusers with no signs of clinical AIDS. Neither one of the patients had opportunistic lung infections or any other cause of secondary pulmonary hypertension. In one case, peculiar clinical and electrocardiographic features of PH were associated with signs of thrombotic thrombocytopenic purpura (TTP). The association between PH and HIV-1 infection might be explained by a severe alteration of pulmonary endothelial cell homeostasis secondary to HIV-1 viral infection.
G Ital Cardiol 1998 Dec
PMID:Pulmonary hypertension associated with human immunodeficiency virus infection. Report of two cases and review of the literature. 988 95

Although supraventricular tachycardias and human immunodeficiency virus infections are common diseases by themselves, a combination is not so common. Such a patient was encountered recently and described in this case report. Because misdiagnosis of tachyarrhythmias is not uncommon and may lead to inappropriate therapy-frequently resulting in acute clinical deterioration or even death, a discussion of management of supraventricular tachyarrhythmias in general was included. The recent introduction of adenosine into clinical use provides an effective agent in, and revolutionizes, the management of patients with supraventricular tachyarrhythmias. Its application, both for diagnostic and for therapeutic purposes, was discussed in some details in this report.
J Cardiol 1999 Jan
PMID:Supraventricular tachycardia in a human immunodeficiency virus-infected man. 1002 58

Several case-reports and small series suggest a causal relationship between human immunodeficiency virus (HIV) infection and pulmonary hypertension. We report on a HIV seropositive man with a high and stable CD4 lymphocyte count (+/- 600/mm3) who developed severe pulmonary hypertension, not attributable to other known causes. This case report underscores the fact that the degree of immunosuppression secondary to the HIV-infection seems to be of little relevance in the pathophysiology of the syndrome. HIV-infected patients with dyspnoea, not related to pulmonary infection, with exercise intolerance, syncope or precordial pain should receive an electrocardiogram and echocardiographic assessment. The exact pathogenetic mechanism of this rapidly progressive disease and whether anti-viral therapy should be promoted is still under investigation.
Acta Cardiol 1998
PMID:Primary pulmonary hypertension in a patient with HIV infection. 1006 33

Human immunodeficiency virus (HIV, lentivirus) type-1 based vectors have a number of attractive features for gene therapy, including the ability to transduce non-dividing cells and long term transgene expression. We used a three-plasmid expression system to generate pseudotyped lentivirus-based vectors by transient transfection of human embryonic kidney 293T cells in the presence of sodium butyrate, which is known to activate the long terminal repeat-directed expression of HIV. Using this system we successfully generated versatile high titer lentivirus at titers of up to 2 x 10(8) transducing units/ml (TU/ml), and improved transduction efficiency in various cell types from seven to over twenty fold. We demonstrate its applicability of these vectors for the efficient transduction of non-dividing cells, including post mitotic beating rat cardiac myocytes and well-differentiated rat L6 myofibers. While both lentivirus-based and murine retrovirus-based vectors effectively transduced dividing cardiac fibroblasts and L6 muscle myoblasts in culture, lentivirus-based vectors also efficiently transduced cardiac myocytes and yielded titers of (6.3 +/- 1.2) x 10(5) TU/ml; however murine retrovirus-based vectors showed low transduction efficiency with titers reaching only (8.9 +/- 2.1) x 10(2) TU/ml. Furthermore, even 12 days after induction of differentiation of L6 myofibers, lentivirus-mediated transduction of beta-galactosidase (beta-Gal) at approximately 30-40% of the maximum expression levels achieved in replicating myoblasts. In contrast, the expression of beta-Gal following transduction of the myofibers by murine retrovirus-based vectors fell to less than 1% of an already reduced level of transduction in undifferentiated confluent myoblasts. These results demonstrate that lentivirus-based vectors can efficiently transduce both well-differentiated cardiac myocytes and differentiated myofibers. This appears to be an efficient method and provides a new tool for research and therapy for cardiovascular diseases.
J Mol Cell Cardiol 1999 Nov
PMID:A high-titer lentiviral production system mediates efficient transduction of differentiated cells including beating cardiac myocytes. 1059 Oct 30

Limited data are available on the electrocardiogram and ambulatory electrocardiogram recording (Holter) in children infected with the human immunodeficiency virus type 1 (HIV-1). The purpose of this study was to estimate the prevalence and cumulative incidence of rhythm and conduction abnormalities in HIV-1-infected children. Electrocardiograms and Holter monitoring studies were performed annually on 205 HIV-1-infected children enrolled after 28 days of life (group I), 93 HIV-1-infected infants enrolled during pregnancy or during the first 28 days of life (group IIa), and 463 HIV-1-uninfected infants enrolled during pregnancy or during the first 28 days of life (group IIb). The 5-year cumulative incidence in the group I children of second-degree atrioventricular block or supraventricular or ventricular tachycardia was 13.4%, and the 5-year incidence was higher for the older infected group I children (16.8% for children > or =4 years old at first study and 11.4% for children <4 years, p = 0.04). The mean corrected QT interval was also longer for the older infected group I children (p = 0.002) and prolonged in the HIV-1-infected compared to the HIV-1-uninfected group II children (p = 0.02). None of the children had atrial fibrillation or flutter. Arrhythmias are uncommon in children infected with HIV-1 and in children of HIV-1-infected mothers and the arrhythmias identified tend to be benign. Therefore, routine Holter monitoring does not appear to be indicated in asymptomatic children.
Pediatr Cardiol
PMID:Electrocardiography and 24-hour electrocardiographic ambulatory recording (Holter monitor) studies in children infected with human immunodeficiency virus type 1. The Pediatric Pulmonary and Cardiac Complications of Vertically Transmitted HIV-1 Infection Study Group. 1081 72

With the advent of more effective therapies for human immunodeficiency virus (HIV) infection, HIV-infected patients are living longer and cardiovascular disease is becoming more obvious in this population. Patients with HIV infection represent one of the most rapidly developing groups with cardiovascular disease globally. Cardiovascular disease complicating HIV infection is likely to contribute to burgeoning healthcare costs. Pericarditis, myocarditis, cardiomyopathy, atherosclerotic coronary vasculopathy, arterial aneurysms, pulmonary hypertension, and endocarditis occur with increased frequency in these patients. Pericardial tamponade, dilated cardiomyopathy, endocarditis, and vasculopathy can lead to fatal outcomes in this population. The advent of cardiomyopathy heralds a very poor prognosis in patients infected with HIV. Coronary vasculopathy without obvious risk factors can lead to myocardial ischemia in young patients infected with the virus. Moreover, the protease inhibitors used to treat HIV infection induce a syndrome of lipodystrophy and dyslipidemia that may be associated with accelerated atherosclerosis as well as insulin resistance. All these factors contribute to increased cardiovascular morbidity and mortality in the HIV-infected population. HIV infection, opportunistic infections, secreted viral proteins such as gp120 (envelope protein) or Tat (transactivator of viral transcription), and cytokines elaborated during the course of HIV infection of the immune system all contribute to pathogenesis of these disorders. Further basic and clinical studies are required to understand the pathogenesis of cardiovascular complications and develop appropriate management strategies for these patients.
Cardiol Rev
PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4


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