Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed a prospective study including cytochemical, bacteriologic and pathologic observations in 25 patients with ascites of different causes. Activity of adenosine deaminase in ascitic fluid was higher in tuberculous (103 +/- 61 mu/l) than in neoplastic (16 +/- 8), inflammatory (16 +/- 13) and portal hypertension (15 +/- 6) etiologies (p less than 0.05). Inflammatory cases included patients with lupus and spontaneous peritonitis. Activity of adenosine deaminase was higher in every patient with tuberculosis than in any other patient. Thus, a high sensitivity and specificity of this test in the diagnosis of tuberculous peritonitis is confirmed.
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PMID:[Adenosine deaminase activity in peritoneal tuberculosis]. 251 74

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

A 51-year-old woman was admitted to our hospital complaining of fever and general fatigue. Physical examination revealed butterfly-like erythema in face, facial edema and diffuse purpura all over her body. Laboratory data showed renal dysfunction, nephrotic syndrome and active phase of SLE. She was administered first methylprednisolone (1g/day/3 days by intravenous drip) then prednisolone (60 mg/day/month, orally) and had immune adsorption therapy for eight times. However, 14 days after the last session of immune adsorption, she developed fever of 39 degrees C and mild headache, and then 3 days later, she gradually became unconscious. Brain CT showed hydrocephalus. We diagnosed her as having tuberculous meningitis based on the detection of acid-fast bacillus in cerebrospinal fluid, and began treatment with antituberculous agents. We suspected that tuberculous meningitis had caused hydrocephalus. We tried percutaneous drainage of the left ventricle for hydrocephalus. Brain MRI showed a tuberculoma depicted as a mass of low intensity in the right cerebellum on the T1-weighted image, and of high intensity on the T2-weighted image, and the meninx in the basal cistern was enhanced. After treatment with antituberculous agents, we performed serial brain MRI and examined cerebrospinal adenosine deaminase activity (ADA). Despite treatment with antituberculous agents, new intracerebral tuberculomas had developed in some areas, whereas they had disappeared in other areas. After treatment for 4 months, the level of cerebrospinal ADA became normal, and the patient recovered consciousness despite the presence of multiple tuberculomas. Both the cell counts and the level of ADA in cerebrospinal fluid are the good indicators of the activity of tuberculous meningitis and reflected its clinical course. Furthermore, the level of ADA in cerebrospinal fluid changed with brain MRI image. Serial brain MRI and examination of ADA in cerebrospinal fluid were useful to know the activity of tuberculous meningitis and to evaluate the response to treatment.
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PMID:[Tuberculous meningitis developed during treatment for systemic lupus erythematosus (SLE)]. 1006 53

A 54-year-old male patient was admitted to Osaka University Medical School Hospital for interferon treatment for chronic hepatitis C and the daily administration of recombinant interferon-alpha 2a started at the dose of 9 megaunits per day. Fourteen days later, moderate right pleural effusion was detected by abdominal magnetic resonance imaging study. He had experienced no symptom to suggest pleural effusion or any pulmonary lesions during interferon treatment. The pleural fluid was serous, showing the character of slightly bloody, turbid and positive Rivalta test, and the levels of lactic dehydrogenase and adenosine deaminase were not elevated. His serum titer of anti-nuclear antibody increased to 80 in homogenous staining, but anti-DNA antibody and anti-liver kidney microsome-1 antibody remained negative. Other laboratory tests or physical findings could not satisfy the criteria of any autoimmune diseases, such as systemic lupus erythematosus. After discontinuation of interferon administration, his pleural effusion resolved gradually and disappeared completely by use of no specific drugs. This is the first case that pleural effusion developed during interferon administration without any other clinical signs indicating autoimmune diseases. The increase of serum titer of anti-nuclear antibody prompted us to elucidate that pleuritis might be induced by immunological activation of interferon.
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PMID:Pleural effusion during interferon treatment for chronic hepatitis C. 1110 Mar 69

