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)

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation. The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status. During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.
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PMID:Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University. 1207 15

The incidence of myocardial infarction in patients who have the aquired immunodeficiency syndrome (AIDS) is increasing. However, no effective therapeutic agents have been discovered to reduce myocardial ischemia-reperfusion (I/R) injury in pathologies associated with AIDS. The aim of this study was to determine if infarct size is increased in murine AIDS after I/R injury and if I/R injury could be attenuated with vitamin E supplementation. Three groups of mice were studied: control, murine AIDS, and murine AIDS with vitamin E supplementation. Anesthetized mice were subjected to 30 min of left anterior descending coronary artery occlusion and 120 min of reperfusion. The hearts in mice that had murine AIDS had a larger infarct size compared to controls after I/R injury. Vitamin E supplementation significantly reduced infarct size and inhibited polymorphonuclear neutrophil (PMN) CD11b expression (p < 0.05). However, vitamin E supplementation did not affect PMN reactive oxygen species (ROS) production and platelet CD62p expression. These results suggest that the reduction of myocardial I/R injury with vitamin E supplementation may be the result of the inhibition of PMN CD11b expression. Vitamin E may be a promising prophylactic agent for the reduction of the severity of myocardial I/R injury in patients who have AIDS.
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PMID:Vitamin E attenuates myocardial ischemia-reperfusion injury in murine AIDS. 1227 Nov 55

Scientific analyses fortified by interpretations of immunodeficiency diseases as 'experiments of nature' have revealed the specific immune systems to be comprised of T cells subserving cell-mediated immunities plus B cells and plasma cells which produce and secrete antibodies. These two separate cellular systems regularly interact with each other to produce a coordinated defense which permits mammals to live within a sea of microorganisms that threaten the integrity and the survival of individuals. We have shown that bone marrow transplantation (BMT) can be used as a form of cellular engineering to construct or reconstruct the immune systems and cure otherwise fatal severe combined immunodeficiency. When severe aplastic anemia complicated the first BMT which was performed to cure a fatal severe combined immunodeficiency, a second BMT cured for the first time a complicating severe aplastic anemia. Subsequently, BMT has been used effectively to treat some 75 otherwise fatal diseases such as resistant leukemias, lymphomas, inborn errors of metabolism, and genetic anomalies of the hematopoietic development such as sickle cell anemia, thalassemia, congenital neutropenias, and many other diseases. More recently, we have employed BMT in mice both to cure and cause autoimmunities, and, together, these experiments showed that autoimmunities actually reside in the hematopoietic stem cells. We have also found that mixed BMT or mixed hematopoietic stem cell transplantation (HSCT) can be used to prevent and cure the most complex autoimmunities such as those occurring in BXSB mice and in (NZW x BXSB)F1 W/BF1 mice. Untreated, the former develop fulminating lethal glomerulonephritis plus numerous humoral autoimmunities. Mice of the (W/B)F1 strain develop autoimmune thrombocytopenic purpura, coronary vascular disease with myocardial infarction, glomerulonephritis, and numerous autoantibodies. All of these abnormalities are prevented or cured by mixed syngeneic (autoimmune) plus allogeneic (normal healthy) BMT or mixed peripheral blood HSCT. Thus, the most complex autoimmune diseases can be prevented or cured in experimental animals by mixed syngeneic plus allogeneic BMT or HSCT which produce stable mixed chimerism as a form of cellular engineering.
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PMID:Mixed bone marrow or mixed stem cell transplantation for prevention or treatment of lupus-like diseases in mice. 1238 26

Worldwide, human immunodeficiency virus (HIV) infection is one of the main health subjects. Even, the human immunodeficiency virus primarily effects the immune system, HIV infection also has an impact on other organs. Cardiovascular manifestations in HIV-infected patients could occur by the HI-virus itself or by opportunistic infections. Reports of myocardial infarction in young HIV-infected patients, who received protease inhibitors, have raised concerns about premature arteriosclerosis and coronary artery disease in this population. In the pre-protease inhibitor era, autopsy reports were the first to describe an association between coronary artery disease and HIV infection. Long-term antiretroviral therapy, including protease inhibitors, significantly reduced mortality, morbidity and revolutionized the care of HIV-infected patients. However, class-specific metabolic side effects, such as elevated total cholesterol and triglyceride levels and insulin resistance, have been described. These metabolic alterations of antiretroviral therapy impair the cardiovascular risk profile of HIV-infected patients. Even epidemiological studies found no significant effect of antiretroviral treatment type on coronary heart disease or myocardial infarction, an increase of arteriosclerosis in HIV-infected patients is suspected. Recent results of autopsy studies and analyses of endothelial function in patients with HIV infection described an effect of HIV and antiretroviral therapy on premature arteriosclerosis. The present article gives an overview about arteriosclerosis and coronary events in HIV-infected patients and the impact of antiretroviral therapy.
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PMID:[Atherosclerosis in HIV-positive patients]. 1244 90

