Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kawasaki Disease (KD) is a potentially fatal acute vasculitis of childhood. Although KD is the leading cause of acquired heart disease in children in developed nations, its pathogenesis remains unknown. We previously reported the novel observation that IgA plasma cells infiltrate the vascular wall in acute KD. We have now examined the clonality of this IgA response in vascular tissue from three fatal cases of KD to determine whether it is oligoclonal, suggesting an Ag-driven process, or polyclonal, suggesting nonspecific B cell activation or a response to a superantigen. We first sequenced VDJ junctions of 44 alpha genes isolated from a primary, unamplified KD vascular cDNA library. Five sets of clonally related alpha sequences were identified, comprising 34% (15 of 44) of the isolated alpha sequences. Furthermore, point mutations consistent with somatic mutation were detected in the related sequences. Next, using formalin-fixed coronary arteries from two additional fatal KD cases, we sequenced VDJ junctions of alpha genes isolated by RT-PCR, and a restricted pattern of CDR3 usage was observed in both. We conclude that the vascular IgA response in acute KD is oligoclonal. The identification of an oligoclonal IgA response in KD strongly suggests that the immune response to this important childhood illness is Ag-driven.
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PMID:Oligoclonal IgA response in the vascular wall in acute Kawasaki disease. 1114 18

A 74-year-old woman was referred to our department in December 1999 for a pyoderma gangrenosum (PG) arising at the edges of chronic leg ulcer. The history was positive for benign monoclonal gammopathy, ischemic hypertensive cardiopathy, polyarthrosis and venous lower leg deficiency. Monoclonal gammopathy of IgA Kappa type was diagnosed 10 years before with a continued benign nature. In 1990 a post traumatic PG of the left leg was diagnosed and a therapy with Cyclosporine A was started with healing of the lesion. In June 1999, 6 months before the hospitalization, a typical venous ulcer of the right leg appeared and was treated with bed-rest, compression bandaging and topical desloughing therapy. In the last month, after a minor surgical debridement of the wound, the lesion developed pustules evolving into a painful, necrotic ulcer with ragged, purple-red, undetermined borders (Fig. 1). A relapse of PG was suspected. Histological examination was consistent with pyoderma gangrenosum and showed massive neutrophilic infiltration, hemorrhage and necrosis of the overlying epidermis. Wound culture was negative. Other laboratory examinations only showed IgA = 8.15 g/L. Investigation of other underlying medical conditions were normal or negative. The venous leg ulcer gradually healed with antiseptic and compression-bandage therapy. After a 4-month course of topical steroid therapy with good results, the PG recurred also involving the proximal area of the leg. Methylprednisolone 50 mg/day was started. Healing began 10 days later and 2 months later the wound healed and epithelialized. Steroid was reduce to 5 mg daily for 4 months. No recurrence was seen when the drug was stopped.
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PMID:Pathergic pyoderma gangrenosum in a venous ulcer. 1201 Mar 42

Trypanosoma cruzi, the causative agent of Chagas' disease, is an important cause of heart disease in Latin America. The parasite is transmitted mucosally, with both intra- and extracellular life stages in the human host. Cruzipain, the major cysteinyl proteinase of T. cruzi, has been shown to be antigenic in both humans and mice during infection with the parasite. We extend these observations, showing here that multiple murine immune subsets of potential importance for vaccine-induced protection can be induced by cruzipain. Cruzipain-specific serum IgG responses were induced during chronic infection with T. cruzi. In addition, T. cruzi mucosal infection stimulated the development of cruzipain-specific secretory IgA detectable in fecal extracts from infected mice. Cruzipain-specific type 1 cytokine responses characterized by the production of IFN-gamma but not IL-4 were also detectable during murine infection. Furthermore, immunization of mice with a DNA vaccine encoding cruzipain was shown to stimulate cytotoxic T lymphocyte (CTL) responses capable of recognizing and lysing T. cruzi-infected cells. The induction of serum antibody, mucosal IgA, Th1 cytokine and CTL responses by cruzipain in mice supports the use of this parasite protein for further efforts in T. cruzi vaccine development.
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PMID:Induction of B- and T-cell responses to cruzipain in the murine model of Trypanosoma cruzi infection. 1227 Jul 27

