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:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive leukocytosis has been reported in patients with non-Hodgkin's lymphoma of different histologic types. On the other hand, the blastic crisis of chronic myelocytic leukemia (CML) can sometimes be localized outside the bone marrow and simulate lymphoma, particularly when the blasts are of lymphoid lineage and the blastic crisis is the presenting feature of the disease. We report two patients in whom the differential diagnosis between lymphoblastic lymphoma with reactive leukocytosis and blastic crisis of CML outside the bone marrow was raised. They were two males aged 32 and 22 years, respectively, with lymphadenopathy (and one with splenomegaly), who were initially diagnosed of T lymphoblastic lymphoma. In both cases, leukocytosis was detected with myelemia and dysgranulopoiesis in the onset in one of them and when lymphadenopathy reappeared after remission in the other one. In addition, one patient had marked eosinophilia. In the bone marrow there was marked granulopoietic hyperplasia, with a reduction of fatty cells, and the granulocyte alkaline phosphatase index was reduced. However, the cytogenetic study did not disclose the existence of Philadelphia (Ph) chromosome, and bcr/abl molecular rearrangement was also not observed in the molecular study of both cases. We discuss the basic aspects of differential diagnosis between T lymphoblastic lymphoma with leukemoid reaction and T lymphoid lymphadenopathic blastic crisis of Ph-negative, bcr/abl-negative CML.
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PMID:[T lymphoblastic leukemia with leukemoid reaction or the extramedullary blast crisis of Philadelphia chromosome-negative chronic myeloid leukemia? Comments apropos 2 cases]. 209 54

This study examines the effect of leukemia inhibitory factor (LIF) on preosteoblastic rat calvaria (RCT-1) cells, which acquire osteoblastic properties when treated with retinoic acid (RA). LIF potentiated the increase in alkaline phosphatase (AP) activity produced by RA. The LIF effect was time and dose dependent (EC50, approximately 1 pM). The earliest effects on AP activity were detected at 48 h, and maximal effects were observed after 72 h. RA increased AP mRNA about 2-fold at 3 h and 6-fold at 6 and 12 h. LIF further increased AP mRNA to 18-fold at 12 h. After RA treatment AP mRNA returned to control levels at 24 h, but in the presence of LIF, AP mRNA remained elevated at 24 and 72 h of treatment. When given alone, LIF had no effect on either AP activity or mRNA levels. Tumor necrosis factor-alpha and 1,25-dihydroxyvitamin D3 also potentiated the RA induction of AP, and interleukin-6 had a small effect, whereas granulocyte macrophage colony-stimulating factor had no effect. LIF alone had a small inhibitory effect on type 1 collagen mRNA, but did not oppose the stimulatory effect of RA. Consistent with these biological actions, LIF receptors were demonstrated on these cells. [125I]LIF bound to RCT-1 cells at 0 C with an apparent dissociation constant of 20 pM, and it was found that these cells express an average of 300 receptors/cell. Scatchard analyses showed a single class of high affinity binding site. LIF was internalized with an endocytic rate constant for occupied receptors of 0.03 min-1, and the apparent equilibrium dissociation constant at 37 C was 358 pM. These findings suggest that osteoblast precursor cells are among the target cells of LIF.
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PMID:Leukemia inhibitory factor binds with high affinity to preosteoblastic RCT-1 cells and potentiates the retinoic acid induction of alkaline phosphatase. 211 91

DDT administration (30 mg/kg per day, po, for 21 consecutive days) to rabbits showed an increase in peak plasma concentration and a decrease in time to reach peak plasma concentration of isoniazid whereas no change was observed in elimination rate constant and area under the plasma concentration-time curve. DDT treatment caused increased absorption of isoniazid. Early signs of hepatic damage were also observed. Since there was no change in the levels of serum glutamate oxaloacetate transaminase and serum glutamate pyruvate transaminase, it can be concluded that DDT does not significantly affect liver function at the dosage used. The observed elevated levels of alkaline phosphatase could be due to direct activation of the enzyme. Leukopaenia and neutropaenia with relative lymphocytosis indicated that DDT might have suppressant effect on granulocyte cell line of WBCs.
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PMID:Effect of subacute DDT on pharmacokinetics of isoniazid and liver function in rabbits. 227 76

