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)

We describe a 44-year-old male patient with human immunodeficiency virus (HIV) infection and pulmonary arterial hypertension who was treated with several protease inhibitors and with sildenafil. In order to guide treatment with sildenafil, the pharmacokinetics and dynamics of sildenafil were monitored at various time points. In comparison with healthy subjects, the maximal concentration in plasma (Cmax), area under the curve (AUC), and elimination half-life of sildenafil were approximately doubled in the patient. After increasing the sildenafil dose to ensure therapeutic drug levels over 24 hours, the pulmonary arterial hypertension and physical performance of the patient improved significantly. We conclude that the elimination of sildenafil is impaired in patients treated with protease inhibitors, but to a lesser extent than predicted from single-dose studies reported in the literature. Patients treated concomitantly with protease inhibitors and sildenafil need close monitoring of plasma levels, pharmacodynamics, and toxicity of sildenafil in order to be treated optimally.
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PMID:Pharmacokinetics and pharmacodynamics of sildenafil in a patient treated with human immunodeficiency virus protease inhibitors. 1822 77

As survival has improved in the highly active antiretroviral therapy (HAART) era, the prevalence of kidney disease is increasing in the aging HIV-infected population. Since HIV-specific kidney disease, particularly human immunodeficiency virus-associated nephropathy (HIVAN), incidence has remained stable if not declining in the HAART era, the rising rates reflect to a great extent increases in kidney disease seen in the general population due to hypertension and diabetes. In addition, HIV-infected patients are exposed to toxicities of antiretrovirals and other drugs. There is also a disproportionate prevalence of HIV in black Americans, who have a higher risk of kidney disease and the associated risk factors. Because of the high rates of kidney disease, screening for kidney dysfunction is recommended at the time of HIV diagnosis. Because kidney disease is usually asymptomatic, effective screening will include assessment of risk factors and markers of kidney disease, specifically estimations of glomerular filtration rate using serum creatinine and quantification of urine protein. Upon identification of renal dysfunction, the differential diagnosis may be broad, including etiologies common in the general population as well as HIV-specific causes. Although clinical diagnoses can be made, a kidney biopsy is often necessary. Regardless of the cause of kidney disease, early identification, accurate diagnosis and consequent appropriate management are likely to result in improved outcomes. Success in confronting this growing problem can only be achieved with better understanding of kidney diseases affecting the HIV population.
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PMID:Kidney disease in the HIV-infected patient. 1824 Aug 91

The infection with the human immunodeficiency virus (HIV) is not only associated with a dysfunction of the immune system. Other organs are often affected in patients with HIV-infection, as well. In particular, an increased cardiovascular risk profile leads to an increasing rate of morbidity and mortality due to cardiac disorders, including heart failure and HIV-associated cardiomyopathy in this patient population. However, not only classic risk factors such as smoking, hypertension or dysregulation of lipid and glucose metabolisms are the reasons of HIV-associated myocardial dysfunction. Especially these subjects are also prone to opportunistic infections, side effects of antiretroviral therapy or the HI-virus itself.
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PMID:[HIV, AIDS and the cardiovascular risk]. 1830 15

Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure (PAPm) superior than 25mmHg at rest or superior than 30mmHg with exercise. The classification of PH differentiates between "secondary" PH which results from a well-known disease, such as PH due to thromboembolic disease (obstructive PH), left cardiac failure (passive PH), or chronic respiratory diseases (hypoxic PH), and pulmonary arterial hypertension (PAH). PAH is a rare disease characterized by a progressive increase of pulmonary vascular resistance leading to right ventricular failure. PAH is classified as idiopathic, familial, or associated with various conditions (connective tissue diseases, congenital heart diseases with systemic-to-pulmonary shunts, portal hypertension, infection with the human immunodeficiency virus, or appetite-suppressant drugs). Transthoracic Doppler echocardiography is the investigation of choice for non invasive detection of PAH but right-heart catheterization is necessary to confirm the diagnosis of PAH and determine its mechanism. Pulmonary function tests and chest CT scan may detect an underlying chronic pulmonary disease (hypoxic PH). Lung perfusion scan and contrast-enhanced chest spiral CT scan can lead to the diagnosis of thromboembolic PH, which is to be confirmed by pulmonary angiography. Assessment of the severity of PH is based on clinical parameters (NYHA, right heart failure), functional tests (six-minute walk test), echocardiography and hemodynamics. Characterization of PH is essential in the management of PH because it determines the appropriate treatment: an etiological treatment in passive, obstructive or hypoxemic PH, or vasodilatator and antiproliferative therapies in PAH.
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PMID:[Investigation of pulmonary hypertension]. 1865 91