The immunologic profile of patients with congenital heart disease complicated by protein-losing enteropathy (PLE) is undefined. The aim of this study was to assess the lymphocyte subpopulation and immunglobulin (Ig) pattern in patients with PLE complicating congenital heart disease. The immunologic profile of six patients with congenital heart disease complicated by PLE was compared to that of controls without PLE matched for age and cardiac interventions. Enteric protein loss was documented by Tc99m-labeled albumin scintigraphy. The lymphocyte subpopulations were enumerated using flow cytometry, whereas serum IgG, IgA, and IgM concentrations were measured by the turbidimetric technique. The cardiac diagnoses included complex cyanotic heart disease post-Fontan procedure (n = 3), and one each of tetralogy of Fallot, restrictive cardiomyopathy, and valvar pulmonary stenosis. In patients with PLE, the T lymphocyte (CD3+) count was significantly lower (300 +/- 186 vs 2070 +/- 1171/microl, p = 0.017); both the helper/inducer lymphocytes (CD4+) (127 +/- 158 vs 927+/- 377/microl, p = 0.006) and suppressor/cytotoxic lymphocytes (CD8+) (129 +/- 49 vs 850 +/- 695/microl, p = 0.057) reduced with reversal of CD4(+)/CD8(+) ratio (0.81 +/- 0.68 1.64 +/- 0.89, p = 0.027). Furthermore, IgG level was significantly reduced (5.12 +/- 2.84 vs 12.5 +/- 1.58 g/L, p = 0.005) and IgA level tended to be lower (1.36 +/- 1.37 vs 2.50 +/- 0.80 g/L, p = 0.095). In contrast, the B lymphocyte (CD19+) count (340 +/- 151 vs 618 +/- 427/microl, p = 0.25), natural killer cell count (CD16(+) 56(+) CD3(-)) (252 +/- 212 vs 276 +/- 251/microl, p = 0.85), and IgM level (0.98 +/- 0.59 vs 1.12 +/- 0.25 g/L, p = 0.67) were similar for both groups. None of the patients developed opportunistic or severe viral infections. Abnormal immunologic profile of both the cellular and humoral arms of the immune system occurs in patients with congenital heart disease complicated by PLE. Nonetheless, these abnormalities perhaps appear quantitative rather than qualitative in nature, although further functional studies of antibody production and lymphocyte proliferation assays are required to support this proposition.
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PMID:Immunologic profile of patients with protein-losing enteropathy complicating congenital heart disease. 1253 Apr 89

The possible role of inflammation in coronary artery disease (CAD) is being recognised, while markers of inflammation (e.g., CRP) and infection with Chlamydia pneumoniae (C. pneumoniae), cytomegalovirus (CMV) and Helicobacter pylori (H. pylori) have been proposed as risk factors for CAD. However, these associations require further evaluation. It is a known fact that diabetic patients suffer from impaired immune response to some pathogens and a high incidence of atherosclerosis. In this case-control study we investigated serological markers of infection with C. pneumoniae, CMV, and H. pylori in a group of 140 patients with unstable angina pectoris (UA), 52 of them having type 2 diabetes mellitus, and in a matched control group. Anamnestic (IgG) and acute infection (IgA) antibodies against the above agents were tested using ELISA or indirect immunofluorescence tests. In patients with UA we found a significantly higher seroprevalence and titres of IgG antibodies against C. pneumoniae (p = 0.04) and increased titres of IgG antibodies against CMV (p = 0.007). No differences were found in IgA antibody response to these pathogens. Antibody response to H. pylori was similar in both groups tested. In diabetic patients with UA, the frequency of group-common IgG antibodies against C. pneumoniae was higher than in the non-diabetic UA patients. The other serological markers studied were comparable in the patients with or without diabetes mellitus. Our findings confirmed association of C. pneumoniae and CMV with cardiovascular heart disease. Moreover, diabetes mellitus may predispose the patients to C. pneumoniae infection. However, serological markers observed do not indicate that destabilisation of angina pectoris is associated with acute C. pneumoniae or CMV infection. No relationship was found between UA and H. pylori infection.
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PMID:Serological markers of Chlamydia pneumoniae, cytomegalovirus and Helicobacter pylori infection in diabetic and non-diabetic patients with unstable angina pectoris. 1288 57