Systemic candidiasis with Candida-induced abscesses, predominantly in the liver and the spleen, was diagnosed in 27 patients with haematologic malignancies after intensive cytostatic therapy. Specific features included septic fever unresponsive to antimicrobial therapy, hepatosplenomegaly with multiple lesions in the liver and spleen (diameter up to 2 cm) as detected by computed tomography (CT) or ultrasound, and an elevation in liver enzymes. During treatment, induced neutropenia, hepatic and splenic foci were poorly defined histologically and were not identified by imaging procedures. After granulocyte recovery these foci showed characteristic histological patterns. Ultrasound and/or CT investigations of the abdomen now revealed characteristic lesions in the liver and the spleen. Gamma-GT and alkaline phosphatase were early indicators of hepatic involvement in Candida septicaemia and were often already elevated in aplasia.
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PMID:Hepatosplenic candidiasis, a late manifestation of Candida septicaemia in neutropenic patients with haematologic malignancies. 233 85

The major initial clinical, hematological and cytogenetical features of a series of 80 patients with blastic crisis (BC) in chronic myelocytic leukemia with positive Philadelphia chromosome (Ph) were evaluated, and also were their outcome and response to therapy. Mean age of patients was 45 years (SD: 14.3). Ten patients fulfilled the criteria for initial BC, and 14 had extramedullary blastic infiltration. In one third there was an acceleration phase before the development of BC. The mean leukocyte count was 69 (SD 75) X 10(9)/l. In 40% there was anemia with hemoglobin less than 90 g/l, and 37.5% had thrombopenia with less than 100 X 10(9) cells/l. In most patients, serum lactic dehydrogenase activity was increased, and in one fourth the index of granulocyte alkaline phosphatase was high. In 9 patients, blast cells had a lymphoid phenotype and in 47 (59%) cytogenetic abnormalities in addition to Ph chromosome were found, usually consisting of 8 trisomy, duplication of Ph chromosome, and the presence of a 17q isochromosome. The median survival of the series was 4.8 months. When analyzed as a time-dependent variable, the achievement of a favorable therapeutic response (found in 26% of patients) was associated with a longer survival.
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PMID:[Blast crisis of chronic myeloid leukemia with positive Philadelphia chromosome: course and clinico-hematologic profile in 80 patients]. 238 91

Recombinant human granulocyte colony-stimulating factor (rhG-CSF) was administered at a dose of 1-60 micrograms/kg of body weight to 22 patients with transitional cell carcinoma before chemotherapy as part of a Phase I/II study. In all patients, a specific dose-dependent increase in the absolute neutrophil count (ANC) of 1.8-12 fold was seen. In addition, this augmentation in the ANC was accompanied by an increase in leukocyte alkaline phosphatase, a marker of secondary granule formation. In six of eight patients analyzed, an increase in bone marrow myeloid to erythroid cell ratio was seen. Day 14 peripheral blood cell derived colony forming unit granulocyte macrophage were also increased by day 6 of rhG-CSF treatment. Circulating levels of eosinophils and basophils were unchanged; however, a 10-fold increase in monocytes was observed in patients treated at the highest doses. There was also a small increase in CD3+ lymphocytes that was not dose dependent. Hemoglobin, hematocrit, and platelet count remained near baseline throughout the period of rhG-CSF administration. These findings demonstrate that rhG-CSF is a potent stimulus for normal neutrophil proliferation and maturation.
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PMID:Phase I study of granulocyte colony-stimulating factor in patients with transitional cell carcinoma of the urothelium. 245 63

Congenital agranulocytosis is a disorder characterized by severe neutropenia and a profound deficiency of identifiable neutrophil progenitors in bone marrow. In an attempt to stimulate neutrophil production and thereby reduce the morbidity and mortality associated with this disease, we administered recombinant human granulocyte colony-stimulating factor (rhG-CSF) in doses of 3 to 60 micrograms per kilogram of body weight per day to five patients with congenital agranulocytosis. In all five patients, an increase in the number of neutrophils was noted eight to nine days after the initiation of the effective dosage (the dose at which the neutrophil count reached 1000 cells per microliter or more and the bone marrow showed granulocyte maturation beyond the myelocyte stage). The absolute neutrophil counts rose from less than 100 to between 1300 and 9500 cells per microliter. Marrow aspirates obtained after 14 days at the effective dosage showed maturation to the mature neutrophil stage. The side effects that were observed were medullary pain, splenomegaly, and an elevation of levels of leukocyte alkaline phosphatase. All five patients have had sustained neutrophil counts of 1000 cells per microliter or more for 9 to 13 months while receiving subcutaneous maintenance therapy. Preexisting chronic infections have resolved clinically, and the number of new infectious episodes and the requirement for intravenous antibiotics have decreased. We conclude that treatment with rhG-CSF can lead to a large increase in the numbers of functional neutrophils in patients with congenital agranulocytosis.
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PMID:Effects of recombinant human granulocyte colony-stimulating factor on neutropenia in patients with congenital agranulocytosis. 247 Oct 75

