Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukocyte acid phosphatases were investigated in 146 patients with different chronic diseases. The method of investigation used was that of Kaplow and Burstone slightly modified by the authors in what regards the pH of the incubation medium. Normal or slightly increased scores were observed in the granulocytic series of patients with chronic myeloid leukemia. In patients with rheumatoid arthritis, chronic hepatitis, lupus erythematosus disseminatus and chronic lymphocytic leukemia a moderate enzymatic activity was generally observed in the lymphocyte and more marked in severe forms of disease. A marked increase of the enzyme activity was observed in patients with myeloma. The possibility of a correlation between the intensity of enzyme activity and immunoglobulin formation is discussed.
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PMID:Behaviour of leukocyte acid phosphatase in various chronic diseases. 98 26

Leukocyte acid phosphatases were investigated in 146 patients with different chronic diseases. The method of investigation used was that of Kaplow and Burstone slightly modified by the authors in what regards the pH of the incubation medium. Normal or slightly increased scores were observed in the granulocytic series of patients with chronic myeloid leukemia. In patients with rheumatoid arthritis, chronic hepatitis, lupus erythematosus disseminatus and chronic lymphocytic leukemia a moderate enzymatic activity was generally observed in the lymphocyte and more marked in severe forms of disease. A marked increase of the enzyme activity was observed in patients with myeloma. The possibility of a correlation between the intensity of enzyme activity and immunoglobulin formation is discussed.
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PMID:Behaviour of leukocyte acid phosphatase in various chronic diseases. 107 75

Genetic polymorphism of transferrin (Tf) was investigated in Han nationality population in Guangzhou area using isoelectric focusing technique. In addition, three diseases (Leukaemia, Heptocarcinoma, Systemic-lupus-erythematosis, SLE) were also typed for Tf and compared with that in normal population. The increased TfC1 gene frequency in acute myelocytic leukaemia (AML) patients was found (chi 2 = 4.16, P less than 0.05). The increased frequency of TfC1C1 was also observed (P less than 0.05). Relative Incident(RI) was 1.9 But TfC1 gene and TfC1C1 phenotype frequencies did not increase in ALL, CML and primary heptocarcinoma patients. It suggests that TfC1 may relative to AML in this area. Besides, the increased TfC1 gene frequency was observed in SLE patients (chi 2 x 6.15, P less than 0.025). RI of TfC1C2 was 2.3. It suggests that Tfc2 may relate to SLE in this area.
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PMID:[Studies of the relationship between transferrin genetic polymorphism and diseases]. 152 51

Interferon alpha (INF-alpha)--In systemic diseases, most indications for INF-alpha result from its effect on haematological or hepatological manifestations. The spectacular effect of INF-alpha in chronic myeloid leukemia has led to its use for the treatment of hypereosinophilia syndrome and systemic mastocytosis. Over the last 6 years, we have treated 7 patients with the hypereosinophilia syndrome who were resistant to corticotherapy and had markers of myeloproliferation. Although both hydroxyurea and INF-alpha can be effective alone, their combination led to a decrease in the eosinophilia count to 1,000/ml, a decrease which was long-lasting in most cases. INF-alpha is also used in histiocytosis X alone or in combination with retinoids or with etoposide and has been found effective in several observations. In carcinoid syndromes whether treated priorly or not with a 5-fluoro-uracil-streptozoticin combination, INF-alpha leads to an objective response in two-thirds of the patients. Several multicentric protocols are currently assessing the efficacity of INF-alpha in mixed cryoglobulinaemias. In most observations these cryoglobulinaemias are seen in patients with markers of hepatitis C (mainly HCV) and the early results are encouraging. Temporary improvement has been reported in discoid or subacute lupus in 8 out of 10 cases. Haemangiomas of the infant, when life-threatening and corticoresistant, may be a good indication for INF-alpha. Thus 20 newborns or infants (including 4 with Kasabach-Merrit syndrome) have been treated with good results in 18. Interferon gamma (INF-gamma).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Interferons. Interferons alpha and gamma: indications in systemic diseases]. 817 44

