Literatura académica sobre el tema "HIV, cardiovascular disease, interleukin-6"
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Artículos de revistas sobre el tema "HIV, cardiovascular disease, interleukin-6"
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Zaaqoq, Akram M., Faisal A. Khasawneh y Roger D. Smalligan. "Cardiovascular Complications of HIV-Associated Immune Dysfunction". Cardiology Research and Practice 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/302638.
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Prolonged survival in HIV infection is accompanied by an increased frequency of non-HIV-related comorbidities. It is suggested that cardiovascular diseases (CVD) occur earlier among HIV-positive patients compared with HIV-negative patients, and at a higher rate. Several factors have been proposed which can be categorized into traditional and nontraditional risk factors. Immune dysfunction is a nontraditional risk factor that contributes significantly to cardiovascular pathology. Markers of inflammation are elevated in HIV-infected patients, and elevations in markers such as high-sensitivity C-reactive protein, D-dimer, and interleukin-6 (IL-6) have been associated with increased risk for cardiovascular disease. However, the data currently suggest the most practical advice is to start antiretroviral therapy early and to manage traditional risk factors for CVD aggressively. A better understanding of the mechanisms of CVD in this population and further efforts to modify chronic inflammation remain an important research area.
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Funderburg, Nicholas T., Elizabeth Mayne, Scott F. Sieg, Robert Asaad, Wei Jiang, Magdalena Kalinowska, Angel A. Luciano et al. "Increased tissue factor expression on circulating monocytes in chronic HIV infection: relationship to in vivo coagulation and immune activation". Blood 115, n.º 2 (14 de enero de 2010): 161–67. http://dx.doi.org/10.1182/blood-2009-03-210179.
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Abstract HIV infection is associated with an increased risk of thrombosis; and as antiretroviral therapy has increased the lifespan of HIV-infected patients, their risk for cardiovascular events is expected to increase. A large clinical study found recently that all-cause mortality for HIV+ patients was related to plasma levels of interleukin-6 and to D-dimer products of fibrinolysis. We provide evidence that this elevated risk for coagulation may be related to increased proportions of monocytes expressing cell surface tissue factor (TF, thromboplastin) in persons with HIV infection. Monocyte TF expression could be induced in vitro by lipopolysaccharide and flagellin, but not by interleukin-6. Monocyte expression of TF was correlated with HIV levels in plasma, with indices of immune activation, and with plasma levels of soluble CD14, a marker of in vivo lipopolysaccharide exposure. TF levels also correlated with plasma levels of D-dimers, reflective of in vivo clot formation and fibrinolysis. Thus, drivers of immune activation in HIV disease, such as HIV replication, and potentially, microbial translocation, may activate clotting cascades and contribute to thrombus formation and cardiovascular morbidities in HIV infection.
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Kounatidis, Dimitris, Dimitra Rontogianni, Dimitrios Sampaziotis, Maria Vardaka, Chara Giatra, Christodoulos Dolapsakis, Evangelia Margellou y Natalia G. Vallianou. "An HHV-8 Positive HIV Negative Multicentric Castleman’s Disease, who Responded well to Rituximab Alone". Cardiovascular & Hematological Disorders-Drug Targets 20, n.º 1 (26 de febrero de 2020): 84–86. http://dx.doi.org/10.2174/1871529x19666190227185318.
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Background: Multicentric Castleman Disease (MCD) presents with enlarged lymph nodes in multiple regions and systemic inflammatory symptoms, due to the dysregulation of cytokines, most commonly interleukin-6 (IL-6). Human herpes virus-8 (HHV-8) is strongly related to MCD (HHV-8-associated MCD) and is being implicated in cytokine dysregulation in patients, the majority of whom are HIV positive or immunosuppressed. Preferred treatment of HHV-8- associated MCD depends on the presence or not of concurrent Kaposi sarcoma and on whether the patient has life-threatening organ failure or poor performance status thought to be related to HHV- 8-associated MCD. Case Presentation: Herein, we describe a female patient with HHV-8 positive, HIV negative MCD, who responded well to the administration of rituximab once weekly for four weeks alone for three cycles. Conclusion: HHV-8 positive, HIV negative MCD treatment modalities are only anecdotal due to the rarity of this form of MCD. Administration of rituximab alone seems to be beneficial among patients with good performance status and the absence of life-threatening organ failure in cases of HHV-8 positive, HIV negative MCD.
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Triant, Virginia A. "Cardiovascular Disease and HIV Infection". Current HIV/AIDS Reports 10, n.º 3 (25 de junio de 2013): 199–206. http://dx.doi.org/10.1007/s11904-013-0168-6.
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Arzhakova, M. A., T. A. Shekhovtsova y D. V. Duplyakov. "Coronary Heart Disease in HIV-Infected Patients". Rational Pharmacotherapy in Cardiology 15, n.º 6 (3 de enero de 2020): 900–905. http://dx.doi.org/10.20996/1819-6446-2019-15-6-900-905.
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Currently, there are methods of drug exposure to the infection caused by the human immunodeficiency viruses (HIV), that allow to suppress the active replication of the virus in the patient's body. The era of antiretroviral therapy, which has allowed HIV-infected people to live longer, has begun. This led to an increase in their cardiovascular diseases, which occur at an earlier age and are more severe than in people without HIV. Specific or “nontraditional” risk factors damaging vascular wall occur in HIV patients along with traditional risk factors. These factors include: the negative impact of HIV on endothelium, an imbalance of inflammatory mediators, pathological immune activation, a decrease in the level of CD4 cells, a change in the number and function of platelets. The question of the effect of antiretroviral therapy on the occurrence of atherosclerotic vascular lesions remains debatable. Acute coronary syndrome (ACS) is one of the most frequent and most severe cardiovascular events in HIV-infected patients. The risk of myocardial infarction is highest in patients with a viral load of HIV-1 ribonucleic acid (RNA)≥500 copies/ml and a CD4 cell count of <200/ml. The most common form of ACS in HIV patients is ACS with ST segment elevation. Treatment of ACS in HIV patients has some difficulties: a high frequency of stent thrombosis, the frequent occurrence of thrombocytopenia, drug interactions with antiretroviral therapy. The high risk of developing cardiovascular diseases in HIV patients necessitates the introduction of active measures of primary and secondary prevention, taking into account the specific interaction of all drugs taken by the patient.