Seventeen patients with advanced malignancy were treated with recombinant human granulocyte colony stimulating factor rhG-CSF (KRN 8601) infused intravenously over a period of 30 minutes once daily at the dose level/25 micrograms, 50 micrograms, 100 micrograms, 200 micrograms, 400 micrograms, 800 micrograms/m2 for 14 consecutive days, and the effect was compared to the period without rhG-CSF treatment. The maximum numbers of peripheral leukocyte (granulocyte) showed a dose-related increase and the nadir of leukocyte counts escalated with shortening of the period. After stopping infusion, the neutrophil count dropped to the base line level within two or three days. RhG-CSF did not affect other components of peripheral blood such as monocyte, lymphocyte, eosinophil, and hemoglobin value and platelet counts. Transient bone pain occurred in two patients receiving a dose of 800 micrograms/m2. The biochemical changes detected were increased total alkaline phosphatase activity in serum, which appeared in parallel with the increase of neutrophil numbers, and less elevation of total uric acid values. We conclude that an optimal dose of rhG-CSF is 100 micrograms/m2 (average maximum peripheral granulocyte count, 10799/microliters; nadir granulocyte count, 3772/microliters; period of neutropenia, 2.6 days), and rhG-CSF is useful for acceleration of neutrophil recovery and prevention of infection from chemotherapy.
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PMID:[Effect of recombinant human granulocyte colony stimulating factor (rhG-CSF) in patients receiving chemotherapy--phase I study]. 247 61

The end-stage maturation of neutrophilic granulocyte precursor cells isolated from normal human bone marrow by Ficoll density centrifugation was studied in a liquid culture assay system used previously to study the maturation of guinea pig granulocyte precursors. Dialyzed normal human serum induced end-stage morphological maturation of human granulocyte precursors and this induction was proportional to a serum level of up to 5.0% in the assay medium. At serum concentrations greater than 5.0% a pronounced inhibition of maturation was observed. Passage of serum through a DEAE-Fractogel 650S column equilibrated with 0.01 M phosphate buffer (pH 7.0) resulted in the binding of the end-stage granulocyte maturation factor to the column. The activity eluted from the column in a fraction containing 17% of the starting serum protein that was inhibitor-free and was also capable of inducing the appearance of granulocyte alkaline phosphatase, a specific biochemical marker for granulocyte end-stage maturation. GMF is most likely a protein since it was destroyed by protease digestion. The data also indicate that neither purified human transferrin nor human recombinant granulocyte colony-stimulating factor can substitute for human serum GMF as a granulocyte end-stage maturation factor in this assay system. It was observed, however, that purified human transferrin greatly potentiated the effect of GMF suggesting that transferrin plays a supporting role in the end-stage maturation of human granulocytes in vitro. To our knowledge the evidence presented here indicates for the first time the existence of a neutrophilic granulocyte end-stage maturation factor in normal human serum.
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PMID:Evidence for a factor in normal human serum that induces human neutrophilic granulocyte end-stage maturation in vitro. 247 45

Polymorphonuclear leukocytes (PMNs) from 29 patients with mixed connective tissue disease (MCTD) were studied "in vitro" for their phagocytic and chemotactic function as well as for granulocyte alkaline phosphatase (GAP) activity. Fc-receptor expression detected by EA-rosette formation was comparable to the control. Yeast-phagocytosis, C3b-receptor mediated phagocytosis and chemotaxis of PMNs, however, significantly decreased in MCTD. At the same time, photometric measure of alkaline phosphatase activity indicated a nearly two fold increase in PMNs from patients with MCTD. Although no correlation was found between PMN functions and the activity of the disease, PMN disorders may play a role in pathogenesis of these connective tissue disorders.
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PMID:Polymorphonuclear functions in patients with mixed connective tissue disease. 253 Aug 62


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