Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to discriminate between malignant and benign effusions, the values of carcinoembryonic antigen (CEA), ferritin, beta2-microglobulin (BMG), acid-soluble glycoprotein (ASP), tissue polypeptide antigen (TPA), adenosine deaminase (ADA), and immunosuppressive acidic protein (IAP) were measured in the pleural fluid of 54 patients with lung cancer, 20 with malignancies other than lung cancer, 18 with tuberculous pleurisy, and 22 with benign diseases other than tuberculosis. CEA levels in malignant effusions were significantly higher than those in benign effusions. At a cutoff level of 5 ng/ml, 68% of the patients with lung cancer and 44% of the patients with other malignancies showed elevated pleural fluid CEA levels. In 13 lung cancer cases with negative pleural fluid cytology, nine cases had elevated pleural fluid CEA levels. The mean pleural fluid BMG level of patients with benign diseases was significantly higher than that of patients with malignant diseases, but there was a marked overlap between those with malignant and benign diseases. No significant differences were found in the pleural fluid ferritin, ASP, TPA, and IAP levels between malignant and benign conditions. ASP and IAP pleural fluid levels showed significant correlations with the pleural fluid C-reactive protein (CRP) concentrations suggesting that they also reflect inflammatory activity. The mean ADA activity in tuberculous effusion was significantly higher than that resulting from other causes of pleural effusion.
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PMID:Tumor markers in pleural effusion diagnosis. 327 87

The activity of adenosine deaminase (ADA) was investigated in pleural effusions from 10 patients with tuberculous pleurisy and 76 patients with pleural effusions of other aetiology. The ADA activity in the tuberculous patients was significantly higher than in the other groups, with the exception of those with empyema. Specificity (87%) and sensitivity (100%) of this test for tuberculosis is high when a reference limit of more than 53 U/l is taken.
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PMID:Adenosine deaminase activity in tuberculous pleural effusions: a diagnostic test. 331 Mar 48

The activity of adenosine deaminase was studied in nine cases of rheumatoid pleural effusion, showing an increase in enzyme activity in all. Rheumatoid arthritis seems unique, however, as it cannot be differentiated from pleural tuberculosis on the basis of this test. Selective increase of adenosine deaminase in both conditions is attributed to stimulation of T lymphocytes in the pleural fluid.
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PMID:Adenosine deaminase activity in rheumatoid pleural effusion. 280 4

We have measured adenosine deaminase (ADA) in pleural effusions of 95 patients, using a method optimalised for rapid determination on a Hitachi 705 analyzer. High ADA activity was found in four of the five patients with tuberculous pleurisy, in four of the seven with empyema and in three of the seven patients with mesothelioma. One patient with very high serum ADA activity due to liver disease also had a high activity in the pleural effusion. Low activity was found in all patients with other neoplastic pleural effusions, parapneumonic pleural effusions, transudates, and in pleural effusions due to some other diseases. We conclude that in a country with a low tuberculosis incidence a high ADA activity in pleural effusion in neither sensitive nor specific enough to rely on the diagnosis of tuberculous pleurisy. Routine determination of ADA is not recommended; in selected cases, however, it may be useful.
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PMID:Adenosine deaminase activity, not diagnostic for tuberculous pleurisy. 365

As an aid in the differential diagnosis of exudative pleural effusions, tumor markers were investigated. We measured immunosuppressive acidic protein (IAP), carbohydrate antigen 19-9 (CA 19-9), tissue polypeptide antigen (TPA), carcinoembryonic antigen (CEA), adenosine deaminase (ADA), and alpha 1-acid glycoprotein (AGP) in the pleural fluid of 36 patients with carcinomatous pleural effusions and of 35 patients with tuberculous pleurisy because we have frequently found these diseases to be associated with exudative pleuritis. Tuberculous pleural effusions had significantly higher levels of IAP, ADA, and AGP than carcinomatous effusions (p less than 0.005). On the other hand, CEA, CA 19-9, and TPA were significantly higher in carcinomatous pleural fluids than in tuberculous fluids (p less than 0.05). There was a correlation between IAP and AGP levels, and their specificity was low. Therefore, combined assays of CEA, CA 19-9, and ADA may be useful in distinguishing pleural effusions due to malignancies from those of tuberculous origin.
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PMID:Carcinomatous and tuberculous pleural effusions. Comparison of tumor markers. 397 60

