Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe two patients demonstrating a granulomatous inflammation of bronchial mucosa characterized clinically by a persistent dry cough, lack of manifestations of bronchial asthma, normal level of serum IgE and serum ACE, inflamed bronchial mucosal appearance consisting of edema, erythema, bleeding and narrowing and recovering without specific treatment. Histopathological findings of the bronchial inflammation of our patients were characterized by noncaseating granuloma formation consisting of epithelioid cells and multinucleated giant cells with infiltration of lymphocytes, plasma cells and eosinophils. The bronchial granulomatous inflammation of our patients was thought to differ from that of diseases which have been known, to our knowledge, as diseases demonstrating a granulomatous inflammation of bronchial mucosa. Although the pathogenesis of the disease could not be clarified by a careful search of special staining and culturing for the infective agent, it was most suggestive of non-specific inflammation with a granulomatous response to some sort of inhaled agents.
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PMID:Idiopathic granulomatous bronchitis. An unusual form of known granulomatous lung diseases or an unknown disease? 134 46

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 first inhibitor of angiotensin converting enzyme (ACE) was found in and isolated from the venom of the South American pit viper Bothrops jararaca. This was done after it was discovered that bites of the pit viper inhibit the breakdown of a proinflammatory peptide, bradykinin, in prey. Treatment with newly developed orally active ACE-inhibitors has been reported to cause symptoms such as adverse skin reactions, angioneurotic oedema, coughs and, in asthmatics, rapidly decreasing lung function. In this thesis the ACE-inhibitor MK 422 (active parent diacid of enalapril) was demonstrated to potentiate wheal and flare reactions induced by allergens, bradykinin or capsaicin, and to increase infiltration of "inflammatory cells", like eosinophils and neutrophils, into inflammatory dermal test sites in sensitized guinea pigs. MK 422 also augmented spontaneous and allergen-triggered histamine release in vitro from guinea pig skin and lung tissue. Capsaicin "desensitization" of guinea pig skin markedly reduced the wheal and flare reactions to allergens and attenuated the proinflammatory effect of the ACE-inhibitor. The histamine release in vitro from capsaicin-pretreated skin was also decreased, and no clear potentiating effect of MK 422 was demonstrated. In man, enalapril augmented anti-IgE-induced wheal and flare responses and increased bronchial reactivity to histamine. The drop of circulating eosinophils in venous blood was more pronounced after the provocations performed during enalapril treatment, and plasma substance P tended to increase. The alpha 2-adrenoceptor agonist clonidine, known to attenuate "neurogenic inflammation", reduced the wheal and flare reactions in guinea pig skin and decreased infiltration of neutrophils and eosinophils into inflammatory test sites. Furthermore, clonidine abolished the proinflammatory effect of MK 422 on the allergen- evoked wheal and flare reactions in guinea pig skin without counteracting the blood pressure lowering effect of the ACE-inhibitor. Contrarily, an additive hypotensive effect was demonstrated when clonidine was combined with MK 422. It is suggested that the proinflammatory properties demonstrated by ACE-inhibitors is due to augmentation of "neurogenic inflammation".
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PMID:New aspects on inflammatory reactions and cough following inhibiton of angiotensin converting enzyme. 246 91

The intradialytic symptoms that can be linked to components of the extracorporeal circuit of greatest clinical importance are the Type A (anaphylactoid) reactions. Most of these are IgE-mediated reactions due to ethylene oxide and are preventable by adequate degassing of the dialyzer by the manufacturer and by adequate rinsing of the dialyzer just prior to use. AN69-associated reactions are a second group, and are probably mediated by membrane-induced bradykinin generation coupled with ACE-inhibitor induced prolongation of bradykinin half-life. Type A reactions occur in a reuse setting, alos, and these may be related to some as yet poorly understood interaction between bleach, reuse sterilants, and certain dialyzer membranes, again, with ACE inhibitors playing an amplifier role. There is no compelling evidence linking membrane-induced complement activation to type A dialyzer reactions. However, there is a large body of evidence in animal models that exposure to complement fragment-releasing membranes can increase the pulmonary artery pressure and increase thromboxane formation. Thus, at least in principle, a case can be made for using unsubstituted cellulose membranes with caution in patients with a history of atopy or eosinophilia, particularly if acetate dialysate is to be used. Such a caution, however, must be viewed as conjectural in the absence of definitive evidence. Type B dialyzer reactions (mild back and chest pain 20-60 min into the dialysis session) is a phenomenon that is in the process of vanishing. The reason why is unclear. These reactions may have been due to some sort of dialyzer contaminant, or they may have been due to complement fragment release and required the use of acetate dialysate as a cofactor. In any event, recent well designed studies fail to find any differences in symptoms between unsubstituted cellulose and synthetic membranes. Membrane-induced complement fragment release also may play a minor role in dialysis hypoxemia, but evidence is conflicting in this area. Again, the use of acetate dialysate appears to be an important cofactor. Post-dialysis events which may be conceivably linked to the delayed effects of complement fragment releasing membranes need to be evaluated in controlled studies. Studies suggesting increased post-dialysis catabolism with use of unsubstituted cellulose membranes need to be confirmed in dialysis patients, and symptomatic correlates should be sought and evaluated.
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PMID:Adverse effects of dialyzers manifesting during the dialysis session. 806 4

