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

Respiratory syncytial virus (RSV) infection is the most frequent reason for hospitalization of infants in developed countries. Premature birth without or, especially, with chronic lung disease of prematurity, congenital heart disease, and T-cell immunodeficiency are conditions that predispose to more severe forms of RSV infection. Incomplete development of the airway, damage to the airway, and airway hyperreactivity underlie the increased morbidity of RSV infection in prematurely born infants. Pulmonary hypertension and cyanosis are associated with worse outcomes in infants with congenital heart disease, and prolonged viral replication accounts for more severe illness in immunocompromised individuals.
...
PMID:Review of epidemiology and clinical risk factors for severe respiratory syncytial virus (RSV) infection. 1461 9

As antiretroviral therapy has improved life expectancy in human immunodeficiency virus (HIV) infection, the life-limiting complication of HIV-related pulmonary hypertension has come into focus. Inhalation of the stable prostacyclin analogue iloprost is an effective treatment for various forms of precapillary pulmonary hypertension. The main objective of the present study was to evaluate the safety and efficacy of inhaled iloprost in HIV-related pulmonary hypertension. In eight patients with severe pulmonary hypertension related to HIV infection, right heart and femoral artery catheterisation were performed. The acute effect of oxygen, inhaled nitric oxide and aerosolised iloprost was investigated. Four patients underwent long-term treatment with inhaled iloprost. The rank order of pulmonary vasodilatory potency was iloprost>NO>O2, with a maximum reduction (mean +/- SEM) in pulmonary vascular resistance of 30.6 +/- 3.1% (p < 0.001), 5.9 +/- 3.9% and -0.6 +/- 3.9%, respectively. Concomitantly, inhaled iloprost significantly increased the cardiac index and central venous oxygen saturation. Chronic treatment with inhaled iloprost tended to improve the 6 min walking distance and decreased pulmonary vascular resistance in all patients (although not significantly). No serious adverse events and no major interactions with the ongoing antiretroviral therapy were noted. In conclusion, inhaled iloprost is a potent pulmonary vasodilator in human immune deficiency virus-related pulmonary hypertension. Future studies are warranted to confirm the encouraging long-term beneficial results observed in the present limited number of patients.
...
PMID:Inhaled iloprost is a potent acute pulmonary vasodilator in HIV-related severe pulmonary hypertension. 1497 11

The pathogenesis of preeclampsia stems from aberrant changes at the placental interface. The trophoblastic endovascular invasion of tonic spiral arteries that converts them to passive conduits falters. Uteroplacental insufficiency and fetoplacental hypoxemia result. Secondary maternal oxidative stress and an excessive inflammatory response to pregnancy generate the clinical syndrome of preeclampsia. Current treatment focuses on preventing seizures, controlling hypertension, preserving renal function and delivering the baby. We propose that the pathophysiological changes induced by preeclampsia in the placenta parallel those caused by persistent hypoxemia in the lungs at high altitude or with chronic obstructive pulmonary disease. Unrelenting pulmonary hypoxic vasoconstriction induces pulmonary hypertension and cor pulmonale. Inhalation of nitric oxide and phosphodiesterase-5 inhibitors opposes pulmonary hypoxic vasoconstriction, alleviates pulmonary hypertension and improves systemic oxygenation. Notably nitric oxide donor therapy also counters hypoxemic fetoplacental vasoconstriction, a biological response analogous to pulmonary hypoxic vasoconstriction. Fetal oxygenation and nutrition improve. Placental upstream resistance to umbilical arterial blood flow decreases. Fetal right ventricular impedance falls. Heart failure (cor placentale) is avoided. Emergency preterm delivery can be postponed. Other than low dose aspirin and antioxidants vitamins C and E no available therapy specifically targets the underlying disease profile. We hypothesize that, like nitric oxide donation, pharmacological inhibition of placental phosphodiesterase-5 will also protect the fetus but for a longer time. Biological availability of guanosine 3'5'-cyclic monophosphate is boosted due to slowed hydrolysis. Adenosine 3'5'-cyclic monphosphate levels increase in parallel. Cyclic nucleotide accumulation dilates intact tonic spiral arteries and counters hypoxemic fetoplacental vasoconstriction. Intervillous and intravillous perfusion pick up. Maternal to fetal placental circulatory matching improves. Enhanced placental oxygen uptake alleviates hypoxemic fetal stress. Appropriate fetal nutrition resumes. Cor placentale and severe intrauterine growth restriction are averted. Increased maternal cyclic nucleotide concentrations promote systemic vasodilatation so that blood pressures fall. Preemption of oxidative stress initiated by "consumptive" oxidation of nitric oxide stabilizes the vascular endothelium and corrects coagulopathy. Anti-inflammatory and immunosuppressant adenosine 3'5'-cyclic monphosphate offsets the extreme gestational inflammatory response. Cellular injury and multi-organ damage are prevented. One tablet a day of the new long acting phosphodiesterase-5 inhibitor, tadalafil (half life of 17.5 h) theoretically should allow a preterm pregnancy affected by preeclampsia to continue safely. Selective monitoring of vital organ functions guards against life-threatening maternal complications. Regular biophysical profiling warns the obstetrician of impending fetal compromise. Fetal growth and vital organ maturation can continue. As a result workloads imposed upon neonatal intensivists will lighten. Parental anxiety and concern will be allayed. The cost of treating preeclamptic mothers and their extremely low birth weight infants will decrease. Money saved by midwifery services in poorer states can be used to pay for better prenatal care. Severe preeclampsia/eclampsia will be less common. Maternal and perinatal morbidity and mortality will be reduced. Because the human immunodeficiency virus often infects individuals at a workforce eligible age, the global acquired immunodeficiency syndrome pandemic has already brought many nations to the brink of economic ruin. Potentially productive lives saved for the future will help restore them fiscally.
...
PMID:Hypothesis: selective phosphodiesterase-5 inhibition improves outcome in preeclampsia. 1550 76

