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: UMLS:C0031154 (peritonitis)
15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The value of ascites gamma interferon concentration and ascites adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a prospective study of 86 patients with ascites, including 16 with tuberculous peritonitis. Gamma interferon concentration was higher in tuberculous peritonitis than in the other causes of ascites (p less than 0.0001), and a cut-off between 3 and 9 u/ml reached a sensitivity and a specificity of 100%. The mean (+/- SD) gamma interferon level in tuberculous ascites was 39.3 +/- 18.3 u/ml in patients seronegative for HIV and 14.2 +/- 4.7 u/ml in patients with AIDS (p = 0.01). Adenosine deaminase activity in tuberculous ascites was also higher than in the other causes of ascites (p less than 0.0001), and a cut-off of 40 u/l reached a sensitivity of 100% and a specificity of 97%. The two false positives for adenosine deaminase test were true negatives for the gamma interferon test. There was no significant correlation between gamma interferon concentration and adenosine deaminase activity either in tuberculous ascitis or in any other group. This study suggests that ascites gamma interferon determination may be very useful in the screening of tuberculous peritonitis, but its cost makes it advisable to use adenosine deaminase activity as a routine test, at least in areas where tuberculosis is endemic.
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PMID:Diagnostic value of ascites gamma interferon levels in tuberculous peritonitis. Comparison with adenosine deaminase activity. 177 79

Tuberculous peritonitis is a rare disease, which often goes unrecognized because of the subtle clinical clues and its insidous onset. We retrospectively analyzed the records of 37 cases of tuberculous peritonitis diagnosed over a 15-year period, and compared the clinical and diagnostic features of cirrhotic and noncirrhotic patients. In cirrhotic patients, tuberculous peritonitis can simulate ascites from liver disease or spontaneous bacterial peritonitis. The diagnosis is difficult in these patients because the ascitic fluid may not be of the exudative type as a result of the low albumin level in serum, and lymphocytes do not predominate in all cases. Adenosine deaminase (ADA) activity in ascitic fluid was elevated (higher than 40 U/L) in all 11 patients (four patients with hepatic cirrhosis). The time required to achieve a correct diagnosis was significantly longer in cirrhotic than in noncirrhotic patients. The overall mortality was 13%, with deaths occurring exclusively among cirrhotic patients. We emphasize that tuberculous peritonitis in cirrhotic patients can present an atypical picture. A considerable element of suspicion is necessary.
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PMID:Tuberculous peritonitis: a study comparing cirrhotic and noncirrhotic patients. 214 14

We studied the activity of adenosine deaminase in the peritoneal fluid of 66 patients who were divided into five groups according to causes of ascites as follows: tuberculous peritonitis (group I), septic peritonitis (group II), secondary to malignant tumours (group III), miscellaneous conditions (group IV), and control subjects of transudates (group V). In patients with tuberculous peritonitis the enzyme activity was significantly higher than for the rest of the groups (p less than 0.001), and enzyme concentrations in all patients were well above the upper non-tuberculous value. Adenosine deaminase activity in the peritoneal fluid has proved to be a simple and reliable method for early diagnosis of tuberculous peritonitis.
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PMID:Adenosine deaminase activity in the diagnosis of tuberculous peritonitis. 375 18

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

Adenosine deaminase (ADA), which catalyzes the irreversible deamination of adenosine to inosine, is related to various human diseases such as tuberculous peritonitis and leukemia. Therefore, the method used to detect ADA activity and screen the effectiveness of various inhibitor candidates has important implications for the diagnosis treatment for various human diseases. A simple and rapid assay method for ADA, based on the enzymatic formation of a luminescent lanthanide complex, is proposed in this study. Inosine, an enzymatic product of ADA with stronger sensitization efficiency for Tb³⁺ than adenosine, produced a strong luminescence by forming an inosine-Tb³⁺ complex, and it enabled the direct monitoring of ADA activity in real-time. By introducing only Tb³⁺ to adenosine and ADA in the buffer, the enhancement of luminescence enabled the detection of a low concentration of ADA (detection limit 1.6 U/L). Moreover, this method could accurately determine the inhibition efficiency (IC₅₀) of the known ADA inhibitor, erhythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), and the inhibition of ADA could be confirmed by the naked eye. Considering its simplicity, this assay could be extended to the high-throughput screening of various ADA inhibitor candidates.
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PMID:Development of a Simple Assay Method for Adenosine Deaminase via Enzymatic Formation of an Inosine-Tb³⁺ Complex. 3121 43

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