The presence of Chlamydia pneumoniae infection was examined in 66 patients with unstable angina pectoris (UAP), 155 patients with acute myocardial infarction (AIM) and 112 controls without signs of a heart disease. Besides evaluation of anamnestic data, ECG and coronarographic examination, serologic examination of C. pneumoniae by the microfluorescent method anti-MOMP and ELISA of anti-LPS of globulin IgA and IgG serum classes in every patient was performed. Moreover, in patients with UAP, routine biochemical methods for the detection of total cholesterol levels and its lipoprotein fractions LDL, HDL and triacylglycerols were used. The levels of anti-MOMP C. pneumoniae antibodies and anti-LPS of the IgA class in sera of patients with UAP were statistically highly significantly increased (chi 2 = 19.54; chi 2 = 12.92; p < 0.01) and anti-LPS of the IgG class significantly increased (chi 2 = 6.15; p < 0.05) in comparison with controls. It can be assumed that the participation of C. pneumoniae is aetiologically possible. Total cholesterol levels, LDL, HDL and triacylgylcerols were increased above the normal range in 34.8%, 48.5%, 39.4% and 28.8% of patients, respectively. The anti-LPS C. pneumoniae ELISA test of globulin class IgA in patients with UAP seems to be the most suitable method for the determination of infections with C. pneumoniae.
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PMID:[Occurrence of chlamydia infection in relation to lipidemia indicators in the etiology of unstable angina pectoris]. 1293 30

Antiphospholipid syndrome (APS) is defined by the presence of arterial and venous thromboses, recurrent fetal death, cerebrovascular accidents, hemolytic anaemia, thrombocytopenia and various other manifestations in different organs. APS is a clinical entity that can appear commonly alongside systemic lupus erithemathous on it can occur as a primary disease. The syndrome is defined by the presence of antiphospholipid antibodies in serum, a group of immunoglobulins (IgG, IgM, IgA or an mixture of them) that adopt an hexagonal configuration when they are incubated at 37grades C. In APS, it is rather common to find cardiac lesions such as non-verrucous endocarditis, valvular lesions (especially of the mitral valve), microvascular cardiac disease and more risk of thrombosis at this level, myxomas that could be the cause of a systemic inflammation in relation to the production of antiphospholipid antibodies, intracardiac thrombii and congenital heart disease. We present the case of a woman with APS associated with interauricular communication whose initial diagnosis were pulmonary thromboembolism and cerebrovascular stroke. We were able to diagnose the cardiac abnormality by the use of transesophagic echocardiography. We propose the use of this imaging technique for patients with APS even though the transthoracic Doppler echocardiography was found to be normal. In this way we will be able to rule out cardiac lesions which could also be the cause of embolic manifestations.
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PMID:[Antiphospholipid syndrome. The use of transesophageal echocardiography]. 1458 41

