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)

Chronic cough may be the sole presenting manifestation of bronchial asthma (reference 3; Corrao et al, 1979), and "cough variant asthma (CVA)" has been used to categorize such patients. In order to clarify the clinical picture of CVA, we evaluated the clinical history, laboratory data, sputum cytology and pulmonary function in 14 subjects (5 males and 9 females, aged 14 to 65 years) compatible with the following diagnostic criteria: (1) chronic cough persistent for more than 8 weeks, (2) no wheeze nor dyspnea, (3) no rales, (4) no past history of asthma, (5) bronchial hyperreactivity to methacholine proven by Takishima's method (reference 13), (6) effectiveness of bronchodilators against cough, (7) normal chest X-ray film, (8) afebrile and negative CRP, (9) absence of sinusitis and postnasal drip, or if present, they are proved not to be responsible for the cough, and (10) no other causes of cough such as heart disease, prescription of ACE inhibitors, current smoking. The results were as follows. 1) Many of the subjects were atopic, with positive skin tests to one or more common allergens in 10 subjects, elevated serum IgE in 4 subjects, and past history and family history of atopy in 4 and 7 subjects, respectively. 2) Respiratory infection preceded the onset of CVA in 3 subjects. 3) Cough was generally nocturnal, but 2 subjects coughed only in the daytime. 4) FEV1.0% was decreased (less than 70%) in only 2 subjects, whereas V25 was decreased (less than 80% of predicted value) in 11 out of 12 evaluable subjects, which suggested peripheral airway obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical study on cough variant asthma]. 150 83

The occurrence of cancer, immunodeficiency, and diseases with possible autoimmune aetiology were studied in 355 blood relatives of 12 patients with common variable immunodeficiency (CVID). The family members were identified through the patients and interviewed after completing a questionnaire, their diseases were medically confirmed by local general practitioners. In two families consanguineous marriages were identified with the coefficients of inbreeding of 0.03125 and 0.01563, respectively: one patient, a dizygotic twin of an unaffected sister, was a granddaughter of first cousins, the second patient was the third daughter of second cousins. These cases of CVID strongly support the autosomal recessivity of the underlying genes. One male patient with CVID was shown to be related to a patient with X-linked hypogammaglobulinaemia, both sharing a common carrier. The different clinical courses of their diseases suggest two genetically determined immunodeficiencies and genetic heterogeneity. No family had an unusual clustering of cancer. The occurrence of tumours in the blood relatives of CVID patients was not significantly higher than in the relatives of spouse controls. Immunological examination of 30 first degree relatives of the CVID patients revealed three children (2 males and 1 female) with selective IgA deficiency, in one boy combined with elevated serum IgE level. Four relatives with rheumatoid heart disease, 12 cases of gastric or duodenal ulcer, and 14 relatives with thyroid disease represented the most often encountered diagnoses with a possible autoimmune component in their aetiology.
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PMID:Family studies in common variable immunodeficiency. 188 Apr 4

The evidence reviewed here indicates that the eosinophil has the ability to kill many species of helminths and likely does so during worm infection. This toxic ability appears to be regulated by several other cells including mast cells, monocytes, and T lymphocytes. Eosinophils kill helminths through their ability to generate potent oxidants and through their content of cationic proteins, which likely achieve high concentrations at points of granule deposition. Eosinophils also participate in inflammation in human disease especially asthma, skin diseases, and heart disease. Though present concepts hold that the mast cell is the cornerstone of the allergic inflammatory response (450), the findings that eosinophils bind IgE and are activated by antigen-IgE complexes and that the eosinophil can elaborate many inflammatory mediators raise the possibility that the eosinophil might also be involved in the initiation of inflammatory responses. Finally, an eosinophil-related protein appears to play an undefined role in human reproduction.
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PMID:The eosinophilic leukocyte: structure and function. 353 19

The prognosis of the hypereosinophilic syndrome (HS) depends mainly on the development of endomyocardial fibrosis (EMF). This complication may be overlooked at an early stage, although its presence is an indication for steroid or antimitotic therapy of the HS. Even at an advanced EMF and associated intracardiac thrombi may not be visualised by angiography. This study was undertaken to assess the diagnostic value of 2D echocardiography in 12 patients. The patients were all men (12 of them) aged 22 to 64 years with unexplained eosinophilia 1 500/mm3 for over 6 months, and visceral lesions. The patients were divided into 3 clinical groups. Group A comprised 4 "allergic" patients with chronic asthma and a significant elevation of IgE; Group B comprised 5 "myeloproliferative" patients with splenomegaly and/or hepatomegaly and a significant elevation of serum B12 levels. The 3 remaining patients who could not be allocated to either Group A or B formed the third group (Group C). 2D echocardiography was carried out on average 30 months after diagnosis of the HS and six planes of examination were used systematically (two parasternal, two apical, one extreme apical and one subcostal). Right and left ventriculography was performed in 6 patients (less than one month before or after 2D-echo). Anatomical studies were obtained in 4 cases (2 operations, 3 autopsies). Echocardiographic signs of EMF were observed in 8 cases. Four patients had a restrictive cardiopathy associated to a large LV thrombus in 2 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac manifestations of the hypereosinophilic syndrome. The value of 2-dimensional echography (12 cases)]. 643 27

