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)

Twenty-six patients with hairy cell leukemia (HCL) were treated with 2-chlorodeoxyadenosine (2-CdA), a purine analogue resistant to adenosine deaminase, at 0.1 mg/kg/d for 7 days by continuous intravenous infusion. Fifteen patients were previously untreated, while 11 patients had received prior treatment with splenectomy alone (three patients), interferon alpha alone (four), splenectomy, then interferon alpha (two), or splenectomy, interferon alpha, then 2-deoxycoformycin (2-DCF) (two). Sixteen (80%) of 20 patients evaluable at 3 months achieved complete remission (CR), and four (20%) achieved partial remission (PR) following a single cycle of therapy. All four patients in PR had complete recovery of their peripheral blood counts (except one patient whose platelet count remained 84,000/microL), but had residual HCL in the bone marrow (three patients) or residual splenomegaly (one). Patients with bulky adenopathy, massive splenomegaly, and severe pancytopenia responded as well as those with only modest marrow involvement. The three patients with residual marrow disease received a second cycle of 2-CdA, and two have attained CR. Therefore, 18 of 20 (90%) achieved CR with either one or two cycles of therapy. No patient achieving CR has relapsed at a median follow-up of 12 (+/- 2.1) months. Toxicities included myelosuppression and culture-negative fever. A community-acquired pneumonia was the only infectious complication. Since a single cycle of 2-CdA induces sustained CR in the vast majority of patients with minimal toxicity, this agent is emerging as the treatment of choice for all patients with HCL.
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PMID:A single cycle of 2-chlorodeoxyadenosine results in complete remission in the majority of patients with hairy cell leukemia. 135 62

ATL is a unique T-cell malignancy first described by Takatsuki and colleagues in 1970s. We estimate that more than 300 patients a year have been detected in the endemic areas of Kyushu, Japan. The surface phenotype of ATL cells characterized by monoclonal antibodies is T3+, T4+, T8-, T11+ and Tac+. In all cases the serum is positive for anti-HTLV-I antibodies and the ATL cells contain the proviral DNA of HTLV-I. Variations in the clinical features of atypical ATL suggested a division of the spectrum of ATL into five types: acute; chronic; smoldering; crisis; and lymphoma. Typical ATL takes an acute course. The survival time is short, with 50% mortality within approximately 5 months. In general a poor prognosis is indicated by the elevation of serum lactate dehydrogenase, calcium, and bilirubin, as well as by high WBC. Smoldering ATL is characterized by the presence of a few abnormal cells (0.5%-3%) in the peripheral blood over a long period. Crisis in chronic or smoldering ATL means the progression of the disease to acute ATL. The lymphoma type of ATL is considered to be a form of T-cell-type non-Hodgkin's lymphoma in which malignant cells contain proviral DNA of HTLV-I. Screening of the sera from healthy adults for presence of the anti-HTLV-I antibodies revealed that 3.6% of healthy individuals in Kumamoto Prefecture, which is located in the middle of Kyushu, were HTLV-I carriers. Family studies showed that the routes of natural infection of HTLV-I are from mother to child and also from husband to wife. The borderline between the healthy carrier state and smoldering ATL remains unclear. Smoldering ATL is frequently diagnosed in patients with fungus infection of the skin, chronic lymphadenopathy, interstitial pneumonitis, chronic renal failure and strongyloidiasis. Five patients with ATL refractory to conventional chemotherapeutic agents were treated with 2'-deoxy-coformycin (DCF), a potent inhibitor of adenosine deaminase. Two patients showed a good response, and three were resistant to DCF. In addition our experiences with a concurrence of lymphoma-type ATL in three sisters and spontaneous remissions in a patients with chronic ATL will be referred.
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PMID:[Overview of ATL (adult T-cell leukemia) research]. 288 29