Studies describing posttraumatic stress disorder (PTSD) as a result of physical illness and its treatment were reviewed. PTSD was described in studies investigating myocardial infarction (MI), cardiac surgery, haemorrhage and stroke, childbirth, miscarriage, abortion and gynaecological procedures, intensive care treatment, human immunodeficiency virus (HIV) infection, awareness under anaesthesia, and in a group of miscellaneous conditions. Cancer medicine was not included as it had been the subject of a recent review in this journal. Studies were reviewed in terms of the prevalence rates for PTSD, intrusive and avoidance symptoms, predictive and associated factors and the consequences of PTSD on healthcare utilization and outcome. There was considerable variability both in the study methodology and design and in the results. The highest prevalence rates were identified in patients treated in intensive care units (ICUs) and those with HIV infection. Irrespective of the physical illness, posttraumatic symptomatology is more common than PTSD caseness. Existing characteristics of the patient may well predispose individuals to the development of PTSD as do other factors such as poor social support and negative interactions with healthcare staff. Generally, the severity of the illness itself is not predictive of PTSD. Issues relating to sampling, attrition, diagnosis, the course of symptoms, aetiological pathways, and the consequences of the disorder are discussed. The presence of PTSD most probably influences the patient's use of healthcare resources and may affect their clinical outcome.
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PMID:Posttraumatic stress disorder following medical illness and treatment. 1272 79

The article describes the clinical, virological and immunological data confirming the etiological role of herpes virus in the initiation of atherosclerosis. 226 patients with atherosclerosis of the predominantly coronary localization were examined; hypertension and stenocardia were found in a part of them, while myocardial infarction was diagnosed in 22% of the patients. The control group consisted of patients with other diseases related with infections (bronchial asthma, rheumatism etc.) as well as of healthy persons. A total of 558 patients were examined and it was established that there is a reliable relation between atherosclerosis and the infection of patients with, mainly, herpes virus. The correlation was of the seasonal nature, it was linked to the specific features of an infection process and it was confirmed by the condition of the cholesterol supply and by immunodeficiency in patients. The infectious nature of atherosclerosis demands further research for the sake of finding proof of the etiological role of viruses and bacteria and for the sake of working out the means of prophylaxis and treatment of atherosclerosis aimed at removing the infectious etiological factor.
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PMID:[Role of viral-herpetic infections in the etiology of atherosclerosis: clinical, virological and immunological evidence]. 1274 52

Protease inhibitor (PI) therapy for patients infected with the human immunodeficiency virus has been associated with lipid disorders and insulin resistance. We compared the incidence of myocardial infarction (MI) among participants receiving treatment with PIs with or without nucleoside reverse transcriptase inhibitors (nRTIs) to nRTI therapy alone in 30 phase II/III double-blind, randomized studies conducted before 1999 for the first 4 PI drugs. In most trials included in this analysis, participants could receive combination therapy with a PI plus nRTIs in open-label extensions after the blinded phase concluded. Person-years (PY) of follow-up were calculated from treatment initiation to the diagnosis of MI, or to the end of the randomized phases for nRTI-only therapy or to the conclusion of the studies for PI-containing regimens. Separate analyses were conducted for the randomized and the randomized-plus-extension phases. Among 10,986 participants, 7951 (72%) received PI drugs at some point for an average duration of 12 months. There were 10 MIs (1.31/1000 PY) in the randomized phases and 19 MIs (1.63/1000 PY) in the randomized-plus-extension phases. The overall stratified relative risk of MI for PI-containing (1.82 MI/1000 PY) versus nRTI-only (1.05 MI/1000 PY) regimens of 1.69 was not significantly increased (95% confidence interval [CI], 0.54 to 7.48). The absolute difference in MI risk was +0.77 (95% CI, -0.71 to +2.26) MIs/1000 PY. Compared with NRTI-only therapy, patients receiving PI-containing regimens for an average of 1 year did not have significantly more MIs, but the upper bound of the 95% CI indicates there may be up to 2.3 additional MIs per 1000 PY. Although studies with a longer duration of PI therapy are in progress to assess whether a later increase in MI incidence occurs, our analysis did not demonstrate a dramatic increase in MI risk during the first year of PI therapy.
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PMID:Incidence of myocardial infarction in randomized clinical trials of protease inhibitor-based antiretroviral therapy: an analysis of four different protease inhibitors. 1288 53