An assay of adenosine deaminase activity in pleural effusions is described. For the continuous determination of adenosine deaminase, the liberated ammonia is estimated by coupling the liberated NH3 with 2-oxoglutarate. The reaction is followed by the decrease of NADH absorbance at 340 nm. The assay was optimized for a Hitachi 705 analyser, with respect to pH, adenosine concentration and glutamate dehydrogenase activity. The assay is linear to an adenosine deaminase catalytic concentration of 110 U/l. Elevated adenosine deaminase activities are found in pleural effusions of patients with tuberculosis, empyema and mesothelioma. Although elevated adenosine deaminase activity in pleural effusion is not pathognomonic for tuberculosis, it may be valuable as a first screening parameter.
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PMID:A continuous method for the estimation of adenosine deaminase catalytic concentration in pleural effusions with a Hitachi 705 discrete analyser. 406 16

The activity of adenosine deaminase (ADA) was determined in serum and pleural fluid of 90 patients with pleural effusions of various aetiology. Tuberculous pleural effusions, empyemas and rheumatoid pleural effusions demonstrated significantly higher activities of ADA than parapneumonic , nonspecific and malignant pleural effusions and effusions in systemic lupus erythematosus and congestive heart failure. In tuberculosis, empyema and rheumatoid arthritis ADA activity was significantly higher in pleural fluid than in serum, indicating a local synthesis of ADA by cells within the pleural cavity in these diseases.
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PMID:Adenosine deaminase in the diagnosis of pleural effusions. 673 Oct 43

We describe a rapid method for the estimation of adenosine deaminase (ADA) activity in cerebrospinal, pleural, peritoneal, and pericardial fluids. Tuberculous effusions show significantly higher levels of ADA activity compared with effusions due to other underlying lesions such as neoplasms, bacterial and viral infections and simple transudates. Similarly, tuberculous meningitis results in raised ADA activity in the cerebrospinal fluid (CSF) when compared with the CSF from patients with other neurological disorders and from normal subjects. The results in 359 cases studied indicated the value of ADA assays in the diagnosis of tuberculous diseases. Levels above 30 IU/I in effusions and above 6 IU/I in the CSF indicate probable tuberculosis.
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PMID:The use of adenosine deaminase assays in the diagnosis of tuberculosis. 708 74

Adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4; ADA) activity is widely distributed in human tissues and is highest in lymphoid tissues. Two ADA isozymes are known as ADA1 and ADA2. Human tissue extracts contained ADA1 predominantly. Meanwhile, ADA2 was the main component of serum ADA. ADA activity was significantly elevated in the sera from patients with hepatic diseases, hematological malignancies and infectious diseases. Serum concentrations of ADA1 were high in patients with acute leukemias, chronic myeloid blast crisis leukemia and acute liver injury. Serum ADA2 levels were raised in patients with adult T-cell leukemia, multiple myeloma (B-J type), infectious mononucleosis, rubella, acquired immunodeficiency syndrome, chronic hepatic diseases and tuberculosis. It is supposed that ADA1 is derived mainly from injured tissues or cells while ADA2 comes from stimulated T-cells.
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PMID:[Adenosine deaminase]. 760 76

We clinico-statistically studied 8 patients (0.77%) with tuberculous peritonitis (3 cases) and tuberculous endometritis (5 cases) aged 50 or older who visited our gynecological clinic for 6 years from July, 1986 to June, 1992 in Tokyo Metropolitan Tama Geriatric Hospital. The mean age was 72 years with a range of 52 to 82 years. Five cases with tuberculous endometritis were diagnosed based on the findings of endometrial cytology and bacteriology, and the incidence was 0.93% of 535 cases in which the uterine cavity could be examined. Three cases with tuberculous peritonitis were strongly suspected by the ascitic findings (cytology and adenosine deaminase level), and culture of ascitic fluid for acid-fast bacilli was positive in 2 of the three cases. Another case with negative culture was diagnosed based on the marked improvement of clinical findings and symptoms during chemotherapy for tuberculosis. No cases were complicated by active lung tuberculosis. All cases had a family and/or past history of pulmonary tuberculosis. The PPD skin test was positive in 7 of the 8 cases. In all cases, the clinical laboratory data and symptoms were markedly improved by chemotherapy for tuberculosis. Endometrial cytology and transvaginal ultrasonography were very effective methods for the diagnosis of tuberculous endometritis and peritonitis associated with ascites.
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PMID:[Clinico-statistical study on tuberculous peritonitis and genital tuberculosis in elderly women]. 773 40


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