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)

Myocarditis is a common occurrence among patients infected with human immunodeficiency virus (HIV). However, it is rare to find HIV-associated myocarditis presenting as ST-segment elevation myocardial infarction with cardiogenic shock. A case of HIV-related myocarditis presenting as an acute inferolateral wall myocardial infarction in a 32-year-old male is described.
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PMID:HIV Myocarditis Presenting as Acute ST-Segment Elevation Myocardial Infarction. 1903 30

Human immunodeficiency virus (HIV)-infected patients are at a significantly higher risk from coronary heart diseases (CHD) and myocardial infarction (MI) compared to gender- and age-matched non-infected individuals. Combination antiretroviral therapy (cART) has transformed a fatal illness into a chronic stable condition. However, cART induces metabolic abnormalities in HIV-infected patients, while its role in vascular atherosclerosis is still under investigation. The use of cART is linked to inflammation - a key mechanism in atherosclerotic progression and destabilisation that precedes clinical events like MI. There is evidence of visceral fat abnormal distribution in HIV infected patients, and inflammatory changes in HIV infected patients drive the initiation, progression and, ultimately, thrombotic clinical complications induced by atherosclerosis. Visceral adipose tissue, a virtual factory for manufacturing pro-inflammatory mediators, affects the liver function. The inflamed liver promotes the development of pro-atherogenic dyslipidaemia. Pro-inflammatory cytokines released by adipocytes travel to the skeletal muscles and other peripheral tissues, worsening insulin sensitivity and leading to hyperglycaemia. Increased high sensitivity C-reactive protein (hs-CRP) inflammatory marker is associated with endothelial dysfunction in HIV-infected patients. Increased levels of monocytic nuclear factor kappa-B (NFkappa-B), a master switch in the inflammatory cascade, are documented in patients with elevated hs-CRP levels. It can be assumed that, as a result of NFkappa-B activation, hs-CRP up-regulates cytokines that contribute to MI by recruiting leukocytes and promoting thrombosis. This review focuses on the association of HIV-infection, metabolic abnormalities and known mechanisms involved in inducing accelerated atherosclerosis and inflammation in HIV-infected patients, as well as the role of lipid lowering agents in potentially preventing CHD.
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PMID:Metabolic-inflammatory changes, and accelerated atherosclerosis in HIV patients: rationale for preventative measures. 1907 47

Myocardial infarction causes a high rate of morbidity and mortality worldwide, and heat shock proteins as molecular chaperones have been attractive targets for protecting cardiomyoblasts under environmental stimuli. In this study, in order to enhance the penetration of heat shock protein 27 (HSP27) across cell membranes, we fused HSP27 with transcriptional activator (TAT) derived from human immunodeficiency virus (HIV) as a protein transduction domain (PTD). We loaded the fusion protein (TAT-HSP27) into microsphere/hydrogel combination delivery systems to control the release behavior for prolonged time periods. We found that the release behavior of TAT-HSP27 was able to be controlled by varying the ratio of PLGA microspheres and alginate hydrogels. Indeed, the released fusion protein maintained its bioactivity and could recover the proliferation of cardiomyoblasts cultured under hypoxic conditions. This approach to controlling the release behavior of TAT-HSP27 using microsphere/hydrogel combination delivery systems may be useful for treating myocardial infarction in a minimally invasive manner.
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PMID:Controlled delivery of heat shock protein using an injectable microsphere/hydrogel combination system for the treatment of myocardial infarction. 1937 30

Patients with human immunodeficiency virus (HIV) who undergo percutaneous coronary intervention have a substantial risk of subsequent cardiovascular events. However, outcome data from HIV-infected patients who receive drug-eluting stents (DESs) are limited. We hypothesized that HIV-infected patients treated with DESs would have fewer recurrent cardiac events compared with those who receive bare metal stents (BMSs). We evaluated 97 HIV-infected patients and 97 non-HIV control patients who had undergone percutaneous coronary intervention between January 2000 and July 2007. Clinical, laboratory, and angiographic data were obtained by chart review. Major adverse cardiovascular events (MACE), defined as clinically driven coronary revascularization, nonfatal myocardial infarction, and cardiovascular death, were adjudicated by 2 independent physicians. The mean age of the HIV cohort was 53 years, and all patients were men. Compared with non-HIV patients, HIV-infected patients were less likely to have hypertension, diabetes mellitus, and previous coronary artery disease and were more likely to have been treated with longer stent length and more stents. During a mean follow-up of 3.1 years, patients who received a DES had a lower rate of MACE compared with those who had received a BMS, regardless of HIV status. After multivariate adjustment for baseline characteristic differences, non-HIV-DES patients had 65% fewer MACE and HIV-DES patients had 60% fewer MACE compared with non-HIV-BMS patients. In conclusion, these data suggest that treatment with DESs in the HIV population is safe and efficacious.
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PMID:Comparison of outcomes using bare metal versus drug-eluting stents in coronary artery disease patients with and without human immunodeficiency virus infection. 1957 50

