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)

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

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.
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PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4

Oxidative modification of DNA, proteins and lipids by reactive oxygen species (ROS) plays a role in aging and disease, including cardiovascular, neurodegenerative and inflammatory diseases and cancer. Extracts of fresh garlic that are aged over a prolonged period to produce aged garlic extract (AGE) contain antioxidant phytochemicals that prevent oxidant damage. These include unique water-soluble organosulfur compounds, lipid-soluble organosulfur components and flavonoids, notably allixin and selenium. Long-term extraction of garlic (up to 20 mo) ages the extract, creating antioxidant properties by modifying unstable molecules with antioxidant activity, such as allicin, and increasing stable and highly bioavailable water-soluble organosulfur compounds, such as S-allylcysteine and S-allylmercaptocysteine. AGE exerts antioxidant action by scavenging ROS, enhancing the cellular antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, and increasing glutathione in the cells. AGE inhibits lipid peroxidation, reducing ischemic/reperfusion damage and inhibiting oxidative modification of LDL, thus protecting endothelial cells from the injury by the oxidized molecules, which contributes to atherosclerosis. AGE inhibits the activation of the oxidant-induced transcription factor, nuclear factor (NF)-kappa B, which has clinical significance in human immunodeficiency virus gene expression and atherogenesis. AGE protects DNA against free radical--mediated damage and mutations, inhibits multistep carcinogenesis and defends against ionizing radiation and UV-induced damage, including protection against some forms of UV-induced immunosuppression. AGE may have a role in protecting against loss of brain function in aging and possess other antiaging effects, as suggested by its ability to increase cognitive functions, memory and longevity in a senescence-accelerated mouse model. AGE has been shown to protect against the cardiotoxic effects of doxorubicin, an antineoplastic agent used in cancer therapy and against liver toxicity caused by carbon tetrachloride (an industrial chemical) and acetaminophen, an analgesic. Substantial experimental evidence shows the ability of AGE to protect against oxidant-induced disease, acute damage from aging, radiation and chemical exposure, and long-term toxic damage. Although additional observations are warranted in humans, compelling evidence supports the beneficial health effects attributed to AGE, i.e., reducing the risk of cardiovascular disease, stroke, cancer and aging, including the oxidant-mediated brain cell damage that is implicated in Alzheimer's disease.
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PMID:Antioxidant health effects of aged garlic extract. 1123 7

Persons with human immunodeficiency virus (HIV) infection might be at risk for ischemic cardiovascular disease (CVD). We reviewed the records of 16 HIV-infected persons with proven CVD (8 cases of angina and 8 cases of myocardial infarctions). This represents 1.7% of HIV-infected persons seen at our institution from 1 April 1999 through 25 April 2000. In comparison with 32 HIV-infected age- and sex-matched controls, case patients had more risk factors for CVD (median number of risk factors for CVD, 3 versus 1; P<.001), lower nadir CD4+ lymphocyte counts (median, 101 cells/mm3 versus 278 cells/mm3; P=.02), and a longer duration of prior exposure to nucleoside analogs (median, 190 weeks versus 130 weeks; P=.02). There was no difference in the duration of exposure to protease inhibitors. Ischemic CVD occurs in HIV-infected persons and appears to be most closely associated with traditional risk factors for coronary artery disease (for example, hypertension and hypercholesterolemia). Lower CD4+ lymphocyte counts and duration of HIV infection might also be risk factors or markers for the development of ischemic CVD.
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PMID:Ischemic cardiovascular disease in persons with human immunodeficiency virus infection. 1217 41

Numerous studies have documented the presence of racial disparities among Americans in health outcomes with respect to cardiovascular disease, infant mortality, cancer, and kidney disease. With regard to kidney diseases, these disparities are more dramatic. African, Hispanic, and Native Americans have the highest risks of end-stage renal disease (ESRD). The incidence of ESRD is four times higher in African Americans than in whites. Diseases causing chronic kidney failure, such as diabetes mellitus, hypertension, systemic lupus erythematosus, and human immunodeficiency virus-associated nephropathy, are particularly prevalent among African-American patients. In addition to the higher prevalence, the morbidity associated with kidney complications of these diseases appears worse in African-American patients. African Americans also have worse outcomes and a relatively reduced access to kidney transplantation--the best therapy for ESRD. It is highly likely that social and environmental factors play a very significant role in the persistence of these disparities. A detailed understanding of these socioeconomic and environmental factors will be critical in formulating rational public health strategies to redress these disparities. This paper reviews the social, economic and environmental factors that impact on the incidence of ESRD in minority groups.
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PMID:Race and kidney disease: role of social and environmental factors. 1215 10

