Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence and incidence of left ventricular (LV) dysfunction was examined in patients infected with the human immunodeficiency virus (HIV). Sixty-nine randomly selected patients diagnosed with HIV infection who were followed in HIV clinics were prospectively evaluated by 2-dimensional echocardiography. Mean follow-up duration was 11 months. Additionally, 39 consecutive HIV-infected patients referred to the Cardiomyopathy Service and found to have LV dysfunction by 2-dimensional echocardiography were also studied. Of the 39 referred patients, 34 (87%) were referred for recent onset, unexplained, congestive heart failure. During this time, the HIV clinic population comprised 1,819 alive and actively followed patients; the 39 cardiomyopathy referrals therefore constituted a crude rate of 2.1% for this population. Of the 69 prospectively studied patients without clinical heart disease, a 14.5% prevalence of global LV hypokinesia and an incidence of 18%/patient-year were found. During a maximal 18-month follow-up period, 4 prospective patients (5.8%) developed symptoms of congestive heart failure. A greater proportion of prospective and referred patients with LV dysfunction had CD4 counts < 100/mm3 (62 and 79%, respectively) than did that of those without LV dysfunction (35%). In conclusion, the high rate of unexpected LV dysfunction in this HIV-infected population suggests that early cardiac contractile abnormalities may involve a significant number of patients, most of whom have low CD4 counts. A subgroup of these patients appears to progress to symptomatic congestive heart failure.
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PMID:Prevalence and incidence of left ventricular dysfunction in patients with human immunodeficiency virus infection. 846 88

Infection and fever evoke a cytokine-mediated host response resulting in negative nitrogen balance, muscle protein degradation, which includes the skeletal muscles as well as the heart muscle, and deteriorated muscle function. Physical training has an opposite effect. Moderate physical training also stimulates the immune system, whereas exhaustive and longlasting exercise is followed by a temporary immunodeficiency and an increased susceptibility to respiratory tract infections. Exercise in the acute phase of an infection may promote complications including myocarditis. Exercise in myocarditis is associated with increased organism-associated as well as immune mediated tissue damage. An increased sudden death (SUD) rate among young Swedish male orienteers existed in 1979-92, suggesting (a) common underlying cause(s). Myocarditis was one of the most conspicuous histopathological features. Chlamydia pneumoniae, or a similar organism cross reacting in diagnostic tests, is hypothesized to be a factor causing this increased death rate. High frequency of intense exercise sessions, which was a common practice among the deceased, may have been immunosuppressive, promoting the development of severe myocardial disease.
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PMID:Interaction between infection and exercise with special reference to myocarditis and the increased frequency of sudden deaths among young Swedish orienteers 1979-92. 925 81

The heart is frequently involved in the acquired immunodeficiency syndrome (AIDS). This study was planned to assess the prevalence of cardiac involvement in a large and selected population of patients who died of AIDS. Of 440 AIDS patients who underwent autopsy, cardiac involvement was documented in 82 patients. Dilated cardiomyopathy was found in 12 patients; lymphocytic interstitial myocarditis was documented in 30 patients, and in 10 of 12 patients with dilated cardiomyopathy. Inflammatory infiltrate was predominantly composed by CD3+ and CD8+ with a positive staining for major histocompatibility class I in 70% of the cases. Infective endocarditis was documented in 28 patients, pericardial effusion in 53 patients, myocardial Kaposi's sarcoma in 2 patients, myocardial B-cell immunoblastic lymphoma in 1 patient. Sequences of human immunodeficiency virus (HIV) nucleic acid were detected using the technique of in situ hybridization in the myocytes of 29 autopsy patients and in 25 of 29 patients with a positive hybridization signal an active myocarditis was documented. Among them, 7 presented a coinfection with Coxsakievirus group B, 2 with Epstein-Barr virus, and 1 with cytomegalovirus. HIV-associated cardiomyopathy may be related either to a direct action of HIV on the myocardial tissue or to an autoimmune process induced by HIV even in association with other cardiotropic viruses.
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PMID:Cardiac involvement in the acquired immunodeficiency syndrome: a multicenter clinical-pathological study. Gruppo Italiano per lo Studio Cardiologico dei pazienti affetti da AIDS Investigators. 971 23

