Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.4.17 (adenosine deaminase)
 5,206 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

YK-176 is a newly isolated 2'-deoxycoformycin (DCF), a potent inhibitor of adenosine deaminase, produced by Aspergillus nidulans. In a cooperative phase I study, YK-176 was administered to 22 patients, comprising 18 with adult T-cell leukemia-lymphoma (ATL), two with cutaneous T-cell lymphoma (CTCL), one with lymphoblastic lymphoma of T-cell type and one with carcinoma of the uterine cervix. Doses of YK-176 ranged from 3.0 to 9.0 mg/m2 and were given intravenously for three consecutive days. General malaise, anorexia, nausea, vomiting and low grade fever were frequently encountered, but were transient and not dose-related. At all dose levels hematological toxicities were mild. Two of seven patients receiving 7.0 mg/m2 for three consecutive days developed hepatocellular enzyme elevations (grade 2) and one patient, proteinuria (grade 2). One of two patients given 9.0 mg/m2 for three consecutive days manifested a life-threatening (grade 4) disturbance of consciousness and dyspnea, presumably ascribable to the drug-related toxicity of YK-176. The results suggest that 7.0 mg/m2 i.v. for three consecutive days is the maximum acceptable dose of YK-176. Central nervous system, pulmonary and possibly renal toxicities appeared to be dose-limiting. Out of the 20 patients evaluable for therapeutic response, partial remissions were observed in four, three with ATL and one with CTCL, who received less than 7.0 mg/m2 for three consecutive days. We conclude that YK-176 is an active agent against ATL at doses that may not be associated with prohibitive toxicity. A starting dose of 5.0 mg/m2 for three consecutive days is recommended for further phase II studies on ATL.
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PMID:Phase I study of YK-176 (2'-deoxycoformycin) in patients with adult T-cell leukemia-lymphoma. The DCF Study Group. 151 64

This review summarizes current strategies in the treatment of patients with pleural effusion. To determine whether a patient has a transudative or exudative pleural effusion, Light's criteria should be applied to measure the concentrations of protein and lactate dehydrogenase (LDH) in the pleural fluid and serum. If the effusion is transudative, therapy should be directed toward the underlying congestive heart failure, cirrhosis, or nephrosis. Consideration should be given to pleurodesis with a sclerosant if patients with recurrent transudative effusion have severe dyspnea due to their effusion. If the effusion is exudative, attempts should be made to define the etiology. The diagnosis of pleural malignancy is most easily established via pleural fluid cytology. If this is negative and the patient is suspected of having pleural malignancy, thoracoscopy is indicated. The concentrations of adenosine deaminase and gamma-interferon in pleural fluid are useful in the diagnosis of pleural tuberculosis. Patients with pneumonia and pleural effusion should undergo therapeutic thoracentesis; the pleural fluid should be Gram-stained and cultured, and the differential cell count, glucose and LDH concentration, and pH should be determined. Indicators of a poor prognosis include the presence of frank pus, a positive Gram-stain, a pleural glucose concentration of less than 2.2 mmol/L, a pH less than 7.00, the presence of pleural loculations, and an LDH concentration greater than three times the upper limit of normal in serum. If the pleural fluid cannot be completely evacuated because of loculations, intrapleural thrombolytic therapy should be considered. If thrombolytics are ineffective, thoracoscopy or thoracotomy with decortication should be performed. Dyspneic patients with malignant pleural effusions whose dyspnea is relieved with therapeutic thoracentesis should be considered for pleurodesis using a tetracycline derivative. Talc is not recommended because it induces acute respiratory distress syndrome in about 5% of patients, with an overall mortality of 1%.
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PMID:Management of pleural effusions. 1092 61