Cardiovascular manifestations in patients infected with human immunodeficiency virus (HIV) have been altered by the introduction of highly active antiretroviral therapy regimens that allow more effective prophylactic treatment and an increased time of survival. Because of this, noninfectious cardiac conditions associated with HIV disease are being recognized with increasing frequency in these patients. Cardiac involvement in HIV-infected patients varies from clinically silent to overtly symptomatic disease. By some estimates a direct cardiac cause of mortality is between 1% and 6% of all cases. Pericardial effusion, pericarditis, myocarditis, cardiomyopathy, endocarditis, and pulmonary hypertension are well-recognized cardiac illnesses associated with HIV infection. Echocardiography has been crucial in evaluating HIV-infected patients to assess the extent of cardiac involvement. This case report illustrates atypical echocardiographic manifestations of endocarditis and paravalvular abscess in an immunocompromised patient.
...
PMID:Atypical echocardiographic findings of endocarditis in an immunocompromised patient. 1554 72

Recent advances in the knowledge of human immunodeficiency virus (HIV) replication and transmission as well as the emergence of effective antiretroviral therapies are leading to longer survival times for HIV-infected individuals. As a result, organ related manifestations of late stage HIV infection, including HIV-related heart diseases have emerged. It is now clear that cardiac involvement in HIV seropositive patients is relatively common and is associated with increased morbidity and mortality. Cardiac involvement in HIV infection is multifactorial. The epidemiology has changed dramatically since the introduction of highly active antiretroviral therapy (HAART), but studies carried out before the introduction of HAART remain relevant because of limited access to this treatment in many areas of the world. A variety of cardiac lesions have been reported in HIV infection and AIDS, including pericardial disease with effusion and tamponade, nonspecific or infectious myocarditis, dilated cardiomyopathy with global left ventricular dysfunction, endocardial valvular disease due to marantic or infective endocarditis, arrhythmias, pulmonary hypertension and neoplastic invasion. In the post HAART-era, coronary artery disease and dyslipidaemia, drug related cardiotoxicity and cardiac autonomic dysfunction are becoming increasingly prevalent. In this review, we highlight the importance of cardiac complications in HIV disease and discuss measures that can be taken to improve survival.
...
PMID:Human immunodeficiency virus (HIV) related heart disease: a review. 1577 20

Pulmonary hypertension associated with human immunodeficiency virus (HIV) infection also involves injury to the lung endothelium. However, the pathogenesis of HIV-induced pulmonary hypertension is not known; we hypothesized that HIV or secreted viral proteins could play a role in vascular injury and the increased frequency of pulmonary hypertension observed in HIV-infected patients. Here, we report that exposure of HIV-1 gp120 proteins to primary human lung microvascular endothelial cells causes apoptosis, as assessed by TUNEL assay, Annexin-V staining, and DNA laddering. Using ribonuclease protection assay and Western blotting we find that gp120-induced apoptosis of lung endothelial cells involves a down-regulation in Bcl-xl mRNA and proteins. In addition, gp120 significantly increases secretion of the potent vasoconstrictor endothelin-1 by human lung endothelial cells. These data suggest that secreted HIV gp120 proteins induce lung endothelial cell injury and could contribute to the development of HIV-associated pulmonary hypertension.
...
PMID:Induction of apoptosis and endothelin-1 secretion in primary human lung endothelial cells by HIV-1 gp120 proteins. 1597 50