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Jalbert, Emilie, Nisha Parikh, Todd Seto, Dominic Chow, Cecilia Shikuma, Lishomwa Ndhlovu y Jason Barbour. "Elevated proinflammatory cytokine production by monocytes in HIV(+) individuals at risk for cardiovascular disease (P3033)". Journal of Immunology 190, n.º 1_Supplement (1 de mayo de 2013): 55.17. http://dx.doi.org/10.4049/jimmunol.190.supp.55.17.
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Abstract Despite virologic suppression by HIV antiretroviral therapy, residual inflammation associated with chronic HIV infection increases the risk of developing cardiovascular disease. Monocytes have been shown to be major players in the development of atherosclerosis due to their proinflammatory responses to oxidized Low Density Lipoproteins. Our study sought to assess the functional properties of monocytes from peripheral blood of HIV-infected individuals. The cohort consisted of 33 HIV(+) subjects on HAART and 14 HIV(-) risk- and age- matched subjects. Our flow cytometry-based functional assay measured monocyte production of IL-1β, IL-8 and IL-6 in the absence of stimulation and in response to LPS or oxLDL. Without stimulation, HIV(+) subjects had a greater frequency of cells producing IL-1β and IL-8. In the presence of either oxLDL or LPS, both groups increased the frequency of responding cells compared to no stimulation, but HIV(+) subjects maintained a higher frequency of IL-1β(+) and IL-8(+) cells compared to HIV(-). There was no IL-6 production in either group in the absence of stimulation, but upon stimulation with either oxLDL or LPS, there was a higher frequency of IL-6 producing cells in the HIV(+) group. The higher level of inflammatory cytokine production in HIV(+) adults compared to HIV(-), both at rest and in the presence of stimulation, may in part account for increased risk of cardiovascular disease seen in the HIV(+) population.
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Abreu, R. Correia. "Characterization of cardiovascular risk factors and Framingham score in an HIV-1 population". Journal of Clinical Research and Reports 5, n.º 5 (21 de noviembre de 2020): 01–04. http://dx.doi.org/10.31579/2690-1919/130.
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With the advent of high-potency antiretroviral treatment introduced in 1996, HIV infection ceased to be an acute and deadly disease to become chronic and controllable. However, the early aging of this population, which according to some authors and cohorts, is 10 years less than in the "normal" population, has been studied. Although the realities of these patients comorbidities are well known, the definition of time, when and how or with what to treat still seems to be a matter of debate. The aim of this study is to evaluate the incidence and prevalence according to the state of the art for the non-HIV population of cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus) and apply the adjusted Framingham Risk Score by recording analytical and clinical factors in an HIV-1 population with more than 50 years of age, followed in the Infectious Diseases Service for more than 6 months.
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Abreu, R. Correia. "Characterization of cardiovascular risk factors and Framingham score in an HIV-1 population". Journal of Clinical Research and Reports 5, n.º 5 (21 de noviembre de 2020): 01–04. http://dx.doi.org/10.31579/2690-1919/0130.
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With the advent of high-potency antiretroviral treatment introduced in 1996, HIV infection ceased to be an acute and deadly disease to become chronic and controllable. However, the early aging of this population, which according to some authors and cohorts, is 10 years less than in the "normal" population, has been studied. Although the realities of these patients comorbidities are well known, the definition of time, when and how or with what to treat still seems to be a matter of debate. The aim of this study is to evaluate the incidence and prevalence according to the state of the art for the non-HIV population of cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus) and apply the adjusted Framingham Risk Score by recording analytical and clinical factors in an HIV-1 population with more than 50 years of age, followed in the Infectious Diseases Service for more than 6 months.
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Polanka, Brittanny M., Suman Kundu, Kaku A. So-Armah, Matthew S. Freiberg, Samir K. Gupta, Tamika C. B. Zapolski, Adam T. Hirsh et al. "Insomnia symptoms and biomarkers of monocyte activation, systemic inflammation, and coagulation in HIV: Veterans Aging Cohort Study". PLOS ONE 16, n.º 2 (9 de febrero de 2021): e0246073. http://dx.doi.org/10.1371/journal.pone.0246073.
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BackgroundInsomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated.MethodsWe examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, “Difficulty falling or staying asleep?,” with the following response options: “I do not have this symptom” or “I have this symptom and…” “it doesn’t bother me,” “it bothers me a little,” “it bothers me,” “it bothers me a lot.” Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI).ResultsWe observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the “Bothers a Lot” group had, on average, 17% higher D-dimer than veterans in the “No Difficulty Falling or Staying Asleep” group in the demographic-adjusted model (exp[b] = 1.17, 95%CI= 1.01–1.37,p= .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95%CI= 0.94–1.26,p= .27).ConclusionWe observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.
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Postorino, Maria Concetta, Filippo Luciani, Carmelo Mangano, Maria Stella Carpentieri, Paolo Scerbo, Armando Priamo, Giuseppina Berardelli et al. "DEMOGRAPHICAL, VIRO-IMMUNOLOGICAL, CLINICAL AND THERAPEUTICAL CHARACTERISTICS OF HIV INFECTED PATIENTS IN A “EPIDEMIOLOGICALLY UNEXPLORED” REGION OF ITALY (CALABRIA REGION): THE CALABRHIV COHORT." Mediterranean Journal of Hematology and Infectious Diseases 7 (8 de octubre de 2015): e2015054. http://dx.doi.org/10.4084/mjhid.2015.054.
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Background and Objectives HIV epidemics may differ among epidemiological contexts. We aimed at constructing an HIV clinical cohort whose main epidemiological, clinical and therapeutical characteristics are described (the CalabrHIV cohort, Calabria Region, Southern Italy). Methods The CalabrHIV cohort includes all HIV patients on active follow-up in all infectious disease centers in the Calabria Region as at October 2014. All information were recorded in a common electronic database. Not-infectious co-morbidities (such as cardiovascular diseases, bone fractures, diabetes, renal failure and hypertension) were also studied. Results 548 patients (68% males; 63% aged <50 years) were included in the CalabrHIV cohort. Major risk factors: sexual transmission (49%) and intravenous drug use (34%). 39% patients had HCV and/or HBV co-infection. An high percentage of late presenters was observed (68.4% patients with CD4+ nadir <350/mm3and 38.5% patients with AIDS at baseline). 83% patients on HAART had actually undetectable HIV-RNA. Hypertension was the most frequent co-morbidity (21.5%). Multi-morbidity was more frequent in >50 years-old patients than in <50 years-old ones (30% vs. 6%; p<0.0001). Co-morbidity was more frequent in HCV and/or HBV co-infected than in HIV mono-infected patients (46.6% vs. 31.7%: p=0.0006). Conclusion This cohort presentation study sheds light, for the first time, on HIV patients’ characteristics in the Calabria Region. Despite a small number of officially reported cases, the size of the cohort was substantial. We showed that HIV infected patients with chronic hepatites, were affected by concomitant not-infectious co-morbidities more than the HIV mono-infected individuals. New HCV treatments are eagerly awaited.
