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)

A study of liver abnormalities in 36 patients with mixed cryoglobulinemia in the absence of underlying infectious, connective tissue, or lymphoproliferative disorders revealed clinical or biochemical evidence of liver dysfunction in 84%. Hepatomegaly was detected in 77%, splenomegaly in 54%, and abnormalities in bilirubin, alkaline phosphatase, or serum glutamic oxalacetic transaminase in 77%. Only four of the patients had overt liver disease. Of 15 biopsies from 12 patients, there was normal tissue structure in two, minimal nonspecific changes in one, portal fibrosis in three, chronic persistent hepatitis in one, chronic active hepatitis in two, chronic active hepatitis with cirrhosis in four, and postnecrotic cirrhosis in two. These findings, together with the previously reported high incidence of serologic evidence of hepatitis B virus (HBV) infection, support the view that the syndrome of purpura, arthritis, and nephritis is often a consequence of immune-complex vasculitis secondary to HBV infection.
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PMID:Liver involvement in the syndrome of mixed cryoglobulinemia. 90 Jun 72

2-Amino-6-methyldipyrido[1,2-a:3',2'-d]limidazole, a potent bacterial mutagen from glutamic acid pyrolysate, when given to male CDF1 mice at a concentration of 0.05% in the diet induced blood vessel tumors characterized histopathologically. These hemangioendothelial sarcomas showed positive alkaline phosphatase activity histochemically and Weibel-Palade bodies ultrastructurally. Neoplasms were predilective for brown adipose tissue and foci of atypical cells, not peliosis-like lesions, appear to be an early stage in tumor development.
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PMID:Hemangioendothelial sarcoma in brown adipose tissue of mouse induced by carcinogenic heterocyclic amine, Glu-P-1. 262 66

A case report is presented of a 43-year-old woman with generalized peliosis hepatitis that developed during longterm use of oral contraceptives (OCs). The patient had been in good health until the last 2 years when she began to experience vague epigastric pains and a feeling of abdominal distension. Several months prior to admission, she had started to complain of itching and fatigue. There was no history of dark urine, white stools, or hepatitis. On physical examination, no jaundice or cutaneous stigmata of chronic liver disease were observed. Laboratory studies showed a normal erythrocyte sedimentation rate and hematological blood count. A radionuclide study of the liver showed hepatomegaly; especially the left lobe was enlarged. A computerized tomographic scan of the liver showed multiple areas of decreased density in both of the enlarged lobes. There was no evidence of a tumor. Selective transfemoral angiography of the celiac artery also showed hepatic enlargement but no signs of a space-occupying lesion. At laparoscopy, the liver was grossly enlarged and had a lumpy appearance, but again there were no signs of a tumor. No evidence of veno-occlusive disease or hepatocellular adenoma was found. The diagnosis was peliosis hepatitis. The OCs were withdrawn, and the patient was discharged. Regular follow-up in the outpatient department showed no decrease in the size of the liver. The alkaline phosphatase level rose. The fatigue became worse, and cholestyramine was prescribed for progressive itching. In September 1980, the patient was admitted for reevaluation. A repeated CT scan and angiography of the liver again yielded no evidence of a tumor. Esophagoscopy showed the presence of varices grade 2. The liver at laparoscopy had the same appearance as it had in 1976. Histological examination of a biopsy specimen showed occasional dilated sinusoids and locally marked periportal and intralobular fibrosis. No regeneration nodules were found. The diagnosis was liver fibrosis. The patient's condition deteriorated gradually in the following years. She experienced increasing fatigue. Steatorrhea developed, and the patient lost weight. She needed increasing doses of cholestyramine and oral supplementation of vitamins A, D, and K. She was admitted for a 3rd time in February 1985. Esophagoscopy revealed varices grade 4. A CT scan of the liver showed no change. The patient successfully underwent an orthotopic liver transplantation in January 1987. The diagnosis of peliosis hepatis was well documented in this patient.
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PMID:Generalized peliosis hepatis and cirrhosis after long-term use of oral contraceptives. 312 33