Between June 1998 and June 2000, 132 consecutive patients with symptomatic exudative lymphocytic pleural effusion were studied to evaluate the diagnostic role of pleural fluid adenosine deaminase (ADAPF) levels. The mean age was 52.2 (SD 16.3) years. The male to female ratio was 1.4:1. The analysis of ADAPF levels was measured base on Giusti's method. Tuberculous pleural effusion was diagnosed in 50 patients (37.9%). Another 59 patients (44.7%) had malignancies, 23 patients (17.4%) had miscellaneous other etiologies (including; 19 with chronic inflammations, 3 with melioidosis, and 1 with systemic lupus erythrematosus). The percentages of pleural fluid lymphocytes and pleural fluid protein in the tuberculous pleural effusion were similar to those with malignancies, but higher than those in the miscellaneous group. The mean value of ADAPF in the tuberculosis group was 93.2 (SD 56.5) U/l, which was significantly higher than for the malignancy and miscellaneous groups (p<0.05, one-way ANOVA). The mean values of ADAPF in the malignancy group were 36.7 (SD 39.2) U/l, and 31.3 (SD 23.4) U/l in miscellaneous group. Three patients were diagnosed with melioidosis and had ADAPF levels of 15, 46.9, and 49.8 U/l, respectively. One patient with systemic lupus erythrematosus had ADAPF levels of 24.1 U/l. A receiver operating characteristic (ROC) curve identified ADAPF level of 48 U/l as the best cut-off value, which in turn yielded a sensitivity of 80% (95% CI, 73 to 87%) and specificity of 80.5% (95% CI, 73.6 to 87.4%). The positive and negative predictive values at this cut-off value were 71.4% and 86.8%, respectively. The likelihood ratios for the diagnosis of tuberculous pleural effusion in patients with ADAPF levels less than 45 U/ l were 1:4, between 45 and 100 U/l were 5:2, and greater than 100 U/l were 7:1. We concluded that ADAPF levels are a useful diagnostic test for tuberculous pleural effusion. In addition, The analyis of ADA levels can be done simply, quickly, and cheaply.
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PMID:Diagnostic role of pleural fluid adenosine deaminase in tuberculous pleural effusion. 1155 92

We evaluated serum total adenosine deaminase, its isoenzymes adenosine deaminase-1 and adenosine deaminase-2, and cytidine deaminase activities in 24 patients with active systemic lupus erythematosus, and in 26 healthy control subjects, and found the means +/- SD values to be 21.38 +/- 5.96 IU/l, 3.74 +/- 2.12 IU/l, 17.72 +/- 5.02 IU/l and 17.89 +/- 4.62 IU/l, respectively in the patients, and 14.97+/- 4.71 IU/l, 4.01 +/- 1.35 IU/l, 10.91 +/- 3.91 IU/l and 7.39 +/- 3.97 IU/l, respectively in the control subjects. When compared to the healthy controls, serum total adenosine deaminase, adenosine deaminase-2 and cytidine deaminase levels were significantly higher (p<0.001) in systemic lupus erythematosus patients, but the decrease of adenosine deaminase-1 level was not statistically significant (p>0.05). The increased adenosine deaminase-2 may be of macrophage origin. It closely correlated with clinical signs of active systemic lupus erythematosus. The membranes of polymorphonuclear neutrophils may be damaged, and cytidine deaminase may be released into serum. In conclusion, serum total adenosine deaminase, adenosine deaminase-2 and cytidine deaminase activities may serve as useful indicators for evaluating disease activity in patients with active systemic lupus erythematosus.
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PMID:Serum adenosine deaminase and cytidine deaminase activities in patients with systemic lupus erythematosus. 1211 94

We report a case of refractory tuberculous meningitis which was markedly improved by intrathecal administration of isoniazid (INH). The patient was a 35-year-old woman diagnosed with systemic lupus erythematosus (SLE) at age 25, who was being managed with steroid therapy. She was admitted to another hospital due to miliary tuberculosis at age 34, and after discharge continued with a regimen of 2 anti-tuberculosis drugs (INH. Rifampicin (RFP)). She was admitted to our hospital with severe headache and fever on June 18, 2001. She showed severe meningeal irritation, and cerebrospinal fluid (CSF) examination revealed cell counts of 207/microliter (72% polynuclear cells), protein level of 300 mg/dl, glucose level of 13 mg/dl, chloride (Cl) level of 104 mEq/l, adenosine deaminase (ADA) level of 10.0 IU/l. The CSF culture was negative for Mycobacterium tuberculosis (M. tuberculosis) and direct polymerase chain reaction (PCR) for M. tuberculosis DNA was negative, but nested PCR was positive in preserved CSF samples. Marked leptomeningeal enhancement at the basilar meninges was noted by cranial MRI on gadolinium (Gd)-DTPA enhanced T1-weighted images. We diagnosed her condition as tuberculous meningitis and administered a total of 5 anti-tuberculosis drugs over about 2 months. However, during this period, both her clinical and CSF findings worsened, and she developed severe consciousness disturbance showing marked hydrocephalus on cranial MRI in August 2001. Therefore, we initiated intrathecal administration of INH 100 mg 3 times a week for progressive tuberculous meningitis. After the initiation of intrathecal therapy, both her consciousness disturbance and CSF findings were improved almost immediately. Ventriculo-peritoneal shunt operation was performed for hydrocephalus on September 26, 2001, and her clinical symptoms were further improved. To our knowledge, this is the first reported case of refractory tuberculous meningitis markedly improved by intrathecal administration of INH. Our findings suggested that intrathecal administration of INH was useful for refractory tuberculous meningitis.
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PMID:[A case of refractory tuberculous meningitis markedly improved by intrathecal administration of isoniazid (INH)]. 1282 May 46