Tesis sobre el tema "HIV, cardiovascular disease, interleukin-6"
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Piira, O. P. (Olli-Pekka). "Effects of emotional excitement on cardiovascular regulation". Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526209708.
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Abstract The incidence of adverse cardiovascular events is higher among spectators of exciting sports events, particularly in patients with coronary artery disease (CAD), but the mechanistic link between the events is not known. We assessed the hemodynamic, autonomic function, plasma catecholamines, endothelin-1, interleukin-6, and markers of platelet activation and blood coagulation of enthusiastic male ice hockey spectators with CAD (n=55, 60±9 years) and healthy subjects (n=16, 48±6 years) during Finnish national league ice hockey final play-off matches and on a control day. Blood markers were also measured before and after a maximal exercise test with a bicycle ergometer. Systolic and diastolic blood pressure (BP) were significantly higher one hour before, during, and one hour after the match than on the control day. During the match the highest systolic BP was 180±14 vs. 145±15 and diastolic BP was 103±13 vs. 82±11 mmHg (respectively, p<0.001 for both). Heart rate (HR) was higher throughout the match (p<0.05) and remained elevated two hours after the match (p<0001), and measures of HR variability were decreased during the match (p<0.01). Plasma endothelin-1 (ET-1), interleukin-6 (IL-6) and noradrenaline (NOR) increased during the match (p<0.01 for all), but markers of platelet activation and coagulation remained unchanged. ET-1 did not change during exercise but NOR, adrenaline, IL-6, and markers of platelet activation and blood coagulation increased statistically significantly (p<0.0001 for all). A statistically significantly more marked increase in both endothelin-1 and interleukin-6 was observed in CAD patients compared with healthy subjects during the match (time x group interaction p<0.05 for both). The high-frequency power of R-peak-to-R-peak intervals decreased in CAD patients (p<0.001) but did not change in healthy subjects during the match. Maximal metabolic equivalens (METs) were most strongly correlated with ET-1 response during the match (β =-0.45, partial correlation r=-0.43, p=0.002) when age, body mass index, METs, left ventricular ejection fraction, basal ET-1 and subjective experience of excitement were entered into the model as independent variables in a linear stepwise regression analysis. In conclusion, autonomic reactions and vasoconstriction may partly explain the vulnerability to cardiovascular events caused by this type of leisure-time emotional excitement. Emotional excitement causes concomitant increases in markers reflecting vulnerability to atherosclerotic plaque complications, while physical exercise causes more prominent changes in markers of coagulation. Emotional excitement causes more significant increases of markers of vasoconstriction and acute inflammation and withdrawal of cardiac vagal regulation in patients with CAD than in healthy subjects. Exercise capacity may protect against further cardiovascular events in CAD patients because it is associated with reduced ET-1 release during emotional excitementTiivistelmä Jännittävän urheilutapahtuman on havaittu lisäävän sydäntapahtumia erityisesti sepelvaltimotautipotilailla. Syyt eivät ole selvillä. Tutkimuksen kohteena oli jääkiekon mestaruussarjan pudotuspelien seuraamisen vaikutus sekä sepelvaltimotautisten (n=55, 60±9 vuotta) että terveiden (n=16, 48±6 vuotta) jääkiekkofanien verenkiertoon, autonomiseen hermostoon, veren katekolamiinien, endoteliini-1:n (ET-1) ja interleukiini-6:n (IL-6) pitoisuuksiin sekä veren hyytymiseen paikan päällä jäähallissa seurattuna. Muuttujat mitattiin jäähallissa ottelun aikana. Ne mitattiin myös ennen ottelua ja eri päivänä sairaalassa ennen kuntopyörällä tehtyä maksimaalista sydämen kuormitustestiä ja heti sen jälkeen. Sepelvaltimotautipotilaiden ylä- ja alaverenpaineet kohosivat tilastollisesti merkitsevästi tuntia ennen jääkiekkopeliä ja sen aikana, ja ne olivat koholla vielä tunnin ajan pelin jälkeen kontrollipäivään verrattuina. Ottelun aikana yläpaineet olivat 180±14 vs. 145±15 ja alapaineet 103±13 vs. 82±11 mmHg (p<0.001 molemmille painetasoille). Sydämen syke oli korkeampi pelin ajan (p<0.05), ja se pysyi koholla kahden tunnin ajan pelin jälkeen (p<0.001). Lisäksi sykevaihtelu heikentyi pelin aikana (p<0.01) kontrollipäivään verrattuna. Veren ET-1-, IL-6- ja noradrenaliinipitoisuudet (p<0.01) nousivat pelin aikana, mutta veren hyytymistä kuvastavat lukemat säilyivät muuttumattomina. ET-1 ei noussut fyysisessä kuormitustestissä, mutta noradrenaliini- ja adrenaliinipitoisuudet sekä IL-6:n ja veren hyytymistä kuvaavat lukemat kasvoivat tilastollisesti merkitsevästi (p<0.0001). Pelin aikana sepelvaltimotautipotilaiden ET-1 ja IL-6 pitoisuudet kohosivat enemmän kuin terveiden vastaavat arvot (p<0.05). Lisäksi ottelun aikana sydämen sykevaihtelu laski sepelvaltimopotilailla (p<0.001), muttei muuttunut terveillä. Polkupyörätestin maksimaalinen suorituskyky (METs) oli voimakkaasti yhteydessä ET-1 vasteeseen pelin aikana (β =-0.45, r=-0.43, p=0.002), kun ikä, painoindeksi, METs, sydämen supistusvireys, ET-1:n lähtötaso ja koehenkilöiden kokema jännitystaso huomioitiin itsenäisinä muuttujina regressiotyyppisessä tilastolaskennassa. Yhteenvetona todetaan itsenäisesti toimivan hermoston muutosten ja verisuonten supistumisen voivan osittain selittää aiemmin havaitun sydäntapahtumien lisääntymisen tutkimuskohteen tyyppisessä vapaa-ajan tunne-elämyksessä. Jääkiekkopelin jännitys aiheuttaa muutoksia sepelvaltimotautialueiden repeämisherkkyyttä kuvaaviin tekijöihin, kun taas fyysinen rasitus vaikuttaa voimakkaammin veren hyytymistä ilmaiseviin lukemiin. Potilailla jännitys lisäsi enemmän suonten supistuvuutta, akuuttia tulehdusreaktiota ja nosti parasympaattisen hermoston vetäytymistä kuvaavia lukemia terveisiin koehenkilöihin verrattuna. Hyvä suorituskyky voi suojata korkean riskin sepelvaltimotautipotilaita sydäntapahtumilta vähentämällä ET-1:n vapautumista jännityksen aikana
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O'Neil, Catherine L. "The Effect of Depression, Inflammation and Sleep Quality on Risk for Cardiovascular Disease". Scholar Commons, 2018. https://scholarcommons.usf.edu/etd/7556.