We report on two sibs and two other unrelated patients with agenesis of corpus callosum, oculocutaneous albinism, repeated infections, and cardiomyopathy. All manifested postnatal growth retardation, microcephaly, and profound developmental delay. Additional central nervous system anomalies present in at least one patient included hypoplasia of the cerebellar vermis, white matter neuronal heterotopia, or bilateral schizencephaly. Repeated viral, bacterial, and fungal infections were consistent with a primary immunodeficiency. However, immunological studies showed variable, nonspecific findings. Cardiomyopathy with progressive heart failure or infection led to death before age 2 years in three of the patients. This syndrome was first described by Vici et al. [1988: Am. J. Med. Genet. 29:1-8]. The four patients reported herein confirm this unique disorder. Affected sibs of both sexes born to unaffected parents provide evidence for autosomal recessive inheritance.
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PMID:Albinism and agenesis of the corpus callosum with profound developmental delay: Vici syndrome, evidence for autosomal recessive inheritance. 1040 46

The frequency and factors associated with cardiomyopathy were studied among inner-city hospital patients with human immunodeficiency virus (HIV) infection. Of 84 patients with HIV infection, 20 (24%) had cardiomyopathy. Fourteen (70%) of the patients with cardiomyopathy did not have clinical evidence of congestive heart failure. There was no significant association between cardiomyopathy and common opportunistic infections or zidovudine treatment. These results indicate that cardiomyopathy is common in patients with HIV infection and often is clinically unsuspected.
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PMID:Frequency and factors associated with cardiomyopathy in patients with human immunodeficiency virus infection in an inner-city hospital. 1051 69

A 27-year-old woman with the acquired immunodeficiency syndrome and endocervical Chagas' disease is reported. The patient was a cocaine addict, and her sexual partner was also human immunodeficiency virus (HIV)-positive. Her past medical history included a son who died 3 days after birth due to congenital Chagas' disease. Seven years later, through a cervical biopsy, a reactivation of Chagas' disease was diagnosed. Giant cells with typical amastigotes were seen; they strongly stained with antibodies against Trypanosoma cruzi. The patient died 5 months later of an acute chagasic myocardiopathy. To our knowledge, this is the first report of this parasitosis in the cervix uteri.
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PMID:Chagas' disease of the cervix uteri in a patient with acquired immunodeficiency syndrome. 1066 23

The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion of taurine has been linked to developmental defects, retinal damage, immunodeficiency, impaired cellular growth and the development of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably very important.
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PMID:Interaction between the actions of taurine and angiotensin II. 1094 14

