Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.4 (deaminase)
 5,113 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 26-year-old woman visited the first hospital due to ascites in August 2003, She had continual abdominal pain diagnosed as Irritable bowel disease after a gastrointestinal and colon fiberscopy was performed. Chest-abdominal CT scan revealed normal chest, massive ascites and swollen ovary. To rule out malignancy, surgical biopsy was performed, which brought no significant findings. We focused on the high value of Adenosin deaminase (ADA) in ascites and strongly suspected tuberculotic peritonitis. Consequently, pathologist confirmed the existence of bacterial bodies stained by acid-fast stain after our consultation. Compared with the poor diagnostic accuracy of surgical biopsy, the value of ADA in ascites has a very high sensitivity and specificity. Considering the high risk of being infertile, to begin diagnostic medication of tuberculotic peritonitis is an acceptable choice for young women with a high value of ADA in the ascites.
 ...
PMID:[A case of a young woman with tuberculous peritonitis diagnosed owing to high value of ADA]. 1556 Mar 83

Adenosin deaminase (ADA) deficiency is the cause for Severe Combined Immunodeficiency (SCID) in about 15% of patients with SCID, often presenting as T (-)B (-)NK (-)SCID. Treatment options for ADA-SCID are enzyme replacement, bone marrow transplantation or gene therapy. We here describe the first patient with ADA-SCID and fatal hepatic failure despite bone marrow transplantation from a 10/10 HLA identical related donor. As patients with ADA-SCID may be at yet underestimated increased risk for rapid hepatic failure we speculate whether hepatitis in ADA-SCID should lead to the immediate treatment with enzyme replacement by pegylated ADA.
 ...
PMID:Hyperbilirubinemia and rapid fatal hepatic failure in severe combined immunodeficiency caused by adenosine deaminase deficiency (ADA-SCID). 2127 5

Diagnosis of tuberculous meningitis (TBM) is always a challenge. We must give importance for duration of clinical manifestations. Cerebrospinal fluid (CSF) has own characteristic and it have to be control several times during the treatment. Adenosin deaminase with cut off more than 15 UI/mL and M. tuberculosis polymerase chain reaction in CSF are the most relevant diagnostic tests. Radiologic test gives diagnostic clues but do not confirm the diagnosis. In the future we can structure a score with all these elements to support the clinician in the diagnostic process. The treatment of TBM because of its high morbidity and high mortality has to be necessarily more intensive and prolonged and we must select drugs with a good penetration into the central nervous system (SNC). A therapeutic scheme with duration of 12 months with two phases is proposed, the diary phase during the first three months of treatment includes isoniacid, rifampicin, pirazinamid and ethambutol or moxifloxacin. Streptomycin must not be included due to own erratic SNC penetration and its known toxicity. The second twice a week phase has to be changed by a three times per week phase during 9 months and it must include isoniacid, rifampicin and pirazinamide. Dexamethasone is added during the first 6 weeks of treatment. Patients with HIV infection than required treatment with antiretroviral drugs have to start ART treatment when diary phase has finished and must not include protease or integrase inhibitors.
 ...
PMID:[Tuberculous meningitis: tips for diagnosis and proposals for treatment]. 2187 50

The aim of the article is to describe the principal findings among patients with M.tuberculosis and M. bovis CNS infection. Mycobacterium tuberculosis is one of the most common infectious agents that cause death and neurological sequelae around the world. Most of the complications of CNS TB can be attributed to a delay in the diagnosis. Unfortunately, there are no specific diagnostic tools to support an early diagnosis. Other prognostic factors different from delay in treatment have not been identified. Clinical, radiological and laboratory characteristics were analyzed retrospectively from the medical files of all the patients admitted with the diagnoses of tuberculosis. Of 215 patients admitted with systemic tuberculosis, 64 (30%) had a neurological infection. Positive cultures were found in 54 (84%) cases, 18 (33%) in the CSF and the rest in other fluids or tissues. Adenosin deaminase (ADA) enzyme determination was more sensitive than M. tuberculosis PCR in the CSF for supporting an early diagnosis. In addition to a later clinical stage and treatment lag, positive CSF cultures (P=0.001) and the presence of M. bovis (P=0.020) were prognostic factors for a worse outcome. Neither older age, the presence of tuberculomas versus meningeal enhancement, or HIV co-infection, was associated to a worse prognosis. The isolation of M. bovis subspecies was more common that previously reported, and it was associated to the development of parenchymal lesions (P=0.032) when compared to M. tuberculosis. In this study, positive CSF cultures for M. tuberculosis and further identifying M. bovis species were additional prognostic factors for worse outcome. Positive cultures in systemic fluids other than CSF, even when the patient had no obvious systemic manifestations, and ADA determination in the CSF were noteworthy diagnostic tools for the diagnosis.
 ...
PMID:Importance of differentiating Mycobaterium bovis in tuberculous meningitis. 2236 76