Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Total adenosine deaminase (ADA) activity and its isozyme (ADA1 and ADA2) activities were measured in pleural effusions and serum samples from patients with tuberculosis and in those from patients with lung cancer as controls. To analyze the cellular source of ADA isozymes in tuberculous pleural effusions, ADA isozyme activities in CD2+ T lymphocytes purified from tuberculous pleural effusions and cultured human cell lines derived from hematopoietic tumors were measured. Tuberculous pleural effusions had a much higher ADA activity than cancerous effusions, and high ADA activity mainly originated from the increase in ADA2 activity. Further, total ADA activity in tuberculous pleural effusions decreased after antituberculosis treatment, because of the decrease in ADA2 activity. On the other hand, measurement of ADA and ADA isozyme activities in T lymphocytes purified from tuberculous pleural effusions and human hematopoietic cell lines showed dominant expression of ADA1 in total ADA activity. In conclusion, we found that ADA2 is a dominant component of tuberculous pleural effusions and that ADA1 is a major component of lymphoid cells. These results suggest that elevation of ADA activity in tuberculous pleural effusions does not always reflect the activation of cell-mediated immunity.
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PMID:Adenosine deaminase isozymes in tuberculous pleural effusion. 865 33

Because of the difficulty in isolating the causative organism, pericardial tuberculosis is rarely diagnosed. Adenosine deaminase activity measured in the pericardial fluid of 108 patients was initially of undetermined origin. Subsequently, we classified five sources: (1) tuberculosis (20 cases); (2) idiopathy (82 cases); (3) neoplasia (three cases); (4) purulent bacterial infection (two cases); and (5) radiotherapy (one case). The highest mean adenosine deaminase value (126 +/- 16.68 U.l(-1) was found in group 1; other values were 29.4 +/- 8.9, 27 +/- 7.21, 29.5 +/- 13.4, 26 U.l(-1) in the idiopathy, neoplasia, purulent bacterial infection and radiotherapy groups, respectively. there was a statistically significant difference between group 1 and the other groups (P less than 0.001), indicating that the adenosine deaminase value has 100% sensitivity and 91% specificity. In addition, there was a positive correlation between high adenosine deaminase values and the development of constrictive pericarditis. In this study, two patients required pericardectomy. Therefore, the adenosine deaminase value is a significant prognostic indicator for the development of constrictive pericarditis in tuberculous pericarditis.
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PMID:The diagnostic and prognostic value of adenosine deaminase in tuberculous pericarditis. 866 76

An exhaustive search for the clinical records of patients diagnosed with tuberculous disease was done in the hospitals of the area under study, which involves 392,000 population. During the years 1992, 1993 and 1994. There were included: 1) patients who had positive bacilloscopy and/or positive Lowenstein's culture in any specimen: 2) patients younger than 35-years-old who had pleural effusion, significant Mantoux and adenosine deaminase (ADA) over 47 U/I in the pleural effusion. In total 814 patients remained in the study with an average age of 38.39(19.39 DE) in 1992, 39.02 (20.04 DE) in 1993, and 34.1 years-old (19.2 DE) in 1994, with extreme ages of 2 months and 87 years-old. The incidence/100,000 H was: in 1992: 67.86, in 1993: 66.58 and in 1994: 73.2. The contagious forms incidence/100,000 H was: 1.5 in 1992 and 1993; and 1.79 in 1994. The hospital mortality incidence/100,000 H was 2.04 in 1992, 2.30 in 1993 and 2.6 in 1994. We conclude that tuberculosis is endemic in our area with moderately high and stationary incidence.
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PMID:[Epidemiological study of tuberculosis in the health area of Santiago de Compostella in 1992, 1993 and 1994]. 909 Oct 37