One third of cases of cerebral ischemia have no clear etiology. A humoral response to the atherosclerotic plaques components beta2-glycoprotein l (beta2-gpl) and heat-shock proteins (Hsp) might be involved in the pathogenesis of stroke. This case-control study includes a complete profile of anti-beta2-gpl antibodies and testing of IgG antibodies to the 60/65 kilodaltons (kDa) Hsp in stroke patients. Ninety-three patients with acute ischemic stroke and 93 controls were evaluated for age, sex, race, hypertension, smoking, previous cardiopathy, diabetes mellitus, hypercholesterolemia and previous history of cerebral ischemia. lgG/lgM/lgA anticardiolipin (aCL) and anti-beta2-gpl antibodies, as well as lgG antibodies to human 60 kDa Hsp and to Mycobacterium bovis 65 kDa Hsp, were detected by immunoassay. Adjusted odds ratios (OR) were calculated by logistic regression. The adjusted OR for IgA anti-beta2-gpl antibodies was 4.6 (90%Cl 1.5 to 14.3; p = 0.025). The non-adjusted OR for IgG antibodies to Hsp 60 was 26.1. The adjusted OR for IgG antibodies to Hsp 65 was 3.2 (90%Cl 1.2 to 8.3; p = 0.044). The adjusted OR for lgG to any Hsp (60 or 65) was 4.8 (90%Cl 1.9 to 12.1; p = 0.006). This study demonstrates that elevated IgA anti-beta2-gpl and lgG anti-Hsp 60/65 antibodies are associated with increased risk of ischemic stroke. The association occurred independently of other risk factors. This humoral response might link autoimmunity, thrombophilia and atherosclerosis in stroke patients.
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PMID:Antibodies to the atherosclerotic plaque components beta2-glycoprotein I and heat-shock proteins as risk factors for acute cerebral ischemia. 1459 78

Chlamydia pneumoniae (C. p.) is very frequently cited as an important factor of the origin of atherosclerosis. To confirm the diagnostic value of the serological examination the following reactions have been used: microimmunofluorescence reaction (MIF) for estimating of antibodies against major outer membrane proteins C. p. (anti-MOMP) and ELISA for detecting antibodies against the lipopolysacharides of C. p. (anti-LPS), both in IgA and IgG immunoglobulin classes of the serum. The ELISA for the detection of the IgG antibodies against chlamydial heat shock protein (cHSP60) has been used. The sera of 155 patients suffering from acute myocardial infarction (AMI) and 69 patients with unstable angina pectoris (UAP) have been examined. The heart disease has been confirmed by anamnesis, electrocardiography and coronarography. As a control group the sera from 112 persons without sings of a heart disease were examined. The antibodies against the cHSP60 have been determined only in the sera 69 patients with UAP and 49 control sera. Statistically higher occurrence of the antibodies anti-MOMP C. p. in the IgA class sera of patients suffering from UAP has been noted compared with those found in the sera of the control group (chi 2 = 18.56; p < 0.01). In the globulin IgG class of the both groups no difference has been found. The anti-LPS C. p. antibodies in the IgA as well in IgG anti-LPS classes of the patients sera with UAP were present significantly more frequently than in the control group (chi 2 = 11.49; p < 0.01, chi 2 = 4.16; p < 0.05). Similarly the incidence of the anti-LPS C. p. antibodies in the IgA class sera of 155 patients suffering from AMI was significantly higher than in the control group (chi 2 = 8.55; p < 0.01). The anti-cHSP60 antibodies have been found in 41 out of 69 patients suffering from UAP (59.4%) and in 21 of 49 control individuals (42.9%). The results seem to confirm an important role of C. p. in atherogenesis. The monitoring of the antibodies against the C. p. may supplement the diagnostics in patients suffering from UAP and AMI and the efficacy of its therapy and prevention as well.
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PMID:[Serologic study of atherosclerosis and its vascular complications]. 1466 61

Kawasaki disease (KD) has emerged as the most common cause of acquired heart disease in children in the developed world. The cause of KD remains unknown, although an as-yet unidentified infectious agent might be responsible. By determining the causative agent, we can improve diagnosis, therapy and prevention of KD. Recently, identification of an antigen-driven IgA response that was directed at cytoplasmic inclusion bodies in KD tissues has provided new insights that could unlock the mysteries of KD.
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PMID:Searching for the cause of Kawasaki disease--cytoplasmic inclusion bodies provide new insight. 1836 28


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