Acquired immunodeficiency syndrome (AIDS) is an often fatal disease caused by a retrovirus frequently resulting in malignancy and/or opportunistic infection. Because the immune deficiency in AIDS is similar to that in some purine enzyme deficiencies, we measured erythrocyte adenosine deaminase (ADA) and purine nucleoside phosphorylase activities in patients with AIDS, heterosexual controls, and a high-risk asymptomatic population. We found that erythrocyte ADA activity was significantly elevated in patients with AIDS (40 +/- 11 nmol/mg of hemoglobin per hr, mean +/- SD) relative to heterosexual controls (25 +/- 10, P less than 0.001). We also measured ADA activity in a group of individuals at high risk for AIDS and found that approximately half had significantly elevated ADA activities (45 +/- 4, P less than 0.002) that correlated with the presence of antibody to the lymphadenopathy retrovirus. Purine nucleoside phosphorylase activity was relatively normal in patients with AIDS as well as in individuals at risk for AIDS. Increased ADA appears to be a diagnostic marker of AIDS and may be useful in conjunction with antibody to the AIDS-related retrovirus in detecting the presence of infection in asymptomatic high-risk individuals. These data also suggest that, in addition to the lymphocyte, the erythroid cell line may also be infected by the AIDS-related retrovirus.
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PMID:Elevated erythrocyte adenosine deaminase activity in patients with acquired immunodeficiency syndrome. 300 27

Deoxycoformycin (DCF) is an inhibitor of adenosine deaminase (ADA). Twenty-one courses of DCF were administered to 13 patients ranging in age from 15 to 78 yr. Eight patients had T-cell disorders, and five patients had non-T-cell malignancies. The i.v. bolus dose was escalated from 5 to 30 mg/sq m/day, and the duration of the courses ranged from 1 to 5 days. The DCF plasma half-life ranged from 4.9 to 6.2 hr and was independent of dose. The dose-limiting toxicities involved the central nervous system (CNS) and the kidneys. Other toxicities included bronchitis, decreases in hematocrit, arthralgias, and myalgias. Mortality was encountered in three patients. These toxic effects may have been secondary to the accumulation of the metabolites adenosine and deoxyadenosine. Deoxyadenosine and adenosine were both detectable in plasma (10(-6) M) and in urine (10(-3) M). Two partial remissions were observed: one in a patient with T-cell ALL and another in a patient with mycosis fungoides. Minimal responses characterized by either declines in peripheral blast counts or partial resolution of adenopathy were observed in five other patients. No responses were observed in six patients. These observations suggest that DCF is effective in the treatment of T-cell lymphoid malignancies.
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PMID:Clinical pharmacology of deoxycoformycin. 626 81

Examining the activity of serum adenosine deaminase in 112 patients with lymphadenopathy of various etiology revealed its increase (at the discriminant level equal or exceeding 20 U/l) in 86% of 50 patients with active tuberculous infection. The specificity of the parameter as a test for tuberculous peripheral lymph nodal lesion is 90.3%, the positive and negative prognostic significances are 83 and 89%, respectively, the diagnostic efficiency is 88.4%.
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PMID:[Adenosine deaminase in differential diagnosis of peripheral lymph node tuberculosis]. 961 80

The authors review 45 pediatric patients with intra-abdominal tuberculosis (ATB) treated between May 1990 and April 1998. The diagnosis was confirmed histologically or by positive culture for Mycobacterium tuberculosis. Clinical presentation was with an abdominal mass (12), subacute obstruction (11), ascites (5), mass and ascites (4), peritonitis (4), and 9 unusual presentations. Mantoux tests were positive in 68% of patients tested. There were radiologic features suggestive of pulmonary TB in 29 patients (64%); abnormal abdominal radiographs were recorded in 21 (47%). Lymphadenopathy was noted on abdominal ultrasound in 23 of 30 patients (77%) and on computed tomography scan in a further 3 of 8 patients investigated. Ascitic fluid adenosine deaminase (ADA) levels were greater than 30 IU/l in 3 of 4 patients (75%), suggesting ATB. All 28 patients screened for human immunodeficiency virus were negative. A surgical procedure was performed in 39 patients. 29 (74%) had an elective diagnostic laparotomy for tissue diagnosis. One (3.4%) developed a postoperative intra-abdominal abscess. Ten (26%) presented with complications requiring surgical intervention including perforated viscus, segmental bowel resection, strictureplasty, adhesiolysis, or ileostomy. One of the latter died due to sepsis after having complications of persistent intestinal obstruction and cecal perforation. The authors recommend an aggressive approach to patients with suspected ATB in order to obtain an early definitive diagnosis, prevent complications, and reduce morbidity and mortality. They emphasize the importance of tissue diagnosis and confirmation by culture.
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PMID:Diagnostic dilemmas in abdominal tuberculosis in children. 1131 66