The rise in adenosine deaminase (ADA) activity in the pleural fluid of tuberculous pleurisy patients, though used for diagnosis, is of unknown origin. In this work, we determined ADA activity and the activities of 2'-deoxyadenosine deaminase and ADA-2 in 350 patients. We also considered whether the results throw light on the origin of high pleural fluid ADA in tuberculous pleurisy and estimated the diagnostic efficiency of 2'-deoxyadenosine deaminase, ADA-2 and total ADA activities with and without the inclusion of the 2'-deoxyadenosine deaminase/ADA activity ratio in a combined criterion. The 350 pleural effusions were classified by previously established criteria as transudates (60 males/18 females) or as tuberculous (49 males/27 females), neoplastic (50 males/39 females), parapneumonic (36 males/19 females), empyematous (11 males/3 females), or miscellaneous (25 males/13 females) exudates. Total ADA, ADA-2 and 2'-deoxyadenosine deaminase activities were, respectively, 127.5 +/- 2.9, 103 +/- 29.5 and 42.8 +/- 14 U.L-1 in tuberculous exudates. With diagnostic thresholds of 47, 40 and 22 U.L-1 respectively, the sensitivities of ADA, ADA-2 and 2'-deoxyadenosine deaminase for tuberculosis were 100, 100 and 95%; their specificities 91, 96 and 92%; and their efficiencies 93, 97 and 93%, respectively. One hundred and one effusions (all 76 tuberculous, 12 neoplastic, 4 parapneumonic and 9 empyematous exudates) had total ADA levels > 47 U.L-1; of these, 8 neoplastic, 1 parapneumonic and all the tuberculous exudates had a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49. The criterion of simultaneously having ADA > 47 U.L-1, ADA-2 > 40 U.L-1 and a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49 was satisfied by all the tuberculous effusions but only eight others (all neoplastic) (sensitivity 100%, specificity 97%, efficiency 98%). We conclude that: 1) high total ADA activity in tuberculous pleural effusions is due mainly to an increase in ADA-2, and, therefore, originated from the only known source monocytes and macrophages; 2) ADA-2 was a more efficient diagnostic marker of tuberculous pleurisy than total ADA activity, although the difference was not statistically significant; and 3) among effusions with high total ADA the 2'-deoxyadenosine deaminase/ADA activity ratio differentiates tuberculous effusions from empyemas and parapneumonic effusions, but fails to discriminate well between tuberculous and neoplastic effusions.
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PMID:Adenosine deaminase (ADA) isoenzyme analysis in pleural effusions: diagnostic role, and relevance to the origin of increased ADA in tuberculous pleurisy. 872 40

In order to evaluate the role of the determination of adenosine deaminase activity (ADA) in ascitic fluid for the diagnosis of tuberculosis, 44 patients were studied. Based on biochemical, cytological, histopathological and microbiological tests, the patients were divided into 5 groups: G1-tuberculous ascites (n = 8); G2-malignant ascites (n = 13); G3-spontaneous bacterial peritonitis (n = 6); G4-pancreatic ascites (n = 2); G5-miscelaneous ascites (n = 15). ADA concentration were significantly higher in G1 (133.50 +/- 24.74 U/l) compared to the other groups (G2 = 41.85 +/- 52.07 U/l; G3 = 10.63 +/- 5.87 U/l; G4 = 18.00 +/- 7.07 U/l; G5 = 11.23 +/- 7.66 U/l). At a cut-off value of > 31 U/l, the sensitivity, specificity and positive and negative predictive values were 100%, 92%, 72% and 100%, respectively. ADA concentrations as high as in tuberculous ascites were only found in two malignant ascites caused by lymphoma. We conclude that ADA determination in ascitic fluid is a useful and reliable screening test for diagnosing tuberculous ascites. Values of ADA higher than 31 U/l indicate more invasive methods to confirm the diagnosis of tuberculosis.
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PMID:The value of adenosine deaminase (ADA) determination in the diagnosis of tuberculous ascites. 872 56

A 69-year-old male of effusive-constrictive pericarditis with a symptom of right heart failure was reported. The patient underwent surgery, as the medical treatment had not been effective. Through median spritting, very thickened pericardium and calcified epicardium of the right atrium, the right ventricle and the left ventricle were resected as largely as possible. In the space between the pericardium and epicardium, there existed yellow and thick fluid of about 50 ml which was evacuated. After surgery hemodynamic improvement was observed and the patient experienced a smooth postoperative course. Although pathological examinations revealed no special findings except the increased activity of adenosine deaminase of the yellow and thick fluid, tuberculosis was mostly suspected as the cause of the disease.
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PMID:[A case of effusive-constrictive pericarditis and its surgical treatment]. 874 57