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Background
Cardiovascular disease (CVD) remains the number one killer even after years of advances and preventative measures. Identifying and reducing modifiable risk factors is a health care priority. CVD Risk assessments are calculated using several traditional risk factors including age, gender, race, blood pressure, cholesterol, history of diabetes, and smoking to estimate a persons’ risk of developing CVD (heart disease or stroke) in the next 10-years. In addition to the traditional risk factors for CVD, there is increasing evidence of metabolic disorders, depressive symptoms, inflammation and sleep quality posing a greater risk for CVD. However, these factors are not included in the current risk prediction models including the Framingham Risk Score, Reynolds Risk Score, and Pooled Cohort Risk Equations. Therefore, this study examined the effect of depressive symptoms, inflammation, and sleep quality on the independent risk for CVD.
Objective
The primary objective of this study was to evaluate the independent relationships between traditional cardiac risk factors, depressive symptoms, inflammation, and sleep quality, on long-term risk of major adverse cardiovascular events (MACE). The secondary objective was to evaluate whether gender modifies the relationships between depressive symptoms, inflammation, and sleep quality on long-term risk of MACE.
Design
A secondary analysis was conducted on data obtained from the Longitudinal prospective cohort study Heart Strategies Concentrating on Risk Evaluation (Heart SCORE) conducted by the University of Pittsburgh. The ongoing Heart SCORE study has been prospectively examining cardiovascular disease (CVD) risk factors and CVD events on an initial cohort of 2,000 enrolled adults ages 45 to 75 at study entry. A Cox proportional-hazard model was used to evaluate the relationship between traditional risk factors as well as independently and collectively for depressive symptoms, inflammation and sleep quality and risk of MACE. Models were reanalyzed adding gender as an interaction term and in stratified analyses to evaluate whether gender modifies the relationships between sleep quality, depressive symptoms, and inflammation and long-term risk of MACE.
Results
The participants (N= 1,895) included in this study were, 1256 females (66%), 639 males (34%), ranging from 45 to 75 years of age with a median age of 60 years, 42% Blacks, 55% Whites and 3% other race. Six percent, (n =113) of the participants experienced a major cardiac event during a mean of nearly 10 year follow up. Results indicated that men as compared with women with high levels of interleukin-6 had particularly high risk for CVD, as defined by two separate definitions of MACE, MACE1: Hazard Ratio (HR) 3.44 vs. 1.72 for males and females, respectively, MACE6: HR 2.51 vs. 1.69 for males and females, respectively. These results suggest the high inflammation in men is strongly associated with future risk of CVD. The addition of depressive symptoms to the initial traditional risk factor model was associated with a modest increase in the risk of both definitions of MACE (HR range from 1.20 to 1.68) with similar results observed by gender. Sleep quality/Insomnia was not associated with long-term risk of MACE overall or when evaluated separately by gender.
Conclusion
Primary prevention with early identification of potential modifiable risk factors is a key strategy in planning interventions to reduce the risk of CVD. Results from this study suggest that depression and inflammation (e.g. IL-6) should be studied in other populations to estimate their independent predictive value in risk stratification. Whereas sleep quality was not associated with long-term risk of CVD in this analysis, future studies should consider the use of objective measures of sleep quality, such as actigraphy in addition to standard use of self-report measures and sleep diaries.
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Teixeira, Andrea Mariana Nunes da Costa. "Efeito da ingestão de chocolate e erva mate na elasticidade arterial de indivíduos com HIV/aids em terapia antirretroviral". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-11102013-103905/.