Worldwide, infection with the human immunodeficiency virus (HIV) is increasing. At the same time, new treatments allow patients to live longer. Consequently, cardiovascular manifestations, most of which occur relatively late in the course of the infection, are becoming more frequent. Pericardial effusion, the most common cardiovascular manifestation of HIV infection, usually is small and causes no hemodynamic compromise or symptoms. It does, however, augur a grim prognosis, as do other cardiovascular conditions associated with the infection: myocarditis, dilated cardiomyopathy, pulmonary arterial hypertension, cardiac lymphoma, and Kaposi's sarcoma of the heart. Highly active antiretroviral therapy (HAART), especially when incorporating protease inhibitors, greatly improves overall outlook in these patients, but appears not only to cause a lipodystrophic syndrome, but to accelerate atherosclerotic cardiovascular disease by inducing glucose intolerance, frank diabetes mellitus, hypertriglyceridemia, hypercholesterolemia, increased lipoprotein (a), and decreased HDL cholesterol. Recent ongoing prospective trials also are showing an association of HAART with increased coronary artery disease and myocardial infarction.
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PMID:Cardiovascular disease in patients infected with the human immunodeficiency virus. 1475 Jul 51

We analyzed the spectrum of clinical features related to antiphospholipid syndrome (APS) in patients with chronic viral infections, such as hepatitis C virus (HCV) infection and human immunodeficiency virus (HIV) infection. We selected patients from the HISPAMEC registry who repeatedly tested positive for antiphospholipid antibodies (aPL) and who had features of APS, and we searched the MEDLINE database for additional cases. A total of 82 patients were included (45 had chronic HCV infection, 32 had HIV infection, and 5 had HCV-HIV coinfection). The main features of APS were avascular bone necrosis (20 patients), peripheral thrombosis (17), thrombocytopenia (15), neurologic features (13), cardiac manifestations (12), pulmonary embolism (9), gastrointestinal manifestations (8), and cutaneous manifestations (8). The main APS-related features in HCV-infected patients were intraabdominal thrombosis and myocardial infarction, whereas, in HIV-infected patients, the main features were avascular bone and cutaneous necrosis. These viruses might act in some patients as chronic triggering agents that induce a heterogeneous, atypical presentation of APS.
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PMID:Clinical features related to antiphospholipid syndrome in patients with chronic viral infections (hepatitis C virus/HIV infection): description of 82 cases. 1503 35

Highly active antiretroviral therapy (HAART) has dramatically improved the life expectancy of patients with human immunodeficiency virus (HIV). Specific toxicities cited for HAART include elevations in serum levels of total cholesterol and triglycerides, reduction in high-density lipoprotein cholesterol, alterations in the distribution of body fat, increases in insulin resistance, and diabetes, which are major risk factors for cardiovascular disease (CVD). The majority of the studies examining the incidence of CV events demonstrated an increase in CV event rate with HAART in the HIV-infected population. Overall, the CVD risk appears to be greater in the HIV-infected population than in the general population, and the increased CV risk is associated with HAART, particularly with protease inhibitor use. Despite the relative risk (RR) for CVD being significantly high (the hazard ratio for myocardial infarction ranging between 1.3 and 7.1), the absolute risk for CVD remains low, with the CV event rates ranging between one and seven events per 1000 person-years. Although there is general consensus that the benefits of HAART far outweigh toxicity-related risks of the treatment with HAART, prolonged survival among HIV-infected patients will likely support the use of different antiretroviral regimens with potentially less CV toxicity in the future.
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PMID:Cardiovascular toxicity with highly active antiretroviral therapy: review of clinical studies. 1547 Feb 72


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