Postinfectious cough has been drawing attention as a factor involved in the etiology of chronic cough in the United States. In Japan, clinical features of postinfectious chronic cough (PICC) have not been described in detail. We investigated 22 patients with PICC diagnosed by the established criteria (Jpn. J. Allergol. 1995; 44: 1418). All patients were nonsmokers and none received ACE inhibitors. None had a history of atopy or sinus diseases. There were four men and 18 women with a median age of 65 years. These 22 patients underwent clinical examinations including chest roentgenograms, respiratory function tests, eosinophil counts in venous blood, serum IgE titers, antibody titers to Mycoplasma pneumoniae, sputum cytologic findings taken from ten patients, and histological features of bronchial biopsy specimens obtained from two patients; all findings were within normal limits. Clinical course of cough in 20 of the patients with PICC was evaluated using a cough diary. One patient did not keep a cough diary. Ten patients improved with dextromethorphan hydrobromide (D) and oxatomide (O). Three of the remaining 9 patients improved with Bakumondo-to (B) only, 4 with D+O+B, and 2 with D+O+B+ozagrel hydrochloride. The duration of cough before treatment showed a significant correlation with the time from the start of treatment to recovery (r = 0.47, p < 0.05). These results indicate that PICC tends to occur in elderly women and to improve with treatment combining with D, O, and B. We hope to establish a standard therapy for postinfectious chronic cough.
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PMID:[Clinical features of postinfectious chronic cough]. 923 11

H1 antihistamines have been shown to have antitussive effects in patients with asthma and postnasal drip. In Japan, no study has been performed to determine whether orally administered oxatomide, H1 antihistamine, can reduce the chronic cough seen in patients with post-upper-airway infection (postinfection). Patients who had chronic cough of more than three weeks' duration and a history of post-upper-airway infection took part in the study. None had any history of nasal disease, gastroesophageal reflux, bronchial asthma, or other chronic pulmonary disease. All patients were non-smokers, and none used ACE inhibitors. They had normal CRP concentrations, peripheral white blood cell and eosinophil counts, serum IgE concentrations, titers of cold agglutinins and antibodies to Mycoplasma pneumoniae, chest roentgenograms, and respiratory function tests. A prospective randomized, open design was used. The effect of one week of treatment with dextromethorphan (D) or with D plus oxatomide (D + O) on the severity of cough, as estimated by cough diary, were examined. Twenty-two patients entered the study, and 20 were eligible for efficacy and side-effect analyses. Nine patients receiving D and 11 receiving D + O completed the protocol. Patients' characteristics before the start of the study, such as severity and duration of cough, and laboratory data, were not significantly different between the two groups. From trial day 5 to 7, improved rates of cough were significantly higher with D + O than with D alone (p < 0.05). Combination therapy with oxatomide and dextromethorphan reduces subjective perception of cough as estimated by cough diary. These results suggest that oxatomide, H1 antihistamine may improve chronic cough in patients with post-upper-airway infection.
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PMID:[Effects of oxatomide, H1-antagonist, on postinfectious chronic cough; a comparison of oxatomide combined with dextromethorphan versus dextromethorphan alone]. 952 65

The role of genetic factors was reviewed with respect to the pathophysiology of bronchial asthma, sarcoidosis and cough induced by angiotensin converting enzyme (ACE) inhibitor administration. The so-called 'atopy gene' in 11q13 is not linked to atopy but is associated with serum IgE levels. The beta2-adrenergic receptor gene on 5q32-33 was found to have polymorphism by Ban I and to be related to beta2-receptor function; a defect of a 2.3 kb allele is related to lowered sensitivity to beta2-agonists. This defect is also related to higher prevalence on non-atopic bronchial asthma. The occurrence of amino acid mutation (Arg16 to Gly) of beta2-receptors was lower and Gln27 to Glu mutation is extremely rare in the Japanese population compared with Caucasians. There is polymorphism of ACE genotypes among normal subjects and patients with sarcoidosis, II, ID and DD. The genotype is a significant determinant of serum ACE activity and may determine the prognosis of sarcoid patients. Genotype II has a higher incidence of coughing induced by ACE inhibitors.
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PMID:Molecular studies of bronchial asthma, sarcoidosis and angiotensin converting enzyme inhibitor-induced cough. 965 60