The relationships of smoking, allergy skin test reactivity, and serum IgE to ventilatory function have been analyzed in 1,182 subjects from a general population sample. The study group consisted of subjects aged 35 or more who deny previous lung surgery, old tuberculosis, or a current diagnosis of heart disease in the absence of chronic bronchitis or emphysema. Impairment of the forced expiratory volume in one second (FEV1) shows a definite relationship to total serum IgE. However, this relationship is significant only for a low FEV1 which is accompanied by symptoms suggesting asthmatic or a chronic bronchitis type disease. Allergy skin test reactivity to a battery of common aeroallergens shows no overall relationship to FEV1. However, after accounting for total serum IgE, positive allergy skin tests tend to be associated with high rather than low FEV1 values. The findings suggest that some type of IgE which is not specific for aeroallergens but which is associated with smoking, may be important in the pathogenesis of the "chronic asthmatic bronchitis" syndrome.
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PMID:Interactions of smoking and immunologic factors in relation to airways obstruction. 664 Dec 98

Eight children with congenital asplenia syndrome have been studied for their cardiac and immunologic status. All patients were greater than 2 years of age and had severe complex cyanotic heart disease. All eight patients had abnormalities of cardiac and/or visceral situs. All patients had evidence of pulmonary stenosis or atresia and a common atrium or large atrial septal defect. Five patients required palliative cardiac surgery. All patients were given prophylactic antibiotics; there were no documented episodes of sepsis. One patient had an isolated deficiency of IgM; two patients had an isolated deficiency of IgE. Seven of eight patients were immunized with a dodecavalent pneumococcal vaccine. Four of the seven patients failed to have a twofold or greater antibody response. Our findings suggest that prophylactic antibiotics may reduce the incidence of sepsis in the asplenia syndrome. Because the prognosis for these patients must be optimistic, we recommend early documentation of splenic function in children suspected of having the asplenia syndrome, prophylactic antibiotics, and parent education. Children immunized with bacterial vaccines should have their antibody responses monitored.
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PMID:Congenital asplenia: immunologic assessment and a clinical review of eight surviving patients. 725 76

The purpose of this study was to determine whether pulmonary hemodynamic abnormalities relate to manifestations of allergic asthma. In 448 patients with congenital heart disease the relationships between asthma and age or pulmonary arterial blood (PA) flow were studied. Asthma (allergic and non-allergic) was more common in 39 (19%) of 201 patients with high PA flow, compared with the incidence in those with normal PA flow (6/117, 5%; P < 0.001) and reduced PA flow (1/130, 1%; P < 0.05). In the high PA flow group, the frequency of asthma declined significantly (P < 0.01) with age, from 25-26% in the 6 month-5 year patient group to 5% in the 6-12 year old patients. The frequency of asthma, including allergic type, was significantly (P < 0.01) greater in patients with pulmonary hypertension (15/24, 63%) than in those without (10/77, 13%) at the age of 6 months to 1 year. Asthma in the high PA flow group was associated with other allergic diseases in 30 (77%) of 39 patients, including food allergy in nine (23%), atopic dermatitis in 14 (36%), allergic rhinitis in seven (18%) and abnormally high total IgE levels in 14 (36%). These findings suggest that high pulmonary flow or pulmonary hypertension enhances the manifestation of allergic disease, particularly asthma.
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PMID:Contribution of pulmonary hemodynamics on manifestation of allergic asthma in patients with congenital heart disease. 810 29

Eosinophilia in humans is often associated with heart disease and cardiac localization of eosinophil granule proteins, and several results suggest that granule proteins mediate endomyocardial damage. Here we investigated the in vitro effects of the four principal eosinophil granule proteins (eosinophil cationic protein (ECP), major basic protein (MBP), eosinophil-derived neurotoxin, and eosinophil peroxidase (EPO)) on the activation of effector cells of inflammation (mast cells) isolated from human heart tissue (HHMC). ECP and, to a lesser extent, MBP (0.3-3 microM), but not eosinophil-derived neurotoxin and eosinophil peroxidase stimulated the release of preformed (histamine and tryptase) and the de novo synthesis of vasoactive and proinflammatory mediators (PGD2) from HHMC. Activation of HHMC by ECP and MBP was Ca2+- and temperature-dependent and was abolished by preincubation (15 min, 37 degrees C) with 2-deoxy-D-glucose (10 mM) and antimycin A (1 microM). There was a significant correlation between the maximal percentage of histamine release induced by ECP and anti-IgE from HHMC (rs = 0.73; p < 0.005), by MBP and anti-IgE (rs = 0.79; p < 0.001), and by ECP and MBP (rs = 0.65; p < 0.005). A positive correlation was also found between histamine and tryptase secretion (rs = 0.71; p < 0.001) and between histamine and PGD2 release induced by ECP from HHMC (rs = 0.85; p < 0.001). This is the first demonstration that some eosinophil cationic proteins, namely ECP and MBP, found at the site of heart damage in patients with eosinophilia, act as complete secretagogues on HHMC. This observation indicates another mechanism by which infiltrating eosinophils and their metabolic products cause inflammatory reactions and thus endomyocardial lesions in patients with eosinophilia.
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PMID:Eosinophil granule proteins activate human heart mast cells. 875 29

