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)

Ninety-three elderly patients with pulmonary tuberculosis were surveyed prospectively to determine the extent and severity of radiological, haematological and biochemical abnormalities. Radiological features of inflammatory changes were present in all patients; 7 per cent of these were purely apical, 48 per cent were in mid and basal zones and in 46 per cent there was a mixed picture. Cavities were seen in 33 per cent of radiographs; half of these occurred in the apical and half in the mid and basal zones. A pleural reaction was present in 46 per cent of cases. Hilar gland enlargement was not seen. Thus radiographs 'atypical' for pulmonary tuberculosis were usual with the major changes being basal and peripheral. Haematological abnormalities were normochromic normocytic anaemia (66 per cent), neutrophilia (69 per cent), thrombocytosis (33 per cent), rapid erythrocyte sedimentation rate (90 per cent), and lymphocytopenia and monocytosis in 22 and 28 per cent respectively. Biochemical abnormalities were hyponatraemia (60 per cent), hypokalaemia (42 per cent), hypoalbuminaemia (83 per cent), and (before treatment) elevation of bilirubin (20 per cent), alkaline phosphatase (62 per cent), aspartic transaminase (77 per cent) and lactic dehydrogenase (74 per cent). The abnormal liver function tests may reflect unsuspected extrapulmonary disease. Radiologically mild opacification occurring frequently in the lower zones and associated with a pleural reaction in half of cases is compatible with tuberculosis. The unexplained presence of any of these haematological and biochemical abnormalities should raise suspicion of the disease.
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PMID:The radiography, haematology and biochemistry of pulmonary tuberculosis in the aged. 260 49

The occurrence of polycythemia vera in a father, mother, and two sons is reported. Thirteen kindreds with familial polycythemia vera in 31 members are reviewed. Comprehensive records were available for all four patients as well as other family members, since all were diagnosed and treated at the author's institution over a period of nearly 50 years. The mean age at diagnosis, sex predominance, symptoms, and incidence of chromosomal abnormalities, leukocytosis, thrombocytosis, and elevated leukocyte alkaline phosphatase levels were similar to those of nonfamilial cases. The mean RBC volume at diagnosis and the incidence of splenomegaly appear to be higher in familial than nonfamilial cases. The mode of inheritance is unclear, but genetic factors may be involved in the pathogenesis of this myeloproliferative disorder.
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PMID:Familial polycythemia vera. 269 Nov 18

A case of primary myelofibrosis complicated with pericardial effusion and proteinuria is described. A 66-year-old female was admitted to our hospital because of abdominal fullness and shortness of breath. On admission, hepatosplenomegaly and pericardial effusion were observed. Blood examination revealed leukoerythroblastic anemia and thrombocytosis with tear drop cells and giant platelets. Bone marrow aspiration was dry tap and its biopsy showed remarkable myelofibrosis. Urinalysis indicated severe proteinuria. Although neutrophilic alkaline phosphatase score was low, no signs of acute blastic crisis of chronic myelogenous leukemia was found. The diagnosis of an atypical type of primary myelofibrosis was obtained. Administration of MCNU was started in August 1987. Hepatosplenomegaly, pericardial effusion and proteinuria were gradually improved after the administration. The etiology of the pericardial effusion and proteinuria were not obvious, however, these facts suggest that these abnormal findings might be related to PMF itself and MCNU was effective to PNF.
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PMID:[The use of MCNU to a patient of primary myelofibrosis complicated with pericardial effusion and proteinuria]. 276 70