Side effects of long-term interferon (IFN) therapy for myeloproliferative disorders may be vasospastic Raynaud's attacks and lupus-like illness. The authors report on a woman with chronic myelogenous leukemia who experienced severe trophic lesions of the fingers after forty-nine months of IFN therapy. Digital artery occlusions could be proven arteriographically.
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PMID:Severe Raynaud's syndrome associated with interferon therapy. A case history. 859 14

Lupus anticoagulant antibodies have never been reported to disappear after either allogeneic or autologous bone marrow transplantation in humans. We report the first case of disappearance of lupus anticoagulant antibodies in a patient without systemic lupus erythematosus or clinical evidence of other autoimmune disorders, who received an allogeneic bone marrow transplant as treatment for chronic myeloid leukemia. Although marrow transplantation is not a recognized therapy for antiphospholipid syndrome, our observation should be considered another example of the capability of intensive chemo-radiotherapy followed by stem cell transplantation to ablate a pathologic marrow clone resulting in an autoimmune disorder and improve, or even cure, some severe autoimmune diseases.
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PMID:Disappearance of lupus anticoagulant after allogeneic bone marrow transplantation. 1003 55

We report a 54-year-old woman who received interferon alpha for haematological relapse of Ph-positive CML, 7 years after allogeneic BMT from an HLA-identical brother. Eighteen months after relapse, cytogenetic and molecular remission was achieved. She received interferon therapy for 25 months and it was discontinued when she developed skin lesions on her face and trunk, dysphagia and fever with respiratory failure and bilateral patchy airspace consolidation of the lung without microbiologic findings. Histologic features showed discoid lupus erythematosis, oesophagitis with pseudomembranes and a mixed pattern of lymphocytic bronchiolitis involving the alveoli and interstitial spaces all compatible with chronic GVHD. The patient was commenced on immunosuppressive therapy with complete clinical and radiological resolution. The available evidence supports an atypical presentation of chronic GVHD and suggests a role for interferon alpha in the pathogenesis of GVHD. To the best of our knowledge, this is the first case reported of severe chronic GVHD occurring during the course of interferon therapy for relapsed CML.
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PMID:Atypical chronic graft-versus-host disease following interferon therapy for chronic myeloid leukaemia relapsing after allogeneic BMT. 1124 42

One hundred and fifty-four patients with erythema nodosum who attended the skin clinic at Ramathibodi Hospital from January 1990 to December 2000 were evaluated retrospectively with regard to the etiology of erythema nodosum. Of 49 patients who attended the skin clinic during that time 26 returned for reevaluation. Of the 154 patients, their ages ranged from 10-72 years old; 138 were females, 16 were males. The most common cause of erythema nodosum was tuberculosis (12.3%). Upper respiratory tract infection was found in 3.9 per cent. Other causes included Behcet's disease, sytemic lupus erythematous, drugs, pregnancy, chronic myeloid leukemia, leprosy, Reiter's syndrome and inflammatory bowel disease. Of the 26 patients who returned for reevaluation, pulmonary tuberculosis was identified in only one patient who had developed erythema nodosum 16 months earlier. In conclusion, it was found that tuberculosis is still a predominant cause of erythema nodosum among Thai patients.
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PMID:Long-term follow-up of erythema nodosum. 1497 15