RSV is the primary cause of hospitalisation in the first year of life for children in most parts of the world, and nearly 100% of children in the USA are infected with the virus by 2 to 3 years of age. The agent is an enveloped RNA virus with a non-segmented single-stranded negative-sense genome. The viral genome encodes 8 structural and 2 non-structural proteins. Important structural proteins include the fusion (F) protein and the attachment (G) protein which are essential for viral penetration and attachment to the host cells. Both proteins are important in development of immune responses. The virus is estimated to cause 3000 to 4000 deaths annually. Primary infections are as a rule symptomatic. The spectrum of clinical manifestations ranges from mild upper tract illness, infection in middle ear which progresses to acute otitis media, croup, to apnoea in premature infants, pneumonia and bronchiolitis. Premature babies born at 30-35 weeks of gestation, infants with cyanotic congenital heart disease, HIV-infected subjects, and patients on intensive immunosuppressive therapy especially after bone marrow transplant are considered to be at risk for increased mortality and morbidity during RSV infection. The virus does not normally replicate outside of the bronchopulmonary tree and the infection is exquisitely restricted to the respiratory mucosa. However, development of extrapulmonary disease has been observed in certain T and B cell immunodeficiency states. The association of RSV with asthma and reversible reactive airway disease in early childhood has attracted significant attention. Recurrent wheezing for up to 5 to 7 years of age and established airway disease has been observed in a significant number of children with a strong family history of allergy, after primary infection or reinfection with RSV. Immune response to primary infection is relatively small but on reinfection, a significant booster effect with sustained immunologic reactivity is observed in serum and respiratory mucosa. Both CD(4)- and CD(8)-specific as well as Th(1)- and Th(2)-cell specific immune responses have been observed during human infection. In addition, proinflammatory as well as immunoregulatory cytokines and chemokines are induced in the respiratory tract after natural and induced (in vitro) infection. Significant progress has been made in understanding the role of Th(1) vs. Th(2), IgE, viral induced cytokines and chemokines in the mechanisms of pathogenesis of the disease, development of wheezing and in the prevention and treatment of the infection and its sequelae. Respiratory syncytial virus (RSV) is one of the commonest human viral infections, and virtually every child is infected by the third birthday. Because of its restricted mucosal immunopathology, and frequent association with bronchial hyperreactivity and development of wheezing, RSV has served as an important model to investigate mechanisms of mucosal immune responses and development of mucosal disease following infection. The importance of RSV in bronchopulmonary disease and development of bronchial hyperreactivity has been the focus of several recent symposia [Kimpen JL, Simoes EAF. Am J Respir Crit Care Med 2001; 163:S1-S6]. This brief report will only summarise, based on selected references, the historical landmarks of its discovery and current understanding of the mechanisms of immunity, and their possible role in the pathogenesis of bronchopulmonary disease.
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PMID:Respiratory syncytial virus: the virus, the disease and the immune response. 1498 Feb 56

Eosinophilia and pleural effusion may suggest pulmonary eosinophilia. We present a case of 42 years old woman with hypereosinophilia history since 5 months and no evidence of parasitic infections. She had no history of heart disease. Laboratory tests revealed eosinophilia (13.0 x 10(9)/l) and elevated serum IgE (2050 IU/ml), ANCA was not detected. ECP was not elevated. Pleural effusion contained 37% of eosinophils. An ECG revealed low voltage of QRS in all leads and Q waves in leads Vi-V-3. An echocardiography showed enlargement of left auricle and left ventricle with ejection fraction = 35%. The only pulmonary manifestation in this case was eosinophilic pleural effusions associated with congestive heart failure. A women was treated with prednisone 1 mg/kg/d and cyclophosphamide 2 mg/kg/d with clinical improvement and normalisation of eosinophil number in peripheral blood. But echocardiographic picture of the heart was nor better during 2 months of observation.
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PMID:[Churg-Strauss syndrome--cardiac problem in lung disease department]. 1505 69


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