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Introdução - Estudos mostram maior ocorrência de complicações cardiovasculares na população HIV/aids. Alguns estudos envolvendo animais e indivíduos saudáveis ou com outras doenças observaram benefícios no consumo de chocolate e erva mate na função endotelial e vasodilatação. Objetivo Avaliar o efeito da ingestão de chocolate e erva mate na elasticidade arterial de indivíduos com HIV/aids em terapia antirretroviral. Métodos Ensaio clínico cruzado, aleatorizado e duplo-cego, envolvendo 89 indivíduos com HIV/aids entre 19 e 59 anos, em tratamento regular com antirretrovirais por no mínimo 6 meses, e carga plasmática do HIV <500 cópias/ml. Os indivíduos receberam suplementação diária com aproximadamente 65g de chocolate amargo, 3g de erva mate ou respectivos placebos por 15 dias, com washout de igual tempo entre as intervenções. A aferição da elasticidade arterial foi realizada por análise do formato da onda de pulso com o equipamento HDI/PulseWaveTM CR-2000®. Também foram avaliados: composição corporal, glicemia, perfil lipídico, proteína C-reativa e concentração plasmática de espécies reativas ao ácido tiobarbitúrico (TBARS). As respostas entre tratamentos foram avaliadas por ANOVA e por teste t de Student pelo Stata® 11.0, considerando-se p< 0,005. Resultados A população foi composta principalmente por homens (62,9 por cento) caucasianos (46,1 por cento) com idade média de 44,6 ± 7,1 anos. O tempo médio de diagnóstico de HIV/aids foi de 13,2 ± 4,8 anos com 10,6 ± 5,1 anos de terapia antirretroviral. Não foram encontradas diferenças significantes na elasticidade arterial dos pequenos e grandes vasos após as suplementações. Conclusão Este é o primeiro estudo a avaliar o efeito da ingestão de erva mate e chocolate na elasticidade arterial de indivíduos com HIV/aids. Apesar das evidências positivas desses alimentos na saúde cardiovascular de animais e indivíduos com outras doenças, os mesmos efeitos não foram observados neste estudo. Provavelmente o tempo de suplementação, a biodisponibilidade das substâncias bioativas e o metabolismo alterado desses indivíduos interferiram nos resultados obtidos, sugerindo a necessidade de melhor investigação desses fatoresIntroduction There has been an increase on cardiovascular diseases occurrence in the HIV/aids population. Some studies involving animals and healthy individuals or individuals with other pathologies have shown benefits on endothelial function and vasodilation under use of chocolate and yerba maté. Objective To evaluate the effect of chocolate and yerba maté intake on HIV/aids patient´s arterial elasticity. Methods Double-blind crossover trial including 89 HIV/aids patients, 19 to 59 years of age, on antiretroviral therapy for at least six months, and with viral load <500copies/ml. The individuals consumed daily approximately 65g of dark chocolate, 3g of yerba maté or placebo during 15 days, followed by a 15-day washout period after each intervention. Arterial elasticity was measured using the HDI/PulseWaveTM CR-2000 CardioVascular Profiling System®, which provides a pulse wave contour analysis. Body composition, glicemic index, lipid profile, C-reactive protein and thiobarbituric acid reactive substances (TBARS) were also assessed. The crossover analysis was performed using analysis of variance (ANOVA) on Stata®. The paired Students t-test was also applied. A p value <0.05 was considered significant. Results Most of the individuals were men (62.9 per cent), caucasian (46.1 per cent) aging 44.6 ± 7.1 years. The mean time of HIV/aids diagnosis was 13.2 ± 4.8 years, with 10.6 ± 5.1 years of antiretroviral therapy. There were no significant alterations on elasticity of either large or small arteries after chocolate and yerba maté intake. Conclusion This is the first research to evaluate the effect of chocolate and yerba maté intake on HIV/aids patient´s arterial elasticity. Despite of the positive evidence of these foods on cardiovascular health of animals and populations with other pathologies, the same effects were not observed in this study. Most probably the time of intervention, the bioavailability of the bioactive substances and the altered metabolism of this individuals interfered on the results, which indicates the need for further investigation
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Andersson, Jonas. "Inflammation and lifestyle in cardiovascular medicine". Doctoral thesis, Umeå universitet, Medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-36221.
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Despite major advances in the treatment and prevention of atherosclerosis the last several decades, cardiovascular disease still accounts for the majority of deaths in Sweden. With the population getting older, more obese and with rising numbers of diabetics, the cardiovascular disease burden may increase further in the future. The focus in cardiovascular disease has shifted with time from calcification and narrowing of arteries to the biological processes within the atherosclerotic plaque. C-reactive protein (CRP) has emerged as one of many proteins that reflect a low grade systemic inflammation and is suitable for analysis as it is more stable and easily measured than most other inflammatory markers. Several large prospective studies have shown that CRP is not only an inflammatory marker, but even a predictive marker for cardiovascular disease. C-reactive protein is associated with several other risk factors for cardiovascular disease including obesity and the metabolic syndrome. Our study of twenty healthy men during a two week endurance cross country skiing tour demonstrated a decline in already low baseline CRP levels immediately after the tour and six weeks later. In a study of 200 obese individuals with impaired glucose tolerance randomised to a counselling session at their health care centre or a one month stay at a wellness centre, we found decreased levels of CRP in subjects admitted to the wellness centre. The effect remained at one, but not after three years of follow-up. In a prospective, nested, case-referent study with 308 ischemic strokes, 61 intracerebral haemorrhages and 735 matched referents, CRP was associated with ischemic stroke in both uni- and multivariate analyses. No association was found with intracerebral haemorrhages. When classifying ischemic stroke according to TOAST criteria, CRP was associated with small vessel disease. The CRP 1444 (CC/CT vs. TT) polymorphism was associated with plasma levels of CRP, but neither with ischemic stroke nor with intracerebral haemorrhage. A study on 129 patients with atrial fibrillation was used to evaluate whether inflammation sensitive fibrinolytic variables adjusted for CRP could predict recurrence of atrial fibrillation after electrical cardioversion. In multivariate iv models, lower PAI-1 mass was associated with sinus rhythm even after adjusting for CRP and markers of the metabolic syndrome. In conclusion, lifestyle intervention can be used to reduce CRP levels, but it remains a challenge to maintain this effect. CRP is a marker of ischemic stroke, but there are no significant associations between the CRP1444 polymorphism and any stroke subtype, suggesting that the CRP relationship with ischemic stroke is not causal. The fibrinolytic variable, PAI-1, is associated with the risk of recurrence of atrial fibrillation after electrical cardioversion after adjustment for CRP. Our findings suggest a pathophysiological link between atrial fibrillation and PAI-1, but the relation to inflammation remains unclear.
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Freitas, Alexandre Magnus Mourao e. "Estado da vitamina D e sua relação com doenças cardiovasculares em indivíduos com HIV/AIDS em tratamento com antirretrovirais: uma revisão sistemática". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-26052015-092359/.
