Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of humoral immune defects and of the antibody deficiency syndrome, respectively, at adult age was examined on 69 patients. As immunological methods the estimation of the immunoglobulins G, A, M, D with Mancini's technique, of IgA-antibodies with Ouchterlony's technique, of T-lymphocytes with the sheep erythrocyte rosette test, of B-lymphocytes with direct immunofluorescence and mouse erythrocyte rosette test were used. The enzyme adenosine deaminase was determined in the plasma, the erythrocytes and the lymphocytes. 31 patients with primary antibody deficiency syndrome, of them 22 patients with selective IgA-deficiency could be diagnosed. 38 patients with secondary antibody deficiency syndrome came from groups of patients with lymphoproliferative diseases (non-Hodgkin-lymphoma and plasmocytoma), chronic dialysis and other haematological diseases. In 80% of the patients clinical symptoms of an immune defect could be proved. Chronically relapsing infections of the respiratory tract are in the first place. Familial accumulation, allergic reactions, antibodies against IgA, statistically significant accumulation of gastric and duodenal ulcers set off the anyway large group of patients with selective IgA-deficiency. An antibody deficiency syndrome with IgA-deficiency could be proved in 5 of 16 patients undergoing the dialysis programme, but clinically it is perhaps insignificant. Disturbances of the cell-mediated immune reaction occurred in a child with teleangiectatic ataxia and lymphoproliferative diseases. A deficiency of adenosine deaminase, which is of importance in combined immune defects syndrome at adult age, but it is to be proved in the plasmocytoma and the non-Hodgkin-lymphoma. The necessity of the knowledge of forms of the antibody deficiency syndrome at adult age results from the increasingly immunosuppressively acting therapeutic measures, correct and well-timed diagnosing as well as the necessity of aimed consultation of the physician in institutions specialised in immunology.
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PMID:[Humoral immune defects in adults]. 711 11

An 80-year-old man developed dysarthria, quadriplegia, sensory disturbance and ataxia in all limbs. Brain and spinal magnetic resonance imaging (MRI) revealed multiple enhanced lesions. Cerebrospinal fluid (CSF) levels of adenosine deaminase (ADA) remarkably elevated. Tuberculosis DNA was not detected, and tuberculosis was not cultured either in the CSF. Brain biopsy revealed the inflammatory demyelinating lesions. With the diagnosis of multiple sclerosis, corticosteroid therapy resulted in rapid improvement of his symptoms and MRI abnormalities. CSF levels of ADA also decreased. Multiple sclerosis should be included in differential diagnosis of disorders with ADA elevation in the CSF.
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PMID:Multiple sclerosis showing elevation of adenosine deaminase levels in the cerebrospinal fluid. 2842 1

The clinical features of autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy remain to be elucidated. We describe here the clinical features of 14 patients with GFAP astrocytopathy confirmed by detection of GFAP-IgG in cerebrospinal fluid (CSF). The novel findings of this study are as follows. First, over half of the patients presented with movement disorders (tremor, myoclonus, and ataxia), autonomic dysfunction (mainly urinary dysfunction), and hyponatremia. Second, most patients showed transient elevation of adenosine deaminase activity levels in CSF. Finally, some patients showed bilateral hyperintensities in the posterior part of the thalamus on brain magnetic resonance imaging.
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PMID:Clinical characteristics of autoimmune GFAP astrocytopathy. 3099 6