Various autoantibodies have been identified in sera from patients with systemic lupus erythematosus (SLE) and autoantibodies against neutrophil have been reported. It was suggested that antineutrophil autoantibodies might be involved in the pathogenesis of neutrocytopenia; however, the role of autoantibodies against neutrophil precursors and their specific target autoantigen(s) remained further characterized. The objective was to investigate the target antigens and clinical associations of autoantibodies against neutrophils and neutrophil precursors in patients with SLE. Sera were collected from 92 patients with SLE and renal biopsy proven lupus nephritis. Cell lysates of peripheral neutrophils (as mature neutrophils) from a normal blood donor and white blood cells from a patient with blast crisis of chronic granulocytic leukemia (CGL) (as neutrophil precursors) were used as antigens in Western blot analysis to detect autoantibodies in sera from patients with SLE. The clinical significance of antineutrophil autoantibodies that recognized different antigens were further analysed. Using normal peripheral neutrophils as antigens, two bands could be blotted: 64 kD (33/92, 35.9%) and 50 kD (13/92, 14.1%). The prevalence of anti-64 kD autoantibody in patients with positive rheumatic factor was significantly higher than that in patients without (54.5 versus 18.8%, P < 0.05). Using CGL white cells as antigen, five bands could be blotted: 60 kD (34/92, 37.0%), 50 kD (32/92, 34.8%), 29 kD (27/92, 29.3%), 42 kD (19/92, 20.7%) and 18 kD (16/92, 17.4%). The prevalence of anti-60 kD autoantibody was significantly higher in patients with neutrocytopenia than that in patients without neutrocytopenia (100 versus 48.3%, P < 0.01). The prevalence of anti-29 kD autoantibody was significantly higher in patients with alopecia than that in patients without alopecia (45.8 versus 20.8%, P < 0.05). Furthermore, the prevalences of anti-60 kD, anti-50 kD and anti-42 kD autoantibodies were significantly higher in patients with anti-Ro autoantibody than those in patients without; the prevalences of anti-29 kD and anti-18 kD autoantibodies were significantly higher in patients with anti-Sm autoantibody than those in patients without. We conclude that there are heterogeneous autoantibodies against both neutrophils and their precursors in sera from patients with SLE. Different autoantibodies may have different clinical significance.
Lupus 2004
PMID:Antineutrophil autoantibodies and their target antigens in systemic lupus erythematosus. 1546 87

Genetic linkage analyses, genome-wide association studies of single nucleotide polymorphisms, copy number variation surveys, and mutation screenings found the human chromosomal 12q24 locus, with the genes SH2B3 and ATXN2 in its core, to be associated with an exceptionally wide spectrum of disease susceptibilities. Hematopoietic traits of red and white blood cells (like erythrocytosis and myeloproliferative disease), autoimmune disorders (like type 1 diabetes, coeliac disease, juvenile idiopathic arthritis, rheumatoid arthritis, thrombotic antiphospholipid syndrome, lupus erythematosus, multiple sclerosis, hypothyroidism and vitiligo), also vascular pathology (like kidney glomerular filtration rate deficits, serum urate levels, plasma beta-2-microglobulin levels, retinal microcirculation problems, diastolic and systolic blood pressure and hypertension, cardiovascular infarction), furthermore obesity, neurodegenerative conditions (like the polyglutamine-expansion disorder spinocerebellar ataxia type 2, Parkinson's disease, the motor-neuron disease amyotrophic lateral sclerosis, and progressive supranuclear palsy), and finally longevity were reported. Now it is important to clarify, in which ways the loss or gain of function of the locally encoded proteins SH2B3/LNK and ataxin-2, respectively, contribute to these polygenic health problems. SH2B3/LNK is known to repress the JAK2/ABL1 dependent proliferation of white blood cells. Its null mutations in human and mouse are triggers of autoimmune traits and leukemia (acute lymphoblastic leukemia or chronic myeloid leukemia-like), while missense mutations were found in erythrocytosis-1 patients. Ataxin-2 is known to act on RNA-processing and trophic receptor internalization. While its polyglutamine-expansion mediated gain-of-function causes neuronal atrophy in human and mouse, its deletion leads to obesity and insulin resistance in mice. Thus, it is conceivable that the polygenic pathogenesis of type 1 diabetes is enhanced by an SH2B3-dysregulation-mediated predisposition to autoimmune diseases that conspires with an ATXN2-deficiency-mediated predisposition to lipid and glucose metabolism pathology.
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PMID:12q24 locus association with type 1 diabetes: SH2B3 or ATXN2? 2493 53


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