BACKGROUND. The risk of myocardial infarction (MI) in patients with human immunodeficiency virus (HIV) infection has been assessed in 13 anti-HIV drugs in the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study. METHODS. Poisson regression models were adjusted for cardiovascular risk factors, cohort, calendar year, and use of other antiretroviral drugs and assessed the association between MI risk and cumulative (per year) or recent (current or in the past 6 months) use of antiretroviral drugs, with >30,000 person-years of exposure. RESULTS. Over 178,835 person-years, 580 patients developed MI. There were no associations between use of tenofovir, zalcitabine, zidovudine, stavudine, or lamivudine and MI risk. Recent exposure to abacavir or didanosine was associated with an increased risk of MI. No association was found between MI risk and cumulative exposure to nevirapine, efavirenz, nelfinavir, or saquinavir. Cumulative exposure to indinavir and lopinavir-ritonavir was associated with an increased risk of MI (relative rate [RR] per year, 1.12 and 1.13, respectively). These increased risks were attenuated slightly (RR per year, 1.08 [95% confidence interval {CI}, 1.02-1.14] and 1.09 [95% CI, 1.01-1.17], respectively) after adjustment for lipids but were not altered further after adjustment for other metabolic parameters. CONCLUSIONS. Of the drugs considered, only indinavir, lopinavir-ritonavir, didanosine, and abacavir were associated with a significantly increased risk of MI. As with any observational study, our findings must be interpreted with caution (given the potential for confounding) and in the context of the benefits that these drugs provide.
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PMID:Risk of myocardial infarction in patients with HIV infection exposed to specific individual antiretroviral drugs from the 3 major drug classes: the data collection on adverse events of anti-HIV drugs (D:A:D) study. 2003 4

Cardiovascular disease has been frequent in HIV-infected patients both before and after the advent of antiretroviral therapy (HAART). The pathogenic basis for the increase of cardiovascular disease, in particular myocardial lesions, may involve HIV-1 itself or other mechanisms including endothelial dysfunction, activation of proinflammatory cytokines, and changes in platelets, which lead to atherosclerotic lesions of blood vessels. In the last decade, among the proinflammatory cytokines, interleukin 18 seems to play a central role in the inflammatory cascade, leading to development of atherosclerotic disease and the occurrence of ischemic heart disease in uninfected HIV-1 people. Increased levels of interleukin 18 were observed in HIV-1 infected patients. This review attempts to evaluate the role of interleukin 18 in cardiovascular disease, especially in myocardial infarction, in HIV-1 infection, as well as the relationship between interleukin 18 and atherosclerotic plaque formation. Two other characteristic aspects in HIV-1 infection, metabolic syndrome and lipodystrophy, will be evaluated in light of activity of interleukin 18. Moreover, the role of platelets and interleukin 18 as an important linkage between chronic inflammation, endothelial dysfunction, and atherogenesis will be highlighted. Finally, experimental an animal model of rhesus macaques infected with simian immunodeficiency virus clearly demonstrates the involvement of interleukin 18 in myocardial lesions, and that circulating levels of interleukin 18 are important predictors of coronary heart disease. In conclusion, interleukin 18 may be considered a partner in crime with other factors, including endothelial dysfunction, increased expression and production of adhesion molecules and proinflammatory cytokines in determining cardiovascular disease.
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PMID:Interleukin 18 and cardiovascular disease in HIV-1 infection: a partner in crime? 2021 8