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Este estudo faz uma revisão sobre a relação das concentrações de vitamina D e doenças cardiovasculares (DVC) em indivíduos com vírus da imunodeficiência humana e/ou síndrome da imunodeficiência adquirida (HIV/AIDS) em tratamento com terapia antirretroviral (TARV). Um total de 1.288 artigos foram recuperados dos bancos de dados do PubMed, EMBASE, OVID, Cochrane Central, ERIC, SIBi, SciELO, LILACS e Grey literature. Nove deles preencheram os critérios de seleção e foram inclusos nesta revisão sistemática. Existe uma alta prevalência da deficiência de vitamina D em indivíduos HIV-positivo, independentemente da região climática que vivem. Tanto a infecção pelo HIV-1 como a TARV podem interferir no metabolismo da vitamina D. Essa vitamina mostrou uma tendência a decrescer do momento antes da TARV ao depois da iniciação da TARV, sua deficiência foi mais prevalente em pacientes que fazem utilização da TARV do que aqueles que nunca a utilizaram e suas concentrações no organismo mostraram significantes associações com medidores da elasticidade arterial, como Espessamento Média-Íntima (EMI) e Dilatação Mediada por Fluxo (DMF). Essas alterações nos vasos e sistema circulatório predispõem doenças cardiovasculares, tais como, aterosclerose, trombose, infarto do miocárdio e acidente vascular cerebral. Portanto, apesar de existirem controvérsias, indivíduos HIV-positivo podem estar mais propensos ao desenvolvimento de DCV, não apenas pelos efeitos colaterais comuns da TARV e da infecção pelo HIV-1, mas também por estarem mais predispostos a terem hipovitaminose D, e as alterações causadas por este quadro em seu organismo.This study reviewed the relationship of vitamin D levels and cardiovascular disease (CVD) in individuals with human immunodeficiency virus and/or acquired immunodeficiency syndrome (HIV/AIDS) in treatment with antiretroviral therapy (ART). A total of 1,288 articles were retrieved from the PubMed, EMBASE, Ovid, Cochrane Central, ERIC, SIBi, SciELO, LILACS and Grey literature databases. Nine of them met the selection criteria and were included in this systematic review. There is a high vitamin D deficiency prevalence in HIV positive individuals, regardless of climate area where they live. Both, HIV-1 infection and ART can interfere with the metabolism of vitamin D. This vitamin has shown a tendency to decrease from the moment before ART to the one after the initiation of ART. Its deficiency was more prevalent in patients who use ART than those who are ART-naïve. Vitamin D concentrations showed significant associations with markers of arterial dysfunction, such as carotid artery intima-media thickness (cIMT) and flow-mediated dilatation (FMD). These changes in vessels and circulatory system predispose CVD, such as atherosclerosis, thrombosis, myocardial infarction and stroke. Therefore, although there are controversies, HIV positive individuals may be more prone to the development of CVD, not just for the common side effects of ART and HIV- 1 infection, but also because they are predisposed to have vitamin D deficiency, and all the metabolic changes caused by this situation in his organism. Key-
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PONTECORBOLI, GIULIA. "Detection and prevention of cardiovascular diseases in HIV-infected patients". Doctoral thesis, 2021. http://hdl.handle.net/2158/1234495.
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Zaidan, Sarah. "Exploring the role of IL-32 in premature age-related cardiovascular diseases in HIV-infected individuals". Thèse, 2018. http://hdl.handle.net/1866/22329.
Texto completoLibros sobre el tema "HIV, cardiovascular disease, interleukin-6"
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Klingenberg, Roland y Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.
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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.
Capítulos de libros sobre el tema "HIV, cardiovascular disease, interleukin-6"
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Lüscher, Thomas F. y Paul M. Ridker. "Anti-inflammatory therapies for cardiovascular disease". En ESC CardioMed, 1112–20. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0272.
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Inflammation involves many blood cells and the molecules released by them such as cytokines, chemokines, and antibodies. In particular, cells derived from monocyte/macrophage lines are involved in atherogenesis, as are numerous chemokines, cytokines, and adhesion molecules expressed in the vasculature or adipose tissue. Different inflammatory pathways have been considered in the prevention and treatment of cardiovascular disease. Specifically, as outlined previously in a review of the authors, several lines of evidence support the concept that inhibition of the central immune pathway linking interleukin 1, tumour necrosis factor alpha, and interleukin 6 might be novel targets.
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Lassner, Dirk, Gerhard R. F. Krueger, L. Maximilian Buja y Uwe Kuehl. "HHV-6 and HHV-7 in Cardiovascular Diseases and Cardiomyopathies". En Human Herpesviruses HHV-6A, HHV-6B & HHV-7, 267–80. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-444-62703-2.00016-1.
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Musonda Chalwe, Joseph, Christa Grobler y Wilna Oldewage-Theron. "Genetic Polymorphisms and Their Interactions with the Risk Factors of Cardiovascular Diseases: Review Chapter". En Risk Factors for Cardiovascular Disease. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100486.
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Cardiovascular diseases (CVDs) have been reported to have a complex pathogenesis by a number of studies. Atherosclerosis and inflammation have been established as the main contributors to CVDs. Furthermore, genetic polymorphisms have been identified and found to have a correlation with an individual’s susceptibility to developing CVD. Some of these polymorphisms and corresponding cardiovascular risk (CVR) factors include: C174G (Interleukin (IL)-6 association), methylenetetrahydrofolate reductase (MTHFR) C667T/A1298C (hyperhomocysteinaemia), VII R353Q (coagulation factor VII association) and rs247616/rs1968905/rs1270922 (cholesteryl ester transfer protein (CEPT) - cholesterol metabolism) amongst others. At a time when disease prediction, diagnosis and prognosis are still being investigated, these polymorphisms have the potential for use in these areas as well as opening more opportunities in the understanding of CVD. The objective of this chapter was to review the current knowledge about the relationship between genetic polymorphisms and cardiovascular disease.
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von Käenel, Roland y Christian Albus. "Mechanisms: psychological factors and outcomes". En ESC CardioMed, editado por Susanne Pedersen, 3049–54. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0791.
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An impressive amount of literature has been accumulating on potential biological mechanisms directly linking psychological factors with atherothrombotic cardiovascular disease, heart failure, arrhythmia, and stress cardiomyopathy. Indirect biological effects of psychological factors due to unhealthy behaviours are also important. For instance, depressed individuals have an increased risk of developing the metabolic syndrome, with those having the syndrome showing elevated interleukin 6 and fibrinogen levels.
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Klingenberg, Roland y Ulf Müller-Ladner. "Mechanisms of inflammation". En ESC CardioMed, 1104–6. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270_update_001.
Texto completoResumen
This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.
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Becker, Richard C. y Frederick A. Spencer. "Venous Thromboembolism Prophylaxis". En Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0030.