The diagnostic value of adenosine deaminase (ADA) activity was studied to evaluate its use in the differential diagnosis of tuberculous meningitis in the local setting. Cerebrospinal fluid (CSF) from 119 patients with meningitis and other conditions with central nervous system symptoms were collected and ADA activity determined by the colorimetric method of Guisti read at 628 nm. The CSF was also subjected to other laboratory examinations so as to provide the aetiological diagnosis. All 14 tuberculous meningitis patients had ADA activity greater than the cut off value of 9.0 IU/L. High ADA activity was also seen in 13 of 105 non-tuberculous cases giving a specificity of 87.6%. Even though the ADA activity determination is sensitive for tuberculosis, it was not specific enough to be used as a rapid diagnostic test. However when interpreted together with clinical signs and symptoms and other laboratory tests, it is a useful adjunctive rapid marker for tuberculosis.
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PMID:The use of adenosine deaminase activity as a biochemical marker for the diagnosis of tuberculous meningitis. 893 28

When performing thoracoscopy in patients with pleural effusion of unknown origin, we used two bronchoscopes simultaneously, one for observation and one for biopsy. A total of 50 patients with pleural effusion of unknown origin were studied. In all of those studies, pleural effusion was exudative, lymphocyte-dominant, had a low level of adenosine deaminase, no malignant cells, and no tuberculosis or other bacteria in pleural effusion smears. Fourteen were out-patients. A catheter was inserted into the pleural space under local anesthesia, and 300 ml to 500 ml of pure oxygen was injected to create a pneumothorax. Two flexible fiberoptic bronchoscopes were used simultaneously, one for observation and one for biopsy. Approximately 1 hour after the examination, the out patients were able to return home. Lesions in the pleural cavity were found in 42 of these 50 patients, and histological diagnosis was possible in 46. This is a simple procedure with no major side effects. The equipment required is familiar to pulmonary physicians, and the diagnostic yield is high.
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PMID:[Thoracoscopy with two bronchoscopes in 50 patients with pleural effusion of unknown origin]. 893 36

Tuberculous peritonitis, although common in Third World countries, remains an uncommon cause of ascites in the United States. Ascitic fluid adenosine deaminase (ADA) activity has been proposed as a useful diagnostic test. The aim of this retrospective study was to determine the clinical utility of ascitic fluid ADA activity in diagnosing tuberculous peritonitis in a U.S. patient population. A total of 368 ascitic fluid specimens from a well-characterized ascitic fluid bank, including tuberculous peritonitis (n = 7), tuberculous peritonitis in the setting of cirrhosis (n = 10), and consecutive specimens of widely varied etiologies (n = 351) were analyzed for ADA activity by ultraviolet spectrophotometry at 265 nm. The overall sensitivity of the ADA determination in diagnosing tuberculous peritonitis was only 58.8%, and the specificity was 95.4%. The accuracy of ADA determination (93.8%) compared favorably with that of the common ascitic fluid tests of white blood cell (WBC) count (>500/mm3), total protein (>2.5 g/dL), and combined WBC count and total protein (45.8%, 74.4%, and 81.3%, respectively). However, ADA was only 30% sensitive in detecting tuberculous peritonitis in the setting of cirrhosis, and cirrhosis was present in 59% of the tuberculous peritonitis patients in our population. In addition, malignancy-related ascites (13%) and bacterial peritonitis specimens (5.8%) occasionally yielded false-positive results. In conclusion, our results indicate that the ascitic fluid ADA activity has good accuracy but poor sensitivity and imperfect specificity in a U.S. patient population in which the prevalence of tuberculosis is low and underlying cirrhosis is common.
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PMID:Ascitic fluid adenosine deaminase insensitivity in detecting tuberculous peritonitis in the United States. 893 71

To investigate the diagnostic utility of adenosine deaminase as a test for tuberculosis, molecular forms of the enzyme indicative of cell-mediated immunity were studied in tuberculosis pleural effusion, peritonitis and meningitis. Twenty-six pleural, 21 peritoneal, and 24 cerebrospinal tuberculous and non-tuberculous fluids were examined for adenosine deaminase and the large and small forms of the enzyme were differentiated on immunoblots. Adenosine deaminase levels ranged from zero to 81 units/L, zero to 31 units/L and zero to 31 units/L in the pleural, peritoneal and cerebrospinal fluids, respectively. The large form of adenosine deaminase (280 kDa) was detected in one of 14 proved tuberculous cases, a peritoneal fluid. The small form of the enzyme (35-39 kDa) was seen in both tuberculous and non-tuberculous conditions in 6 pleural, 7 peritoneal and 8 cerebrospinal fluids. Molecular forms of adenosine deaminase did not appear to help in the diagnosis of tuberculosis in this patient population and may not be suited for analysis in fluids with low enzyme activity.
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PMID:Molecular forms of adenosine deaminase do not aid the diagnosis of tuberculosis. 901 6


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