Peliosis hepatis is described in a renal transplant recipient and in a patient who was receiving long-term haemodialysis. This uncommon liver lesion has been reported in a number of patients, including 18 renal transplant recipients and two patients with chronic renal failure. However, its cause, clinical features, natural history and clinical significance remain to be determined. We emphasize that, although it is rare, peliosis hepatis should be considered in long-term haemodialysis and renal transplant patients who exhibit hepatomegaly and/or splenomegaly and/or disordered liver function (in particular, elevation of hepatic alkaline phosphatase levels).
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PMID:Peliosis hepatis in a renal transplant recipient and in a haemodialysis patient. 354 May 50

A retrospective analysis of 30 patients with chronic myelomonocytic leukemia (CrMML) was performed to define the natural history of the disease and the risk of acute transformation. Our patients fulfilled the following criteria of diagnosis: blood monocytosis over 1 X 10(9)/l, blast cell percentage in bone marrow up to 30, and in peripheral blood less than 5. The most common presenting feature was anemia; seven patients had fever; three patients complained of purpura and bleeding. Anysopoikilocytosis and macrocytosis were frequent. Abnormal granulocyte morphology, defective granulation and abnormal leukocyte alkaline phosphatase were often observed. Blast cells in peripheral blood smears were found in 14 patients. Serum and urine lysozyme levels were increased in 82 per cent and 93 per cent, respectively. Dysplastic changes involving erythroid, granulocytic and megakaryocytic lineages were constant features in all cases. Agranulated blasts above 5 per cent of marrow nucleated cells were seen in 13 patients (43 per cent). Seven of the 20 patients showed non-specific chromosomal abnormalities at diagnosis. Median survival from diagnosis was 18 months (range, 3-112). Evolution into acute myeloid leukemia occurred in 11 patients. No difference in survival was found between patients who developed acute leukemia and patients who did not. A shorter survival has correlated to the following parameters: leukocytes greater than 10 X 10(9)/l, the presence of blasts in peripheral blood and agranulated blasts in the marrow above 5 per cent.
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PMID:Chronic myelomonocytic leukemia: clinical features, cytogenetics, and prognosis in 30 consecutive cases. 386 Apr 66

Purpura was grossly observable in albino mice 6 to 8 h after the intraperitoneal injection of sterile, deoxyribonuclease-treated, cell-free extracts prepared by sodium deoxycholate-induced lysis, sonic disruption, Parr bomb treatment, autolysis without sodium deoxycholate, or alternate freezing and thawing of washed suspensions of Streptococcus pneumoniae type I. Cell-free extracts obtained from sonically disrupted, heat-killed cells (100 degrees C for 20 min) did not contain purpurogenic activity. The reaction was maximal at approximately 24 h postinjection, started to fade slowly after 24 to 48 h, and usually was not grossly observable by 4 to 6 days postinjection. The purpura-producing principle (PPP) in the cell-free extract was purified by sequential ammonium sulfate precipitation, protamine sulfate precipitation, Sepharose 6B gel filtration, wheat germ lectin-Sepharose 6MB affinity chromatography, ribonuclease and trypsin treatment, and a second Sepharose 6B gel filtration step. The final preparation (i) contained glucosamine (5.6%), muramic acid (8.0%), neutral carbohydrate (12.8%), phosphate (8.0%), orcinol-reactive material (6.0%), and Lowry-reactive material (1.6%), and (ii) was free of detectable amounts of deoxyribonucleic acid, capsular polysaccharide, neuraminidase, cytolysin, and hyaluronidase. The isoelectric point and molecular size of the PPP were approximately pI 3.0 and several million daltons, respectively, and the activity remained in the supernatant fluid after centrifugation for 1 day at 105,000 x g. PPP activity was destroyed by incubation with egg white lysozyme and sodium metaperiodate but was resistant to trypsin, pronase, alpha-amylase, deoxyribonuclease, ribonuclease, alkaline phosphatase, pancreatic lipase, 7% trichloroacetic acid, 6 M urea, autoclaving (121 degrees C) for 30 min, and mild acid and alkali exposure. Our observations indicate that the PPP requires intact beta-1,4-glucosidic linkages for activity and support the working hypothesis that activity is associated with pneumococcal peptidoglycan solubilized by the bacterium's autolysin.
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PMID:Characterization of pneumococcal purpura-producing principle. 624 53