Human immunodeficiency virus (HIV) infection is associated with a surprisingly high frequency of myocardial dysfunction. Potential mechanisms include direct effects of HIV, indirect effects mediated by cytokines, or a combination. We have previously reported that interleukin-1beta (IL-1beta) (500 U/ml) alone induced nitric oxide (NO) production by neonatal rat cardiac myocytes (CM). Effects of the HIV-1 envelope, glycoprotein120 (gp120), on inducible NO synthase (iNOS) in CM have not been previously reported. Unlike IL-1beta, recombinant HIV-gp120 (1 microgram/ml) alone failed to enhance NO production in CM (0.5 +/- 0.4 vs. 0.4 +/- 0.5 micromol/1.25 x 10(5) cells/48 h, gp120 vs. control, respectively; n = 12, P = not significant). However, the addition of gp120 to IL-1beta significantly enhanced iNOS mRNA expression (70 +/- 1.5 vs. 26 +/- 2.4 optical units, IL-1beta + gp120 vs. IL-1beta, respectively; n = 3), iNOS protein synthesis (42 +/- 1.4 vs. 18 +/- 0.8 optical units, IL-1beta + gp120 vs. IL-1beta, respectively; n = 3), and NO production (NO(2)(-)) (6.6 +/- 0.6 vs. 4.1 +/- 0.8 micromol/1.25 x 10(5) cells/48 h, IL-1beta + gp120 vs. IL-1beta, respectively; n = 12, P </= 0.5). HIV-gp120 enhancement of IL-1beta-induced NO(2)(-) production was blocked by 10 microM of SB-203580 (SB), a selective p38 protein kinase inhibitor (3.6 +/- 0.2 vs. 6.6 +/- 0.6 micromol/1. 25 x 10(5) cells/48 h, IL-1beta + gp120 + SB vs. IL-1beta + gp120, respectively; n = 12, P </= 0.5). HIV-gp120-enhanced p38 protein kinase activity was associated with an increase in IL-1beta-stimulated NF-kappaB activity (184 +/- 12.7 vs. 92 +/- 10.7 optical units, IL-1beta + gp120 vs. IL-1beta, respectively; n = 3). None of these effects was seen with another recombinant HIV-1 protein, Tat. Thus HIV-gp120 enhancement of IL-1beta-induced NO production is associated with p38-mediated activation of NF-kappaB. Direct effects of HIV-gp120 on CM may provide a previously unrecognized mechanism contributing to HIV cardiomyopathy.
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PMID:HIV gp120 enhances NO production by cardiac myocytes through p38 MAP kinase-mediated NF-kappaB activation. 1108 73

Opportunistic infections are a major source of morbidity and mortality in children and adults infected with human immunodeficiency virus (HIV). In addition, organ-specific complications of HIV infection, such as cardiomyopathy, nephropathy, encephalopathy, and others, contribute substantially to the morbidity and mortality associated with HIV infection. Highly active antiretroviral therapy (HAART) has produced a dramatic decline in the incidence of opportunistic infections among patients with HIV infection. Nevertheless, there is very little information concerning the value of HAART for organ-specific complications of HIV infection. In this report, we describe 3 children with HIV infection in whom the dominant clinical manifestations were cardiomyopathy, red cell aplasia, and nephropathy. HAART produced a decrease in the HIV ribonucleic acid level, an increase in the CD4 cell count, and resolution of the organ-specific complications in all patients. These cases add to our knowledge concerning the benefits of HAART for children with HIV infection.
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PMID:Resolution of organ-specific complications of human immunodeficiency virus infection in children with use of highly active antiretroviral therapy. 1117 Sep 55

With the advent of more effective therapies for human immunodeficiency virus (HIV) infection, HIV-infected patients are living longer and cardiovascular disease is becoming more obvious in this population. Patients with HIV infection represent one of the most rapidly developing groups with cardiovascular disease globally. Cardiovascular disease complicating HIV infection is likely to contribute to burgeoning healthcare costs. Pericarditis, myocarditis, cardiomyopathy, atherosclerotic coronary vasculopathy, arterial aneurysms, pulmonary hypertension, and endocarditis occur with increased frequency in these patients. Pericardial tamponade, dilated cardiomyopathy, endocarditis, and vasculopathy can lead to fatal outcomes in this population. The advent of cardiomyopathy heralds a very poor prognosis in patients infected with HIV. Coronary vasculopathy without obvious risk factors can lead to myocardial ischemia in young patients infected with the virus. Moreover, the protease inhibitors used to treat HIV infection induce a syndrome of lipodystrophy and dyslipidemia that may be associated with accelerated atherosclerosis as well as insulin resistance. All these factors contribute to increased cardiovascular morbidity and mortality in the HIV-infected population. HIV infection, opportunistic infections, secreted viral proteins such as gp120 (envelope protein) or Tat (transactivator of viral transcription), and cytokines elaborated during the course of HIV infection of the immune system all contribute to pathogenesis of these disorders. Further basic and clinical studies are required to understand the pathogenesis of cardiovascular complications and develop appropriate management strategies for these patients.
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PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4


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