Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenosine deaminase (ADA) and terminal deoxynucleotidyl transferase (TdT) activities were determined on 97 biopsy specimens obtained from patients with non-neoplastic diseases (12 cases), Hodgkin (30 cases), and non-Hodgkin lymphomas (55 cases). Thirty additional cases were tested only for TdT. TdT was positive in 10 out of 13 lymphoblastic lymphomas (LL) examined and negative in all the other specimens, including the ten cases of the immunoblastic type. Levels of ADA above 350 U/mg of protein were found in 10 out of 12 LL tested, but not in any other specimen. The 3 TdT- LL had high contents of ADA. Therefore, all LL can be detected using both ADA and TdT markers. The 3 TdT- LL had a heterogeneous phenotype and their possible origin is discussed in view of the possibility that they constitute a rare entity distinct from the more common TdT+ LL. Very low levels of ADA (below 100 U/mg of protein) were found in chronic lymphocytic leukemia and immunocytoma, and in Burkitt's lymphoma. In other B-cell non-Hodgkin lymphomas, intermediate values between 100 and 350 U were often found, and this finding could be relevant to the different cellular origin of the various B-cell neoplasias. We conclude that ADA distribution is solid lymphoid tumors reflects the cellular origin of these neoplasias. Adenosine deaminase alone and in combination with TdT can be useful in the diagnosis and classification of childhood lymphomas in which the immature hystotypes predominate.
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PMID:Adenosine deaminase and terminal deoxynucleotidyl transferase in human lymphomas: an aid to the diagnosis and subclassification of lymphoblastic lymphomas. 401 22

Adenosine deaminase (EC 3.5.4.4. - ADA) deaminates adenosine and deoxyadenosine to inosine and deoxyinosine. The distribution of ADA isoenzymes depends on a binding protein. Purine nucleoside phosphorylase (EC 2.4.2.1. - PNP) catabolizes inosine and guanosine to hypoxanthine and guanine. Patients with severe combined immuno-insufficiency often suffer from a congenital ADA deficiency. The PNP deficiency is associated with severely defective T-cell immunity and normal B-cell immunity. Deficiency of ADA leads to an accumulation of adenosine, deoxyadenosine, adenine nucleotides (cAMP, dATP). In PNP deficiency an increased production of inosine, guanosine, deoxyinosine and deoxyguanosine was found. The pathogenesis of the immuno-insufficiency is to be traced back to disturbances in the purine metabolism interfering with the mitogenically induced lymphocyte transformation and other lymphocyte functions, as determined by in vitro tests. Deoxyadenine inhibits the ribonucleoside diphosphate reductase and synthesis of DNA. The overproduction of S-adenosyl-L-homocysteine inhibits methyltransferase reactions and 2'-deoxyadenosine the S-adenosylhomocysteine hydrolase. A decrease of ADA activities was found in T-lymphocytes of patients with Hodgkin's disease. Measurements of ADA activity in patients with leukemias do not explain the impairment of the cellular immune response in leukemias and may be regarded as indicator of increased purine metabolism. The ADA activities are increased in patients with acute immature and chronic myeloic leukemias depending on the activity of the disease. The ADA activity is low in chronic lymphatic leukemia. ADA inhibitors were used for the treatment of T-cell leukemias.
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PMID:[Immune insufficiency in enzyme defects of purine metabolism]. 630 5

Adenosine deaminase (ADA) has been assayed in plasma, erythrocytes, and lymphocytes from 29 patients with haematological and autoimmune diseases. ADA activity was uniformly low in erythrocytes and lymphocytes from patients with non-Hodgkin lymphoma and multiple myeloma (p less than 0.001). High levels of ADA activity was found in plasma, erythrocytes, and lymphocytes from patients with myeloid leukemia (p less than 0.001). ADA was high in plasma but low in erythrocytes and lymphocytes from patients with autoimmune diseases treated with immunosuppressive drugs (p less than 0.05). 4 adults with congenital immunodeficiency showed decreased ADA activity. In the control group of normal blood donors we found a 34-year-old female with low ADA activity in plasma, erythrocytes, and lymphocytes without any immunological abnormalities. This is the 3rd case of a healthy individual deficient for ADA. 1 patient with Osler's disease and high ADA activity in erythrocytes showed the importance of the purine salvage enzyme not only in lymphocytes.
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PMID:Adenosine deaminase activity in plasma and blood cells of patients with haematological and autoimmune diseases. 678 72

Despite a recent decline, tuberculosis (TB) infection is still a frequent diagnosis in Portugal. Adenosine deaminase (ADA) measurement has become an important tool in the timely diagnosis of this infection. However, ADA elevation in bodily fluids is not pathognomonic of TB infection. We present the case of a 70-year-old woman, undergoing treatment for pleural TB, diagnosed based on elevated ADA levels in a pleural effusion. Due to worsening symptoms she was readmitted, and the previous diagnosis was reconsidered. Thoracocentesis was repeated and cytometry analysis of the fluid was performed, showing the presence of diffuse large B cell lymphoma (DLBCL). DLBCL is the most frequently occurring non-Hodgkin lymphoma (NHL). Pleural involvement is rare in the initial stages. ADA elevation >250 U/l should raise suspicion of malignancy, especially in association with markedly elevated LDH levels. The purpose of this case report is to highlight that in the absence of microbiologic or histologic confirmation, a presumptive TB diagnosis should not be lightly made, and alternative diagnoses should be systematically ruled out.
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PMID:Elevated Adenosine Deaminase in Pleural Effusion A Case of Non-Hodgkin Lymphoma Misdiagnosis. 3278 29