Decreased numbers of natural killer (NK) cells and impaired NK function have been reported in patients with systemic lupus erythematosus (SLE). Since DAP12 plays a pivotal role in activation of NK cells, we analyzed the expressions of DAP12 protein and mRNA in peripheral blood NK cells from patients with SLE. Both DAP12 protein and mRNA expressions in NK cells from the SLE patients were decreased compared with those in NK cells from normal subjects. Sequence analysis of DAP12 cDNA showed increased nucleotide mutations, including both nucleotide substitutions and deletions. In spite of the mRNA mutations, we found no mutations in genomic DNA, suggesting that mRNA was modified during or after transcription. Decreased expression of DAP12 in NK cells from the patients was accompanied by increased expression of ADAR1 (adenosine deaminase that acts on RNA transcripts) and by decreased expression of NKp44. These results suggest that abnormal expression of DAP12 molecules in NK cells may account for the impairment of NK cell function in patients with SLE.
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PMID:Decreased DAP12 expression in natural killer lymphocytes from patients with systemic lupus erythematosus is associated with increased transcript mutations. 1557 31

We and other investigators have demonstrated up-regulation of the expression of the RNA-editing gene 150-kDa adenosine deaminase that acts on RNA (ADAR1) in systemic lupus erythematosus (SLE) T cells and B cells, peripheral blood mononuclear cells (PBMC), natural killer (NK) cells. The presence of a small proportion of activated T cells is the hallmark of SLE. Therefore, it was hypothesized that 150-kDa ADAR1 gene expression is induced by the physiological activation of T cells. To examine this hypothesis, normal T cells were activated by anti-CD3-epsilon plus anti-CD28 for various time periods from 0 to 48 hr. The expression of 110-kDa and 150-kDa ADAR1, and interleukin (IL)-2 and beta-actin gene transcripts was analysed. An approximately fourfold increase in 150-kDa ADAR1 gene expression was observed in activated T cells. ADAR2 gene transcripts are substrates for ADAR1 and ADAR2 enzymes. Therefore, we assessed the role of the 150-kDa ADAR enzyme in editing of ADAR2 gene transcripts. In activated T cells, site-selective editing of the -2 site was observed. Previous studies indicate that this site is predominantly edited by ADAR1. In addition to this, novel editing sites at base positions -56, -48, -45, -28, -19, -15, +46 and +69 were identified in activated T cells. On the basis of these results, it is proposed that 150-kDa ADAR1 gene expression is selectively induced in T cells by anti-CD3-epsilon and anti-CD28 stimulation and that it may play a role in site-selective editing of gene transcripts and in altering the functions of several gene products of T cells during activation and proliferation.
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PMID:Induction of 150-kDa adenosine deaminase that acts on RNA (ADAR)-1 gene expression in normal T lymphocytes by anti-CD3-epsilon and anti-CD28. 1789 25

The aetiopathogenesis of the abnormal immune response in systemic lupus erythematosus (SLE) remains incompletely understood. We and other investigators demonstrated altered expression of adenosine deaminase that act on RNA (ADAR) genes in SLE patients. Based on this information, we hypothesize that the altered expression and function of ADAR enzymes is a mechanism for the immunopathogenesis of SLE. ADARs edit gene transcripts through site-specific conversion of adenosine to inosine by hydrolytic deamination at C6 of the adenosine. Thirteen SLE subjects and eight healthy controls were studied. We assessed the role of ADAR enzymes in editing of PDE8A1 gene transcripts of normal and SLE T cells. These studies demonstrated the occurrence of ADAR-catalysed altered and site-selective editing profile of specific sites in the PDE8A1 gene transcripts of normal and SLE T cells. Two hot spots for A to I editing were observed in the PDE8A1 transcripts of normal and SLE T cells. A fundamental finding of this study is A to I hypo-editing followed by up-regulation of PDE8A1 transcripts in SLE T cells. These results are confirmed by analysing PDE8A1 transcripts of normal T cells activated with type I interferon-alpha. It is proposed that, the altered expression of ADAR enzymes tilt the balance of editing machinery and alter editing in SLE transcriptome. Such altered editing may contribute to the modulation of gene regulation and ultimately, immune functions in SLE and play an important role in the initiation and propagation of SLE pathogenesis.
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PMID:Altered editing in cyclic nucleotide phosphodiesterase 8A1 gene transcripts of systemic lupus erythematosus T lymphocytes. 1846 47


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