The bone morphogenetic protein receptor-2 (BMPR2) is a member of the transforming growth factor-beta receptor family and is expressed on the surface of several cell types including endothelial cells and macrophages. Recently, a cause for familial primary pulmonary hypertension (FPPH) has been identified as mutations in the gene encoding BMPR2. Three forms of pulmonary hypertension (PH) exist, including PPH, FPPH, and PH secondary to other etiologies (sporadic PH) such as drug abuse and human immunodeficiency virus (HIV) infection. It is interesting that these subtypes are histologically indistinguishable. The macrophage is a key target cell for HIV-1, significantly altering macrophage cell function upon infection. HIV-1 trans-activator of transcription (Tat), an immediate-early product of the HIV-1 lifecycle, plays an important role in mediating HIV-induced modulation of host cell function. Our laboratory has previously shown that Tat represses mannose receptor transcription in macrophages. In the current study, we examined activity from the BMPR2 promoter in the macrophage cell line U937 and potential regulation by Tat. Transfection of U937 cells with BMPR2 promoter-reporter constructs revealed dose-dependent repression of BMPR2 promoter activity in the presence of Tat. Experiments using truncations of the BMPR2 promoter localized Tat-mediated repression to the first 208 bases of the promoter. Decreased BMPR2 transcription resulted in altered downstream signaling. Similar to mothers against decapentaplegics (SMAD) phosphorylation and SMAD6 expression, in response to BMP2 treatment, were down-regulated after Tat treatment. Finally, HIV-1 infection and treatment with Tat protein of the U937 human monocytic cell line resulted in a decreased, endogenous BMPR2 transcript copy number.
...
PMID:HIV-1 TAT represses transcription of the bone morphogenic protein receptor-2 in U937 monocytic cells. 1628 33

The heart and great vessels are not the sites most frequently affected by opportunistic infections and neoplastic processes in patients with acquired immune deficiency syndrome (AIDS). However, cardiovascular complications occur in a significant number of such patients and are the immediate cause of death in some. The spectrum of cardiovascular complications of AIDS that may be depicted at imaging includes dilated cardiomyopathy, pericardial effusion, human immunodeficiency virus-associated pulmonary hypertension, endocarditis, thrombosis, embolism, vasculitis, coronary artery disease, aneurysm, and cardiac involvement in AIDS-related tumors. To aid accurate diagnosis and appropriate treatment planning, radiologists should be familiar with the imaging appearance of each of these complications.
...
PMID:Cardiovascular complications of human immunodeficiency virus infection. 1641 53

Pulmonary hypertension (PH), defined as a mean pulmonary arterial (PA) pressure of >25 mmHg at rest or >30 mmHg during exercise, is characterized by a progressive and sustained increase in pulmonary vascular resistance that eventually leads to right ventricular failure. Clinically, PH may result from a variety of underlying diseases (Table 1 and Refs. 50, 113, 124). Pulmonary arterial hypertension (PAH) may be familial (FPAH) or sporadic (idiopathic, IPAH), formerly known as primary pulmonary hypertension, i.e., for which there is no demonstrable cause. More often, PAH is due to a variety of identifiable diseases including scleroderma and other collagen disorders, liver disease, human immunodeficiency virus, and the intake of appetite-suppressant drugs such as phentermine and fenfluramine (72). Other, more common, causes of PAH include left ventricular failure (perhaps the most common cause), valvular lesions, chronic pulmonary diseases, sleep-disordered breathing, and prolonged residence at high altitude. This classification, now widely accepted, was first proposed at a meeting in Evian, France, in 1998, and modified in Venice, Italy, in 2003 (124).
...
PMID:Mediators and modulators of pulmonary arterial hypertension. 1669 50

Severe pulmonary hypertension (PH) mimicking idiopathic PH is an increasingly recognized complication of human immunodeficiency virus (HIV) infection. PH shares several histopathologic features with Kaposi's sarcoma (KS), the most common malignancy in AIDS patients, and molecular evidence of the vasculotropic Kaposi's sarcoma-associated herpesvirus or human herpesvirus 8 (HHV-8) has been found in the lung tissue of patients with the disease. Although the prevalence of HHV-8 infection is increased among HIV-infected patients, no clinical association between KS and PH has ever been reported. Herein, we described a 30-year-old HIV-infected female co-infected with HHV-8 who developed severe PH coincident with occult KS. The clinical presentation of KS was unusual and remained masqueraded for years as an indolent cervical lymphadenopathy, without the typical cutaneous lesions. This is the first ever-reported case of PH associated with KS. Although the co-occurrence of both diseases in this patient could have been just a coincidence, the observation may also indicate that a relationship between HHV-8 infection and HIV-associated PH exists. Coinfection with HHV-8 and occult lymphadenopatic KS should be considered in HIV-infected patients developing PH.
...
PMID:Occult lymphadenopathic Kaposi's sarcoma associated with severe pulmonary hypertension: A clinical hint about the potential role of HHV-8 in HIV-related pulmonary hypertension? 1688 48


<< Previous 1 2 3 4 5 6 7 8 Next >>