Adenosine deaminase inhibitors have proven superior to alkylating agent-based therapies in inducing clinical and hematologic remissions in treated and previously untreated chronic lymphocytic leukemia (CLL) patients, and they have become increasingly accepted as a standard for therapy. We report the case of a 66-year-old patient with a 7-year history of CLL who had been previously treated with alkylating agents. Upon presentation with abdominal lymphadenopathy, a 5-day course of the nucleoside analogue, fludarabine, was administered. Two days after completion, the patient developed acute tumor lysis syndrome (TLS) that induced renal failure with hyperkalemia and hyperuricemia. This resulted in critical, life-threatening complications requiring hospitalization, aggressive hemodialysis and fluid replacement therapy. While only 5 other cases of TLS associated with fludarabine therapy have been reported since 1989, we recommend that adenosine deaminase inhibitor therapy be initiated with the addition of allopurinol, and that hydration with copious amounts of oral fluids during therapy be encouraged in order to help protect against the renal effects of potential TLS induced by these agents.
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PMID:Tumor lysis syndrome (TLS) following fludarabine therapy for chronic lymphocytic leukemia (CLL): case report and review of the literature. 1260 95

A thirty-six year old male patient presented with dyspnea, right-sided chest pain, night sweats and intermittent fever. He has a history of ankylosing spondylitis treated with tumour necrosis factor-alpha (TNF-alpha) antagonist (infliximab). Computed tomography of the chest showed mediastinal lymphadenopathy, right-sided pleural effusion, and atelectasis. The pleural fluid was exudative with lymphocyte dominance. Closed pleural biopsy was nondiagnostic. The adenosine deaminase level of the pleural fluid was 110 U/L. In light of these findings, the patient was diagnosed as tuberculous pleurisy and antituberculous treatment was given. After one month, pleural fluid was markedly reduced.
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PMID:[Tuberculous pleurisy after tumour necrosis factor-alpha antagonist usage: case report]. 1912 83

A 16-years-old Egyptian girl presented with massive pericardial effusion, fever, weight loss and hoarseness of voice. Laryngoscopy showed left vocal cord paralysis. Chest CT revealed pericardial effusion, amalgamated mediastinal lymph nodes and clear lung fields. Pericardial fluid analysis revealed a lymphocytic exudate with high adenosine deaminase enzyme level, negative stains and cultures for bacteria and fungi. Despite a negative nucleic acid test for tuberculosis; antituberculous and corticosteroids therapies resulted in resolution of pericardial effusion after 3 weeks but hoarseness of voice persisted. Few cases of vocal cord paralysis with tuberculous mediastinal lymphadenopathy were reported in English literature.
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PMID:Tuberculous pericarditis associated with hoarseness of voice due to left recurrent laryngeal nerve paralysis. 2267 7

A 62-year-old woman with liver cirrhosis developed ascites. She had been previously treated with a combination of interferon and ribavirin therapy. The ascites was bloody and of exudative nature. Radiological examinations showed supraclavicular, axillar, and mediastinal lymphadenopathy. Biopsy of the axillar lymph node was performed because of suspected malignancy, and the results showed that the lymph node had granulomatous inflammation with caseous necrosis and Langhans giant cells, suggestive of mycobacterial infection. Furthermore, a DNA sequence specific to Mycobacterium tuberculosis was recovered from the same lesion, leading to a diagnosis of tuberculous lymphadenitis. The ascites and the lymphadenopathy subsided with anti-tuberculosis chemotherapy. Although bacilli were not detected in the ascites, a high level of adenosine deaminase in the ascites, the coexistence of tuberculous lymphadenitis, and the response to anti-tuberculosis agents supported the diagnosis of tuberculous peritonitis. Although tuberculous peritonitis is often difficult to diagnose, lymph node biopsy was useful to establish the diagnosis in the present case.
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PMID:[A case of tuberculous peritonitis accompanied by lymphadenitis in a patient with liver cirrhosis in which lymph node biopsy was useful for establishing the diagnosis]. 2335 May 17


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