A 61-year-old man was admitted to our hospital with cough, breathlessness, anorexia and chest pain. Chest radiograph showed right pleural effusion and also a chest CT scan showed right pleural effusion with thickening of the right visceral pleura, pericardial effusion and a liver tumor. The pleural effusion was slightly bloody and exudative. The adenosine deaminase (ADA) level in the pleural effusion was elevated. Because the cytological examintion of the pleural effusion showed no malignancy, we diagnosed pleuritis tuberculosa. The serum-soluble interleukin-2 receptor level was also elevated. His general condition worsened in spite of the chemotherapy with antibiotics and antituberculous drugs. We finally diagnosed the case as natural killer (NK) cell lymphoma from CT-guided needle biopsy just before death, and necropsy. In this case, the high level of ADA in the pleural effusion suggested lymphoma.
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PMID:[A case of natural killer cell lymphoma with high adenosine deaminase level in pleural effusion]. 1599 86

Pleural effusion without occurrence of active pulmonary lesion due to nontuberculous mycobacteria is extremely rare. We report a case of Mycobacterium intracellulare pleurisy in an 84-year-old woman. The patient was admitted to a nearby hospital because of dyspnea. Massive right pleural effusion was observed on chest roentgenogram. Bacteriological examinations, smear and culture of the sputum or pleural effusion were negative. First we thought pleurisy was caused by M. tuberculosis as pleural effusion showed predominant lymphocyte count and high adenosine deaminase level. However, M. intracellulare was identified by the polymerase chain reaction method from pleural effusion. Based on clinical findings and laboratory data, we suspected pleurisy was due to M. intracellulare infection. Clarithromycin, kanamycin, rifampicin and ethambutol were administered. After four months of treatment pleural effusion disappeared without accompanying the active pulmonary lesion. Therefore, we diagnosed this case as pleurisy without pulmonary lesion due to M. intracellulare.
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PMID:[A case of Mycobacterium intracellulare pleurisy without active lung lesion]. 1828 12

Not long ago, primary tuberculosis was considered a rare disease; now with an increasing incidence worldwide, physicians should relearn many of its basic aspects and manifestations. Pericarditis is a rare finding seen with tuberculosis, but its prognosis is excellent with treatment, so early diagnosis is crucial. Pathogenesis is particularly important, and it must be taken in consideration when interpreting diagnostic tools. Herein we report on a healthy 32-year-old woman who presents with a 1-month history of febrile illness, malaise, and weakness; more recently, she also had resting dyspnea, which was progressively worsening. A positive PPD and an abnormal chest radiograph prompted hospitalization, where she was found to have pulsus paradoxus of 20 mm Hg. The echocardiogram showed diastolic right chamber collapse along with respiratory variation of the mitral inflow, consistent with pericardial tamponade. A pericardiocentesis was performed with resolution of her resting dyspnea; more than 1000 mL of serous fluid drained from the pericardial space over the following 24 hours. Although sputum and pericardial fluid cultures and smear for AFB and other organisms were negative, as well as a negative pericardial fluid PCR for Mycobacterium tuberculosis DNA; an elevated (44.4 U/L [normal, 0 to 18]) adenosine deaminase level in the pericardial fluid was consistent with the probable diagnosis of tuberculous pericardial effusion. The patient was treated with resolution of the clinical syndrome and no recurrence of the effusion thereafter. Adenosine deaminase, an enzyme marker of cell-mediated immune response activity to M tuberculosis that includes activated T-lymphocytes and macrophages, appears in pericardial fluid. The diagnosis of probable tuberculous effusion can be made without demonstration of mycobacterium.
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PMID:Adenosine deaminase in the diagnosis of tuberculous pericardial effusion. 1879 13