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Venous thromboembolism represents a true worldwide medical problem that is encountered within all realms of practice. Venous thromboembolism (VTE) occurs in approximately 100 patients per 100,000 population yearly in the United States and increases exponentially with each decade of life (White, 2003). Approximately one-third of patients with symptomatic deep vein thrombosis (DVT) experience a pulmonary embolism (PE). Death occurs within 1 month in 6% of patients with DVT and 12% of those with PE. Early mortality is associated strongly with presentation as PE, advanced age, malignancy, and underlying cardiovascular disease. An experience dating back several decades has provided a better understanding of disease states and conditions associated with VTE (Anderson and Spencer, 2003). Given the potential morbidity and mortality associated with VTE, it is apparent that prophylaxis represents an important goal in clinical practice. A variety of anticoagulants including unfractionated heparin, low-molecular-weight heparin (LMWH), and warfarin have been studied. More recently, two new agents have been developed that warrant discussion. Fondaparinux underwent a worldwide development program in orthopedic surgery for the prophylaxis of VTE. The program consisted mainly of four large, randomized, double-blind phase II studies comparing fondaparinux (SC), at a dose of 2.5 mg starting 6 hours postoperatively, with the two enoxaparin regimens approved for VTE prophylaxis—40 mg qd or 30 mg twice daily beginning 12 hours postoperatively. The results support a greater protective effect with fondaparinux, yielding a 55.2% relative risk reduction of VTE (Bauer et al., 2001; Eriksson et al., 2001; Lassen et al., 2002; Turpie et al., 2001, 2002; ). A European program of three large-scale clinical trials (MElagatran for THRombin inhibition in Orthopedic surgery [METHRO] I, II, and III, and EXpanded PRophylaxis Evaluation Surgery Study [EXPRESS]) (Eriksson et al., 2002a, b, 2003a, b) evaluated the safety and efficacy of subcutaneous melagatran followed by oral ximelagatran compared with LMWH for thromboprophylaxis following total hip replacement (THR) and total knee replacement (TKR) surgery.
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Sharif, Saima, Saira Rafaqat y Shagufta Naz. "Biomarkers of Metabolic Syndrome in Cardiomyopathy: A Leading Cause of Heart Failure". En New Insights on Cardiomyopathy [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.109381.
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Cardiomyopathy is a disease of the heart muscle, which makes the muscles harder to pump blood to the rest of the body leading to heart failure. The main types of cardiomyopathies include dilated cardiomyopathy, hypertrophic cardiomyopathy, ischemic cardiomyopathy, arrhythmogenic right ventricular dysplasia, restrictive cardiomyopathy, and Takotsubo cardiomyopathy. On the other hand, Metabolic syndrome (MetS) is the clustering of different medical conditions, which requires at least three of the five following diseases. These diseases are high blood sugar, high blood pressure, high serum triglycerides, low serum high-density lipoprotein, and central obesity. The risk of developing type 2 diabetes and cardiovascular disease associated with metabolic syndrome. In MetS, many different biomarkers are used in the early detection and risk stratification of MetS patients. It includes adiponectin, leptin, interleukin 6, tumor necrosis factor-alpha, uric acid, interleukin 10, ghrelin, adiponectin, paraoxonase, oxidized low-density lipoprotein, and plasminogen activator inhibitor-1. This chapter provides an overview and focuses on the basic role of major biomarkers of metabolic syndrome in the pathogenesis of different types of cardiomyopathies, which mainly highlights recent pathophysiological aspects in the development and progress of cardiomyopathy which is the leading cause of heart failure. In conclusion, biomarkers of metabolic syndrome play a significant role in the development and progress of cardiomyopathy which is the leading cause of heart failure.
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Weller, Peter F. "Eosinophilia". En Oxford Textbook of Medicine, editado por Chris Hatton y Deborah Hay, 5254–58. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0520.
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Eosinophilia (eosinophil count >0.45 × 109/litre) is associated with some infections, some allergic diseases, and a variety of other conditions, sometimes neoplastic. Parasitic diseases—eosinophilia is a characteristic feature of infection by multicellular helminth parasites (e.g. Strongyloides stercoralis) with diagnosis typically based on geographical/dietary history, serological tests, and examination of stool or tissues for parasite forms. Other diseases—eosinophilia can be caused by the fungal disease coccidioidomycosis, and modest eosinophilia may accompany retroviral infections such as HIV and HTLV-1. Common allergic diseases—asthma, rhinitis, and atopic dermatitis are associated with modest eosinophilia. Drug reactions—these are a frequent cause of eosinophilia, at times in reactions characterized by rashes and pyrexia. More severe reactions may also manifest with (1) pulmonary eosinophilia and lung infiltrates; (2) interstitial nephritis; (3) hepatitis; (4) myocarditis; (5) drug-induced hypersensitivity vasculitis; (6) gastroenterocolitis; and (7) DRESS syndrome. Other conditions—these include (1) eosinophilic granulomatosis with polyangiitis; (2) hyper-IgE syndromes; (3) chronic myeloid leukaemia, acute myeloid leukaemia, and lymphoma; (4) a variety of pulmonary, skin, gastrointestinal, and endocrine diseases. Hypereosinophilic syndromes are defined by (1) eosinophilia (>1.5 × 109/litre) sustained over a month, (2) lack of an identifiable cause precipitating a secondary eosinophilia, and (3) symptoms and signs of organ involvement. About 30% of patients will have either a myeloproliferative condition (chronic eosinophilic leukaemia) or hypereosinophilia mediated by clonal expansion of specific T cells producing interleukin-5 (IL-5). Treatment—patients without organ damage do not require treatment. Aside from supportive care, chronic eosinophilic leukaemia may respond to tyrosine kinase inhibitors (e.g. imatinib), and nonmyeloproliferative hypereosinophilic syndrome may respond to high-dose corticosteroids, with hydroxyurea, interferon-α or anti-IL-5 monoclonal antibody used in refractory cases.
Actas de conferencias sobre el tema "HIV, cardiovascular disease, interleukin-6"
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Hansen, Laura, Manu Platt, Roy L. Sutliff y Rudolph L. Gleason. "The Mechanical and Structural Effects of HIV Proteins on Murine Carotid Arteries". En ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53693.
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Acquired immunodeficiency syndrome (AIDS) is considered a global epidemic with over 65 million people worldwide infected with the HIV-1 virus, the causative agent [1]. The development of highly active antiretroviral therapy (HAART) has significantly increased the life expectancy of people infected with the virus by slowing the progression to the development of AIDS. However, the treatment has also led to the emergence of early onset cardiovascular complications including myocardial infarction [2] and atherosclerotic lesions [3], as well as subclinical markers of atherosclerosis including increased carotid artery intima-media thickness [4], increased arterial stiffness [5–6], and endothelial dysfunction [6]. It appears that HAART and HIV-1-infection are independent risk factors for the development of atherosclerosis in adults [7]; however, the mechanism of disease progression remains unclear. There is a pressing need to identify mechanisms of early on-set cardiovascular disease associated with HIV-1 infection and HAART and to identify therapeutic strategies to reduce cardiovascular disease in HIV patients. The overall goal of this study is to test the hypothesis that over-expression of HIV proteins will lead to alterations in the biomechanical properties of large arteries.