TGF beta 1 from porcine platelets increased alkaline phosphatase (AP) activity in the rat osteoblastic cell line ROS 17/2.8 about three-fold. This effect was dose-dependent with an ED50 of about approximately 0.2 ng/ml and was larger during logarithmic growth than at confluence. TGF beta 1 inhibited cell growth by about 30% with similar dose dependence. Thirty min exposure to TGF beta 1 was sufficient to increase AP activity 3 days later by about two-fold but did not affect cell growth, suggesting dissociation between effects on proliferation and differentiation. The rise in AP activity started 6 h after TGF beta 1 addition and was blocked by cycloheximide and actinomycin D. TGF beta 1 also increased AP mRNA by two- to three-fold and this effect was not blocked by cycloheximide. The half-life of AP mRNA, estimated following the addition of 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole was about ten h in both control and TGF beta 1-treated cells. The mRNAs for type I procollagen and osteonectin were also increased by TGF beta 1 but fibronectin mRNA was decreased. TGF beta 2 effects on AP and cell growth were similar to those of TGF beta 1, except for lack of activity following transient exposure. At saturating concentrations, TGF beta 2 (2 ng/ml) or dexamethasone (10(-7) M), which has similar effects on these cells, did not further augment the effects of TGF beta 1 (at 2 ng/ml). Above findings suggest that TGF beta promotes osteoblastic differentiation in rat osteosarcoma cells at least in part by acting at the pretranslational level.
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PMID:Type beta transforming growth factor (TGF beta) regulation of alkaline phosphatase expression and other phenotype-related mRNAs in osteoblastic rat osteosarcoma cells. 348 Feb 88

A clinicopathological study was performed on 46 patients with chronic myeloproliferative diseases (CMPD) showing a thrombocythemia in excess of 1,000 x 10(9)/liter. When applying rigid diagnostic criteria only 23 patients were compatible with the initially suspected diagnosis of primary thrombocythemia (PTH). Comparison of PTH with the other entities of CMPD (CGL, 10, AMM, 6, and polycythemia, 7 cases) revealed a sustained elevation of the platelet count observable over a period of 2 to 8 years, no marked leukocytosis or abnormalities of the differential blood count, and a normal score of the leukocyte alkaline phosphatase. Episodes of hemorrhage and thrombosis as well as neurological symptoms (paresthesias, dizziness, headache), were encountered frequently as clinical manifestations in PTH. Survival time in PTH was significantly longer than in CGL with accompanying thrombocythemia. In a consecutively biopsied population of patients with CMPD, incidence of PTH was about 8%. In PTH the characteristic histopathology of the bone marrow consisted of an isolated (monolinear) proliferation of the megakaryocytes (density 127 +/- 47/mm2) without gross abnormalities of this cell lineage or a conspicuous increase in neutrophilic granulo- or erythrocytopoiesis. These lesions are significantly different from the morphological findings in the other CMPD with extreme thrombocytosis.
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PMID:Chronic myeloproliferative diseases with an elevated platelet count (in excess of 1,000,000/microliter): a clinicopathological study on 46 patients with special emphasis on primary (essential) thrombocythemia. 350 37

A syndrome of intrahepatic cholestasis leading to death in early childhood was studied in 16 Greenland Eskimo children. The pedigrees are compatible with autosomal recessive inheritance. Jaundice, bleeding, pruritus, malnutrition, steatorrhoea, osteodystrophy and dwarfism were typical clinical features. Eight had died between the ages of six weeks and three years due to bleeding or infections. Hyperbilirubinaemia, profound hypoprothrombinaemia, thrombocytosis and elevated alkaline phosphatase levels were evident. Serum calcium, phosphate and parathyroid hormone levels indicated a secondary hyperparathyroidism. Hepatic fibrosis developed with increasing age. Follow-up of the surviving patients was 4 to 30 months. The aetiology of the disease is unknown. The syndrome has some features in common with previously described patients with familial intrahepatic cholestasis. No specific treatment is available. Genetic counselling is essential.
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PMID:Fatal familial cholestatic syndrome in Greenland Eskimo children. 356 58