It is interesting to study an autoimmune condition like dermatomyositis (DM) in the setting of immunosuppression due to human immunodeficiency virus (HIV) infection. An HIV seropositive female aged 30 years, presented with a nonitchy rash over the face, breathlessness, diarrhoea and difficulty in raising her hands above her head. A heliotrope rash around the eyes, Gottron's papules and proximal muscle weakness were found to be present. C reactive protein, erythrocyte sedimentation rate and lactate dehydrogenase levels were raised, but creatinine phosphokinase and anti-nuclear antibody profile were normal. Her HIV serostatus was confirmed by Western blotting, keeping in mind the potential for false positive HIV serology in an autoimmune disorder. Her CD4 count was 379 cells/mm3. An X-ray of the chest showed bilateral pleural effusion with raised pleural fluid adenosine deaminase levels. Clinical findings and laboratory investigations favored the diagnosis of DM and HIV infection with tuberculous effusion in an HIV seropositive patient. She was treated with antibiotics, four-drug anti-tubercular treatment, systemic steroids and later, antiretroviral treatment. Chances of a false positive antibody test for HIV should be considered in a patient having an autoimmune disease such as DM.
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PMID:Dermatomyositis in a human immunodeficiency virus infected person. 1858 92

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

Pericardial effusion might be the first presentation of various pathologies including malignant tumors. Massive pericardial effusion as the primary manifestation of high-grade malignant lymphoma is a very rare condition. A 53-year-old woman presented with progressive dyspnea of one-week history. Physical examination showed venous distention of the neck veins and diminished heart sounds. The chest X-ray demonstrated increased cardiothoracic index. Transthoracic and transesophageal echocardiographic examinations showed massive pericardial effusion without any other pathology. Hematologic and biochemical tests showed only anemia. The patient underwent pericardiocentesis. Pericardial adenosine deaminase test and cultures were negative. Cytopathologic examination of the fluid showed huge lymphocytes and highly atypical lymphoid cells consistent with high-grade malignant lymphoma (non-Hodgkin's lymphoma). Immunohistochemical analysis showed positivity for leukocyte common antigen. No other primary origin could be determined.
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PMID:Massive pericardial effusion as the primary manifestation of high-grade malignant lymphoma. 2020 Apr 63

A 74-year-old man was referred to our hospital with complaint of dyspnea and left pleural effusion. The pleural effusion was exudative and lymphocytic with elevation of adenosine deaminase (ADA). Antitubercular agents were administered on a diagnosis of tuberculous pleuritis, but the pleural effusion did not improve. After he had been followed up with diuretic agents during about 2 years, he suffered cardiac tamponade and right pleural effusion. We diagnosed primary effusion lymphoma based on the cytology findings of the pleural effusion. The measurement of ADA activity in pleural effusions was useful for diagnosis of tuberculous pleuritis, but not only tuberuculous pleuritis but also lymphoma or other diseases can show elevation of ADA activity in pleural effusions.
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PMID:[A case of primary effusion lymphoma with elevation of ADA activity in pleural effusion]. 2211 19

Ticagrelor, a recently approved platelet antagonist indicated for the reduction of thrombotic cardiovascular events in patients with acute coronary syndrome (ACS), has been reported to cause dyspnea in more than 13% of patients. Dyspnea is not a clinically relevant adverse event with other medications indicated for ACS. One suggested mechanism of ticagrelor-induced dyspnea involves an increase in systemic adenosine concentrations through adenosine deaminase inhibition. Dyspnea, a subjective finding resulting from physiologic and sensory mechanisms, may be a consequence of increased systemic adenosine concentrations, leading to amplified and prolonged receptor activity. Current literature suggests, however, that pulmonary status is not compromised, with no reduction of efficacy seen in patients with ticagrelor-induced dyspnea, thus allowing clinicians to continue therapy without reservation. Still, patients with a history of asthma and chronic obstructive pulmonary disease may be more susceptible to ticagrelor-induced dyspnea, potentially leading to nonadherence and exacerbations of morbidity. Therefore, it is paramount that health care providers continually monitor these patients with the aims of maintaining medication therapy adherence and providing relevant options if dyspnea becomes intolerable.
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PMID:Potential role of endogenous adenosine in ticagrelor-induced dyspnea. 2371 33


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