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Hansen, Laura, Manu O. Platt, Roy L. Sutliff y Rudolph L. Gleason. "The Mechanical and Structural Changes in Murine Arteries due to the Antiretroviral Drug Azidothymidine (AZT)". En ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80799.
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With over 33 million people infected with the human immunodefeciency virus (HIV-1), HIV-1 and autoimmune deficiency syndrome (AIDS) is a worldwide epidemic [1]. However, the development and widespread use of highly active antiretroviral therapy (HAART) has helped transform HIV-1 infection from a terminal disease leading to AIDS to a manageable chronic condition. With the increase in life expectancy, a new set of non-AIDS related complications has emerged including dyslipidemia, lipodystrophy, insulin resistance, diabetes mellitus, and cardiovascular disease (CVD) specifically high risks for myocardial infarction[2] and increased incidence of atherosclerosis [3]. Additionally, patients exhibit markers of subclinical atherosclerosis including endothelial dysfunction [4], carotid artery intima-media thickening [5], and arterial stiffening [4, 6].
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Cardoso, Alicia Marina, João Bosco Ramos Borges, Caroline Gomes de Almeida Rocha y Laura Alejandra Matulevich Santana. "CASTLEMAN DISEASE IN A PATIENT WITH AXILLARY LYMPH NODE ENLARGEMENT". En XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1016.
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Castleman disease represents a group of polyclonal lymphoproliferative entities. Based on clinicopathological associations, the disease can now be clinically divided into two subtypes: unicentric disease and multicentric disease. The multicentric Castleman disease (MCD) involves multiple lymph nodes from different anatomical sites and represents the other 25% of cases, occurring in 5 out of 1 million patients. MCD is multifactorial and can be subdivided according to its clinical association. It is known that interleukin 6 (IL6) plays an important role in the constitution of iMCD symptoms. The cause of the increase in IL6 is unknown. MCD is commonly associated with constitutional symptoms such as night sweats, weight loss, ascites, and pleural effusion. The treatment for MCD is based on the use of IL6 inhibitors. Consideration should be given to the severity of symptoms present to determine the intensity of targeted therapy. Cytotoxic chemotherapy may be a possibility in cases of the disease with severe organ dysfunction. Data from a systematic review published in 2012 of 404 cases of surgery in DC and demonstrated that there was no long-term benefit if patients in the MCD group underwent resective surgery. New prospective research data are needed to further assess the role of surgery in MCD. A female patient, 25 years old, born in Várzea Paulista, SP, came to the mastology outpatient clinic of the University Hospital of Jundiaí in May 2021 with a complaint of the appearance of a hardened nodule in the left breast for 9 months, with progressive increase, pain on palpation, daily afternoon fever, and weight loss of 6 kg in 2 months. A breast ultrasound showed lymph node enlargement in the left infraclavicular region. Physical examination showed good general condition, conscious, oriented, left axilla with the presence of hardened, enlarged, and mobile lymph nodes of approximately 8 cm. She was tested for HIV, syphilis, and hepatitis B and C negative. B2 microglobulin: 2.4. Core biopsy and immunohistochemistry (IHC) were performed on lymph node enlargement, and the result was inconclusive. Computed tomography of the thorax and abdomen: supraclavicular and infraclavicular and axillary lymph node enlargement on the left, measuring the largest 5.7×2.5 cm and 5.9×4.4 cm, some compressing the subclavian vein on the left; paraortic and prevascular mediastinal lymph node enlargement; and presence of inguinal adenomegaly. The patient was undergoing an excisional biopsy in October 2021, whose IHC showed histological aspects of atypical proliferation of epithelioid cells in the context of chronic lymphadenopathy with regression of germinal centers. Fungal research and BAAR were negative. Such lymphoid features are similar to those identified in Castleman disease, hyaline-vascular form. The association of histopathology data, IHC, clinical picture, and the exclusion of other differential diagnoses allowed us to obtain the diagnosis of iMCD. Because of its primordial manifestation in the left armpit, it was essential to differentiate between lymphoma and occult breast carcinoma, since these are more common diagnoses in clinical practice and have a similar initial clinical picture.
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Jan, Zala, Christian Gostečnik y Veronika Kralj-Iglič. "Adverse Human Health Outcomes Associated with Psychologi-cal Trauma: A review". En Socratic Lectures 7. University of Lubljana Press, 2022. http://dx.doi.org/10.55295/psl.2022.d7.
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Until 30 years ago it was believed that psychological stress increases cortisol secretion, but later stud-ies gave contradictory results. Decrease in cortisol levels in post-traumatic stress disorder (PTSD) reflects a nonnormative and inadequate response to severe stressors, with its pathophysiology in-volving maladaptation or dysfunction in stress-regulatory systems. To have more insights in re-sponse of human body to physiological stress, inflammatory signals, oxidative stress parameters and other health parameters were measured. As for the cortisol level results, also inflammatory signals, including proinflammatory and anti-inflammatory cytokines and C-reactive protein (CRP), have been reported to increase and decrease in PTSD. Levels of interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, tumour necrosis factor (TNF)-α, interferon gamma (IFN-γ) and CRP were reported higher and lower in blood samples of individuals with PTSD. Some studies report that dysregulation of the stress axis could have direct effects on brain regions responsible for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Early-life stress, such as child-hood adversity (abuse, neglect, or family disfunction), is a potent risk factor for developing PTSD in response to later trauma, and elevated peripheral markers of inflammation are one of the best-repli-cated findings in children and adults with early-life stress. Those who develop PTSD may have an inability or failure to activate an innate immune response. PTSD can also result in other adverse outcomes, such as heightened oxidative stress (OXS), eating disorders, metabolic disorder, and car-diovascular disease (CVD). Since the results are very contradictory for PTSD and inflammation re-sponse of the human body, further research is important. Small cellular particles that can be isolated from body fluids present potential biomarkers of the clinical status and will be considered in plan-ning the future research. This contribution presents perspectives in assessment of psychological stress by objective parameters. Keywords: Cortisol; Post-traumatic stress disorder; Inflammatory response; Oxidative stress; Cyto-kines; Eating disorders; Metabolic disorder; Cardiovascular disease; Small cellular particles as stress markers, Extracellular vesicles as stress markers