Thrombotic thrombocytopenic purpura (TTP) has been associated with human immunodeficiency virus (HIV) infection. With the high prevalence of HIV in sub-Saharan Africa, HIV-associated TTP is the most common form of this disease seen in the South African population. Several case reports describe myocardial infarction in HIV-negative TTP patients. The case of the first HIV-positive patient who presented with clinical signs and symptoms of TTP and myocardial injury is reported in this study. A patient with fragmentation haemolysis and thrombocytopenia presented with angina. Risk factors for ischaemic heart disease were absent. An electrocardiogram (EKG) revealed ST-segment elevation and a significantly raised Troponin T level. The patient's HIV test was positive and a diagnosis of myocardial injury with HIV-associated TTP was made. The patient was treated with plasma infusion and steroid therapy. Due to poor response, the therapy was changed to plasma exchange. The patient recovered fully and subsequent coronary angiography revealed normal coronary vessels. Treatment of myocardial infarction in TTP is controversial, but the treatment cornerstone should remain plasma infusion or plasma exchange. As patients are often young and do not have the classical risk factors of ischaemic heart disease, a high level of suspicion and routine exclusion of myocardial ischaemia in these patients are advised.
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PMID:Myocardial injury in HIV-associated thrombotic thrombocytopenic purpura (TTP). 2040 74

Patients with lymphoma can develop cardiac involvement that includes malignant pericardial effusions and myocardial infiltration, but extensive myocardial invasion by tumor with resultant rupture has been reported only rarely. We report a case of a patient with human immunodeficiency virus and T-cell lymphoma who presented with signs and symptoms that were suggestive of a non-ST-elevation myocardial infarction. Plans were made for cardiac catheterization, but the patient developed thrombocytopenia after the initiation of heparin and eptifibatide. Cardiac catheterization was deferred, and shortly afterwards he had a witnessed cardiac arrest in the hospital and could not be resuscitated. Autopsy revealed transmural infiltration of the myocardium with lymphoma and resultant rupture of the left ventricular free wall. To our knowledge, this is the 1st reported case of left ventricular free-wall rupture due to transmural infiltration by human-immunodeficiency-virus-associated peripheral T-cell lymphoma.We conclude that noncoronary causes of chest pain, including direct myocardial infiltration, should be considered in immunocompromised patients with lymphoma.
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PMID:Left ventricular rupture due to HIV-associated T-cell lymphoma. 2084 22

Hyper-immunoglobulin E recurrent infection syndromes (HIES) have distinct features, with identified associated mutations of STAT3, TYK2, and DOCK8. Among 197 Taiwanese patients with primary immunodeficiency on a referral-base of over 23 million inhabitants, STAT3 (R382W and Q469R) and DOCK8 mutations (exon 1-9 deletion) were identified in two patients each from six AD-HIES and five AR-HIES patients, respectively. Aside from decreased Th17 and memory B cells, characteristic facies and pneumatocele were not mutually exclusive regardless of STAT3 and DOCK8 mutations. One with novel DOCK8 deletion had notable cytomegalovirus retinitis, cerebral vasculitis, lead deposition, and amenorrhea. In adolescence, three AD-HIES patients without STAT3 mutation died of myocardial infarction, staphylococcus sepsis, and proteus sepsis while receiving chemotherapy for lymphoma. Close follow-up of the HIES phenotype rather than identifying genetic mutations should be the cornerstone of intervention at this juncture because of relatively lower percentage of identifying mutations in Taiwanese HIES (4/11; 36.5%).
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PMID:Clinical, immunological and genetic features in Taiwanese patients with the phenotype of hyper-immunoglobulin E recurrent infection syndromes (HIES). 2132 46

With increasing life expectancy due to highly active antiretroviral therapy (HAART), the spectrum of human immunodeficiency virus (HIV)-associated morbidity and mortality has shifted from opportunistic infections toward associated chronic medical conditions. We report on a 26-year-old female patient receiving HAART for HIV infection, who developed spontaneous thrombosis of the proximal left anterior descending (LAD) artery, resulting in acute ST-elevation myocardial infarction. She had none of the conventional risk factors for the development of coronary artery disease. Following diagnostic coronary angiography that showed a large (16x3.4 mm) spontaneous thrombus in the proximal LAD artery, percutaneous coronary intervention was performed with prior aspiration of the occluding thrombus and implantation of a bare-metal stent. The patient was discharged with instruction of appropriate medical therapy. This case highlights the association between immunosuppression with HAART, particularly protease inhibitors, and the development of accelerated atherosclerosis in patients with HIV infection.
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PMID:ST-elevation myocardial infarction due to a spontaneous thrombus in the left anterior descending artery in a young HIV-infected patient. 2164 32


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