Priority health-risk behaviors, which contribute to the leading causes of mortality and morbidity among youth and adults, often are established during youth, extend into adulthood, are interrelated, and are preventable. This report covers data during February-December 2001. The Youth Risk Behavior Surveillance System (YRBSS) monitors six categories of priority health-risk behaviors among youth and young adults; these behaviors contribute to unintentional injuries and violence; tobacco use; alcohol and other drug use; sexual behaviors that contribute to unintended pregnancy and sexually transmitted diseases (STDs), including human immunodeficiency virus (HIV) infection; unhealthy dietary behaviors; and physical inactivity. The YRBSS includes a national school-based survey conducted by CDC as well as state, territorial, and local school-based surveys conducted by education and health agencies. This report summarizes results from the national survey, 34 state surveys, and 18 local surveys conducted among students in grades 9-12 during February-December 2001. In the United States, approximately three-fourths of all deaths among persons aged 10-24 years result from only four causes: motor-vehicle crashes, other unintentional injuries, homicide, and suicide. Results from the 2001 national Youth Risk Behavior Survey demonstrated that numerous high school students engage in behaviors that increase their likelihood of death from these four causes: 14.1% had rarely or never worn a seat belt during the 30 days preceding the survey; 30.7% had ridden with a driver who had been drinking alcohol; 17.4% had carried a weapon during the 30 days preceding the survey; 47.1% had drunk alcohol during the 30 days preceding the survey; 23.9% had used marijuana during the 30 days preceding the survey; and 8.8% had attempted suicide during the 12 months preceding the survey. Substantial morbidity and social problems among young persons also result from unintended pregnancies and STDs, including HIV infection. In 2001, 45.6% of high school students had ever had sexual intercourse; 42.1% of sexually active students had not used a condom at last sexual intercourse; and 2.3% had ever injected an illegal drug. Two-thirds of all deaths among persons aged > or = 25 years result from only two causes: cardiovascular disease and cancer. The majority of risk behaviors associated with these two causes of death are initiated during adolescence. In 2001, 28.5% of high school students had smoked cigarettes during the 30 days preceding the survey; 78.6% had not eaten > or = 5 servings per day of fruits and vegetables during the 7 days preceding the survey; 10.5% were overweight; and 67.8% did not attend physical education class daily. Health and education officials at national, state, and local levels are using these YRBSS data to analyze and improve policies and programs to reduce priority health-risk behaviors among youth. The YRBSS data also are being used to measure progress toward achieving 16 national health objectives for 2010 and 3 of the 10 leading health indicators.
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PMID:Youth risk behavior surveillance--United States, 2001. 1238 72

Kidney transplantation should be strongly considered for all medically suitable patients with chronic and end-stage renal disease (ESRD). Improvements in outcomes after renal transplantation have resulted in a more liberal selection of patients. High-risk category patients including human immunodeficiency virus (HIV)-positive, highly sensitized patients, T-cell positive cross-match, and ABO blood group-incompatible patients are now considered potential renal transplant candidates. Unfortunately, the demand for kidney transplants far exceeds the supply of available organs, causing a persistent increase in the number of patients on the waiting list with a parallel increase in the waiting time for a cadaveric kidney transplant. This has 2 major consequences. First, patients on the waiting list are getting sicker and older. Second, living donors have assumed increasing importance in renal transplantation. Pre-existing morbidities including malignancies, cardiovascular disease, infections, and coagulopathies should be extensively evaluated before proceeding to transplantation. Special attention should be given to cardiovascular risk factors because the leading cause of death after renal transplant is cardiovascular disease. A full immunologic evaluation with ABO blood group determination, human leukocyte antigen (HLA) typing, screening for antibody to HLA phenotypes, and cross-matching need to be gathered before transplantation to avoid antibody-mediated hyperacute rejection or to proceed with specific protocols in highly sensitized or in positive T-cell cross-match patients. With the increased rate of donation from living donors, regular follow-up evaluation of kidney donors is recommended to detect hypertension or proteinuria in those who may develop it.
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PMID:Pretransplant evaluation of renal transplant candidates. 1243 96

To ascertain the impact of hepatitis C virus (HCV) infection on human immunodeficiency virus (HIV) disease progression and associated death in the era of highly active antiretroviral therapy (HAART), we examined mortality rates, the presence of other diseases, and antiretroviral use in an observational cohort of 823 HIV-infected patients with and without HCV coinfection during the period of January 1996 through June 2001. Analyses were used to compare patient characteristics, comorbid conditions, and survival durations in HIV-infected and HIV-HCV-coinfected patients. HIV-HCV-coinfected persons did not have a statistically greater rate of acquired immunodeficiency syndrome or of renal or cardiovascular disease, but they did have more cases of cirrhosis and transaminase elevations. There were proportionately more deaths in the HIV-HCV-coinfected group. Age, baseline CD4+ cell count, and duration of HAART were significantly associated with survival, but HCV infection was not. HAART use was a strong predictor of increased duration of survival, suggesting that treatment is more important to survival than is HCV coinfection status.
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PMID:Influence of coinfection with hepatitis C virus on morbidity and mortality due to human immunodeficiency virus infection in the era of highly active antiretroviral therapy. 1288 76

The introduction of highly active antiretroviral therapy has significantly reduced morbidity and mortality in patients infected with the human immunodeficiency virus. Treatment with antiretroviral agents--protease inhibitors in particular--has uncovered a syndrome of abnormal fat redistribution, dyslipidemia, and impaired glucose metabolism, collectively termed lipodystrophy syndrome. The cause of the syndrome seems to be multifactorial; however, its exact mechanisms have yet to be elucidated. Accelerated risk for cardiovascular disease is likely to be a major concern in these patients in the future. At this time, no clinical guidelines are available for the prevention and/or the treatment of lipodystrophy syndrome. The available treatment options range from switching the different antiretroviral drugs and lifestyle modifications to the use of pharmacologic agents to treat patients with dyslipidemia, impaired glucose tolerance and/or diabetes, and changes in body composition. This review emphasizes the clinical features, potential molecular mechanisms, and treatment options for patients infected with human immunodeficiency virus who have lipodystrophy syndrome.
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PMID:Lipodystrophy, insulin resistance, diabetes mellitus, dyslipidemia, and cardiovascular disease in human immunodeficiency virus infection. 1263 Jun 45

Dyslipidemia is an important clinical problem in individuals infected with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy. Data suggest that increased cardiovascular disease is occurring in this population. HIV-infected individuals should undergo evaluation and treatment regimens based on the current National Cholesterol Education Program guidelines. In most situations, the first interventions should be nonpharmacological and should include diet, exercise, and management of other hygienic risk factors. If pharmacologic therapy becomes necessary, the choices of lipid-lowering agents should be limited to agents with the least likelihood of adverse drug interactions.
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PMID:Lipid abnormalities. 1265 75


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