Intraabdominal pseudotumor of the plasma cell granuloma type in a 19-year-old man is reported. The patient presented with fever and weight loss lasting months, and the laboratory findings revealed high sedimentation rate, hypochromic, microcytic anemia, thrombocytosis, elevated alkaline phosphatase, decreased thromboplastin time and polyclonal hypergammaglobulinemia. When the plasma cell granuloma was removed, all laboratory findings returned to normal within 3 months and the patient remained asymptomatic during the two-year follow-up.
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PMID:[Abdominal inflammatory pseudotumor (plasma cell granuloma) with anemia and hypergammaglobulinemia]. 370 10

Neutrophil alkaline phosphatase activity was estimated in 194 patients; 59 cases of chronic myeloid leukaemia (CML), 42 cases of polycythaemia vera (PV), 24 cases of primary myelofibrosis, 7 cases of idiopathic thrombocythaemia, 6 cases of leukaemoid reaction, 19 cases of secondary polycythaemia (PS) and 37 cases of the primary myelodysplastic syndrome (MDS). According to NAP activities the groups proved to be separate entities (p less than 0.00025). The incidence of decreased NAP score in the CML group was 85% and differed significantly from the other groups as a whole, as well as separately (p less than 0.001). The MDS group, the only group besides CML that showed decreased scores, also differed significantly from the others (p less than 0.001). The PS group, nearly always showing normal scores, differed significantly from the PV group (p less than 0.0052). A method evaluating single cell NAP activity proved superior to the score method in discriminating between the different groups. Thus, the incidence of decreased activity in the CML group was 93% compared with 85% by the score method and the incidences of increased activity in the PV, MP, IT, and LR groups were 79% to 100% compared with 25% to 67% by the score method. The latter difference was statistically significant (p = 0.029).
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PMID:Evaluation of neutrophil alkaline phosphatase (NAP) activity in untreated myeloproliferative syndromes and in leukaemoid reactions. 404 68

During an outbreak of trichinosis, two young men--one with established trichinosis and the other with suspected infection--were found to have clinical, radiologic and histologic stigmata of a systemic necrotizing vasculopathy equivalent to classic polyarteritis nodosa. The parasitosis manifested as a pentad of fever, myalgias, facial edema, eosinophilia and hyperimmunoglobulinemia E. Features of the arteritis included mononeuritis multiplex, pain in the abdomen and joints, weight loss, hypertension, leukocytosis, thrombocytosis, microhematuria and raised alkaline phosphatase levels. A sustained remission was achieved by the administration of thiabendazole, prednisone and cyclophosphamide. Pathogenetic links between the two diseases are presented: (1) deposition of circulating immune complexes in the vessel wall; (2) adjuvant activity with cross reaction between parasitic antigen and human vessel wall; (3) immunoglobulin E (IgE) aggregates and soluble antigen IgE complexes precipitation in vessel wall; and (4) hypereosinophilia-induced tissue damage. A causal relationship of trichinosis to polyarteritis nodosa is persuasive, and we suggest that cases of hepatitis B surface antigen (HBsAg) negative polyarteritis nodosa, especially those in which myalgias and eosinophilia are prominent, may be related to trichinosis and that, conversely, patients with trichinosis and multiorgan disease should be studied for polyarteritis nodosa.
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PMID:Trichinosis-related polyarteritis nodosa. 611 36

Local inflammation was induced in rats by single (1 x 4 ml/kg) or multiple (14 X 0.2 ml/animal) infections of turpentine. The induction of inflammatory processes in both groups resulted in anemia and granulocytosis following an initial leukopenia. Thrombopenia on the second day, followed by thrombocytosis, was also observed in both groups. Studies on blood chemistry parameters revealed a decline in serum albumin; elevation of alkaline phosphatase in serum was observed only after multiple injection of turpentine. In these animals an elevation in the weights of spleen and adrenals and a reduction in the weight of thymus were also found.
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PMID:[Systemic reactions in rats following the initiation of a local inflammatory process by subcutaneous administration of spirits of turpentine]. 689 Dec 53


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