Previously, we reported the effectiveness of treatment with oxatomide (O), an antihistamine, plus dextromethorphan (D), and that of Bakumondo-to (B), an herbal drug that inhibits the activation of C-fibers, in patients with persistent coughing after upper-airway infection. In this study, we evaluated the efficacy and side effects of combination therapy (O + D + B) in patients with postinfectious persistent cough. Patients who had been coughing for more than three weeks and had a history of upper-airway infection took part in the study. None had any history of nasal disease, gastroesophageal reflux, bronchial asthma, or other chronic pulmonary disease. All patients were non-smokers, and none used angiotensin converting enzyme (ACE) inhibitors. All had normal chest roentgenograms and normal pulmonary function. The following hematological data were obtained before treatment: peripheral eosinophil counts. CRP levels, serum IgE concentrations, and titers of cold agglutinins and antibodies to Mycoplasma pneumoniae. The effects of one week of treatment with O + D + B on the severity of coughing, as estimated with a cough diary, were examined. Thirty-six patients entered the study, but only 18 with normal hematological findings who satisfied the study criteria were eligible for efficacy and side-effect analyses. Cough scores decreased significantly from 5.1 +/- 2.4 (range, 2-9) to 1.2 +/- 1.9 (range, 0-6), and the rate of cough disappearance was 50%. Two patients reported slight drowsiness. Therapy with O + D + B reduced perception of coughing as estimated with a cough diary. These results suggest that this therapy (O + D + B) may be useful in patients with postinfectious persistent cough.
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PMID:[A pilot phase II study of combination therapy with oxatomide, an antihistamine, plus dextromethoraphan and bakumondo-to, an herbal drug, in patients with postinfectious persistent cough]. 969 46

Urticaria and angioedema may be elicited by a considerable number of drugs, particularly nonsteroidal antiinflammatory drugs, angiotensin converting enzyme inhibitors, radiocontrast media and antibiotics. Pathogenic mechanisms involved include pseudoallergy, idiosyncrasy and IgE-mediated hypersensitivity, occasionally also IgG antibodies. In this survey the common problems which still lack established diagnostic in vitro tests such as pseudoallergic reactions to analgesic drugs and idiosyncratic side effects to angiotensin-converting-enzyme inhibitors are presented. In addition some examples of drugs are given where, due to progress in research, instead of a pseudoallergic mechanism an immunological pathogenesis could be demonstrated.
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PMID:Drug-induced urticaria and angioedema caused by non-IgE mediated pathomechanisms. 1058 38

Multiple proteins are proteolytically shed from the membrane, including the amyloid precursor protein (APP) involved in Alzheimer's disease, the blood pressure regulating angiotensin converting enzyme (ACE), the low affinity IgE receptor CD23, and the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). The inhibitory effect of a range of hydroxamic acid-based compounds on the secretases involved in cleaving and releasing these four proteins has been examined to build up a structure-activity relationship. Compounds have been identified that can discriminate between TNF-alpha convertase and the other three secretases (compound 15), between the shedding of CD23 and the shedding of APP and ACE (compound 21), and between the secretases and matrix metalloproteinase-1 (compound 22). The structure-activity relationship for the APP alpha-secretase and the ACE secretase were remarkably similar, and both secretases were activated in whole cell systems by the serine proteinase inhibitor 3,4-dichloroisocoumarin. The basal and carbachol-stimulated shedding of APP and ACE from human SH-SY5Y neuroblastoma cells could not be differentiated by any of the hydroxamate compounds, implying that the same or very similar activities are involved in the constitutive and regulated shedding of these two proteins. By utilizing a key discriminatory compound (compound 15) that potently inhibits TNF-alpha convertase but not alpha-secretase, we show that TNF-alpha convertase is not involved in the regulated shedding of APP from human neuronal cells. The compounds reported here will be useful in future studies aimed at identifying and validating candidate secretases.
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PMID:Structure-activity relationship of hydroxamate-based inhibitors on the secretases that cleave the amyloid precursor protein, angiotensin converting enzyme, CD23, and pro-tumor necrosis factor-alpha. 1193 93


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