Extracellular nucleotides and nucleosides act as signaling molecules involved in a wide spectrum of biological effects. Their levels are controlled by a complex cell surface-located group of enzymes called ectonucleotidases. There are four major families of ectonucleotidases, nucleoside triphosphate diphosphohydrolases (NTPDases/CD39), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPs), alkaline phosphatases and ecto-5'-nucleotidase. In the last few years, substantial progress has been made toward the molecular identification of members of the ectonucleotidase families and their enzyme structures and functions. In this review, there is an emphasis on the involvement of NTPDase and 5'-nucleotidase activities in disease processes in several tissues and cell types. Brief background information is given about the general characteristics of these enzymes, followed by a discussion of their roles in thromboregulatory events in diabetes, hypertension, hypercholesterolemia and cancer, as well as in pathological conditions where platelets are less responsive, such as in chronic renal failure. In addition, immunomodulation and cell-cell interactions involving these enzymes are considered, as well as ATP and ADP hydrolysis under different clinical conditions related with alterations in the immune system, such as acute lymphoblastic leukemia (ALL), B-chronic lymphocytic leukemia (B-CLL) and infections associated with human immunodeficiency virus (HIV). Finally, changes in ATP, ADP and AMP hydrolysis induced by inborn errors of metabolism, seizures and epilepsy are discussed in order to highlight the importance of these enzymes in the control of neuronal activity in pathological conditions. Despite advances made toward understanding the molecular structure of ectonucleotidases, much more investigation will be necessary to entirely grasp their role in physiological and pathological conditions.
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PMID:NTPDase and 5'-nucleotidase activities in physiological and disease conditions: new perspectives for human health. 1880 12

As patients infected with human immunodeficiency virus (HIV) live longer while receiving antiretroviral therapy, kidney diseases have emerged as significant causes of morbidity and mortality. Black race, older age, hypertension, diabetes, low CD4(+) cell count, and high viral load remain important risk factors for kidney disease in this population. Chronic kidney disease should be diagnosed in its early stages through routine screening and careful attention to changes in glomerular filtration rate or creatinine clearance. Hypertension and diabetes must be aggressively treated. Antiretroviral regimens themselves have been implicated in acute or chronic kidney disease. The risk of kidney disease associated with the widely used agent tenofovir continues to be studied, although its incidence in reported clinical trials and observational studies remains quite low. Future studies about the relationship between black race and kidney disease, as well as strategies for early detection and intervention of kidney disease, hold promise for meaningful reductions in morbidity and mortality associated with kidney disease.
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PMID:Kidney disease in patients with HIV infection and AIDS. 1894 27

With the introduction of combination antiretroviral therapy, there have been substantial declines in both morbidity and mortality associated with human immunodeficiency virus (HIV)-1 infection. However, data increasingly indicate that HIV-1-infected individuals are faced with accelerated rates of chronic diseases that afflict the general population such as diabetes mellitus, hypertension, and dyslipidemia, as well as cardiovascular, liver, and kidney diseases. Furthermore, this population is exposed to a variety of adverse effects from long-term use of antiretroviral medications, which may cause clinically important renal toxicities. However, it often is challenging to distinguish antiretroviral-related renal toxicity from either direct effects of HIV-1 on the kidney or from a multitude of non-HIV-related kidney diseases. A timely and coordinated effort by the HIV primary provider and a nephrologist is likely to facilitate the evaluation of HIV-1-infected patients with new kidney problems.
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PMID:Antiretroviral nephrotoxicities. 1901 27

A 97-year-old lady was hospitalized for left leg cellulitis. Comorbidity included hypertension and congestive heart failure. While in hospital, she developed a painless vesicular rash localized to the territory of the left trigeminal nerve (third branch), which evolved to pustules and crusts (Figure 1). A chickenpox-like disseminated eruption of vesicles followed within 4 days, with the same evolution pattern (Figure 2).The diagnosis of disseminated zoster was suspected. A PCR analysis confirmed the presence of varicella-zoster-virus (VZV) in an abdominal vesicle. The patient was treated with oral valacyclovir for 7 days. Clinical examination, laboratory tests (including HIV serology), and a chest radiograph revealed no evidence of underlying immunodeficiency or malignancy.
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PMID:Disseminated zoster in an elderly patient. 1916 30