An 82-year-old woman with essential mixed cryoglobulinemia type II (IgM K IgG) presented with moderate renal failure and nephritic syndrome. Mesangiocapillary glomerulonephritis with mesangial and subendothelial granular deposits containing IgG, IgM, and C3 in conjunction with small-vessel vasculitis was seen on renal biopsy. Renal symptomatology preceded by a period of 10 months the development of leg ulcers and purpura. The onset of the skin lesions was accompanied by an acute decline of renal function and an increase in liver alkaline phosphatase. Plasmapheresis with a 50% plasma exchange each week over 12 weeks led to improvement in renal function, healing of leg ulcerations, disappearance of purpura, and a return to the baseline of alkaline phosphatase in association with the disappearance of circulating cryoglobulins.
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PMID:Plasmapheresis as sole therapy in a patient with essential mixed cryoglobulinemia. 674 40

Many methods have been described to identify platelet antibody, but they are either not very sensitive or too complex for general use. Therefore, we have developed an enzyme immunoassay for the detection of platelet antibodies in serum. The method involves incubating platelets with serum antibody; any attached antibody is shown by the addition of an enzyme (alkaline phosphatase) labeled anti-human IgG, followed by assay of the enzyme reaction with its substrate. The reaction product is indicated by a color change, which is proportional to the antibody concentration. Assay conditions such as the use of paraformaldehyde fixed versus unfixed platelets, conjugate dilutions, and substrate concentration and incubation time were investigated. Positive results were obtained in 16 of 19 sera of patients with various diseases including 2 of 4 patients with idiopathic thrombocytopenic purpura, 2 of 2 with post-transfusion purpura, 2 of 3 with neonatal purpura, and all 9 polytransfused patients. Sensitivity and specificity were 84% and 98%, respectively. Also, enzyme linked immunospecific assay (ELISA) was found to be superior to the lymphocytotoxicity (LCT) and platelet immunofluorescence test (PIIFT) for platelet antibody identification.
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PMID:Application of the enzyme linked immunospecific assay (ELISA) for the detection of platelet antibodies. 719 85

The acute toxic effects of phalloidin, a toxin from the green deathcup, Amanita phalloides, were tested in dogs. No fatalities occurred following intravenous injection; however, the biochemical parameters GPT, GOT, alkaline phosphatase, and total bilirubin yielded pathological values. Histologically the liver parenchyma revealed hemorrhagic necrosis and peliosis-like changes with penetration of red blood cells into hepatocytes.
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PMID:Acute phalloidin poisoning in dogs. 728 49

Diffuse hemangiomatosis of the spleen is a very rare benign tumor in which the whole spleen is permeated by neoplastic blood vessels. It is occasionally accompanied by severe disturbances of blood coagulation. The histogenesis of this tumor remains obscure. No systematic investigations of the immunophenotype of the neoplastic endothelium have been published. We describe a case of isolated benign diffuse hemangiomatosis of the spleen in which the enzyme-histochemical and immunohistochemical findings suggested an origin in the splenic sinus endothelial cells. Some of the tumor endothelial cells reacted with UEA-1, BMA 120, antibodies against the von Willebrand factor, CD34, and CD8, an antigen which, in man, is expressed only by suppressor/cytotoxic T cells and the endothelial cells of the splenic sinuses. Enzyme-histochemical investigations revealed reactivity for nonspecific esterase and lack of reactivity for alkaline phosphatase--a pattern typical of the sinus endothelial cells. The tumor could be distinguished from other tumors/tumor-like lesions of the spleen that exhibit endothelium with characteristics typical of the splenic sinuses (peliosis, splenoma, littoral cell angioma) on the basis of its histological features. The lack of expression of histiocytic antigens by the tumor endothelium is also evidence against a diagnosis of littoral cell angioma, which also derives from the sinus endothelium. Thus, this tumor could not be identified as any of the recognized tumors/tumor-like lesions of the spleen and it is therefore proposed that it should be designated diffuse sinusoidal hemangiomatosis.
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PMID:Diffuse sinusoidal hemangiomatosis of the spleen. A case report with enzyme-histochemical, immunohistochemical, and electron-microscopic findings. 780 69


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