The objective of this study was to determine the effects of highly active antiretroviral therapy (HAART) drugs on pulmonary endothelial function. Porcine pulmonary arteries or human pulmonary arterial endothelial cells (HPAECs) were incubated with eight HAART drugs [ritonavir, indinavir, lopinavir, zidovudine (AZT), abacavir, stavudine, didanosine (ddI), and lamivudine] individually or in combination [three HAART drugs (3-plex; indinavir, stavudine, and ddI)] at their clinical plasma concentrations for 24 hours. Endothelium-dependent vasorelaxation in response to bradykinin was reduced significantly by the ritonavir in a concentration-dependent manner. Five other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly also impaired endothelium-dependent vasorelaxation in response to bradykinin. Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs. Furthermore, both ritonavir and AZT substantially activated ERK2 in HPAECs. Additionally, the antioxidants ginsenoside Rb1 and ginkgolide A effectively reversed HAART drug-induced vasomotor dysfunction and eNOS down-regulation. Inhibition of ERK1/2 also partially blocked ritonavir- and AZT-induced down-regulation of eNOS and vasomotor dysfunction. Thus, HAART drugs significantly impair endothelial functions of porcine pulmonary arteries and HPAECs, which may be mediated by eNOS down-regulation, oxidative stress, and ERK1/2 activation. These findings suggest that HAART drugs may contribute to the high incidence of pulmonary artery hypertension in human immunodeficiency virus-infected patients.
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PMID:Roles and mechanisms of human immunodeficiency virus protease inhibitor ritonavir and other anti-human immunodeficiency virus drugs in endothelial dysfunction of porcine pulmonary arteries and human pulmonary artery endothelial cells. 1921 43

Left ventricular hypertrophy (LVH) is an independent predictor of major cardiovascular events. Cardiovascular risk is increased among human immunodeficiency virus (HIV)-infected patients. To assess LV mass/hypertrophy in HIV infection, 654 women enrolled in the Women's Interagency HIV Study underwent transthoracic echocardiography. There were 454 HIV-infected and 200 uninfected women, mean age 40.8 +/- 9.3 years. LV mass/height(2.7) was similar between the HIV-infected and the HIV-uninfected groups (41.4 +/- 11.1 vs. 39.9 +/- 10.3 g/h(2.7); p = 0.37). The prevalence of LVH was similar between the two groups (LVH by LV mass/height(2.7) criteria 15.0% vs. 13.0%, p = 0.29). Relative wall thickness (RWT), defined as the ratio of LV wall thickness to cavity diameter, was also similar between the HIV-infected and HIV-uninfected groups (0.36 +/- 0.05 vs. 0.37 +/- 0.06, p = 0.16). On multiple linear regression analysis adjusting for age, W/H ratio, triceps skinfold thickness, systolic/diastolic BP, diabetes, hypertension and dyslipidemia; HIV status (b = 2.08, p = 0.02, CI 0.27-3.88); weight (b per kg = 0.15, p < 0.01, CI 0.08-0.22); and smoking duration (b per one-year increase = 0.08, p = 0.03, CI 0.01-0.16) were independent correlates of LV mass/height(2.7) (Model R(2) = 0.20, p < 0.001). Weight (aOR = 1.04, CI 1.01-1.06) and smoking duration (aOR = 1.03, CI 1.01-1.06) were independent correlates of LVH. Being HIV negative, increased age, increased triceps skinfold thickness, and higher W/H ratio were independent correlates of higher RWT. Among HIV-infected women, higher LV mass was not associated with a history of AIDS-defining illness, nadir CD4(+) count <200 cells/microl, or with the duration of highly active antiretroviral therapy (HAART). Women taking NRTIs had higher LV mass. Higher RWT was associated with current CD4(+) count. In conclusion, HIV infection is associated with greater LV mass but not with a higher prevalence of LVH. Among HIV-infected women, RWT, but not LV mass, is associated with the degree of immunosuppression.
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PMID:The association of HIV infection with left ventricular mass/hypertrophy. 1939 99


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