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)

Ten episodes of massive transaminase increase with hepatic necrosis were observed in 7 patients after infusion of megluminioglycamide (Biligram). The patients were 3 men and 4 women aged 49 to 65 years with biliary tract disease (n = 1), recurrent pancreatitis (n = 1), hyperlipidaemia and minimal toxic liver damage (n = 1), pyelonephritis (n = 1), , arteriitis (n = 1), and pseudo-LE (n = 1). In 6 patients there was an increase of the alkaline phosphatase without icterus before the investigation and a slight increase of transaminases in 3 patients. After infusion of 100 ml of Biligram in 5 patients and of 200 ml in 2 patients there was an abrupt increase of GPT (98-2202 U/l) with a lesser increase of GOT. The alkaline phosphatase activity remained unchanged. Three patients showed symptoms such as upper abdominal pain, fever erythema, or conjunctivitis. Histologically all patients showed centrolobular necroses. Transaminases should be checked 2 days after intravenous cholangiograms. In patients with a definite increase reexposure should be avoided.
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PMID:[Hepatic necroses after infusion cholangiography (author's transl)]. 63 57

The distribution and concentration of human tryptase-positive, chymase-negative mast cells (MCTS) and tryptase-positive, chymase-positive mast cells (MCTCS) were examined in conjunctival biopsy specimens from subjects with active vernal conjunctivitis (VC; n = 7), giant papillary conjunctivitis (GPC; n = 6), and allergic conjunctivitis (AC; n = 5), and from asymptomatic soft-contact lens wearers (SCL; n = 6) and normal control individuals (n = 19). Carnoy's fixed tissue sections were stained by a double immunohistochemical method using a biotinylated mouse monoclonal antichymase antibody with immunoperoxidase, followed by an alkaline phosphatase-conjugated mouse monoclonal antitryptase antibody. Epithelial mast cells (MCs) were found in all VC specimens (96% MCTCs) and in three GPC specimens (100% MCTCS) but in none of the other groups. In the substantia propria, MCTCS were the predominant type of MC observed in all specimens, accounting for 95% of the total MCs in the normal control group and 100% of the total MCs in the subjects with GPC, AC, and SCL. No significant differences were found in the total MC concentration of the substantia propria among the normal control subjects (11,054 +/- 6327 MCs per cubic millimeter), subjects in the SCL group (13,168 +/- 4685 MCs per cubic millimeter), subjects with GPC (17,313 +/- 8500 MCs per cubic millimeter), and subjects with AC (15,380 +/- 5660 MCs per cubic millimeter). In subjects with VC, the percentage of MCTs (18% +/- 13%) and the total MC concentration (24,689 +/- 18,978 MCs per cubic millimeter) in the substantia propria were significantly increased as compared to the normal control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human conjunctival mast cells: distribution of MCT and MCTC in vernal conjunctivitis and giant papillary conjunctivitis. 219 2

High doses of calcitriol were used prospectively for 11 to 29 months to raise serum calcium levels in an effort to control renal osteodystrophy in 16 children undergoing CAPD. Serum Ca, P, iPTH and alkaline phosphatase were measured monthly; hand radiographs were obtained every six months, and a semiquantitative score of bone abnormalities was evaluated by two independent observers. During the study, serum Ca increased from 9.9 +/- 0.9 to 11.0 +/- 0.6 mg/dl (P less than 0.001); serum iPTH decreased by 113 +/- 131 microliter Eq/ml (P less than 0.005); serum P was unchanged; and serum alkaline phosphatase fell by 33 +/- 46% (P less than 0.02), 530 +/- 397 to 204 +/- 551 IU/liter. The radiographic score fell from 4.8 +/- 4.6 to 0.9 +/- 1.2 (P less than 0.005). The average and maximal doses of calcitriol were 0.61 +/- 0.37 and 0.95 +/- 0.56 microgram/day or 28 +/- 18 and 46 +/- 28 ng/kg body wt/day, respectively. Transient and asymptomatic hypercalcemia occurred in nine patients and two patients had reversible conjunctivitis in association with the hypercalcemia. Thus, "high dose" calcitriol prevented or controlled progression of hyperparathyroid bone disease in most pediatric CAPD patients. The failure to suppress PTH or reverse secondary hyperparathyroidism until the serum Ca rose to 10.5 to 11.0 mg/dl could reflect an increase in the "set point" for PTH suppression by serum calcium in many uremic children.
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PMID:"High-dose" calcitriol for control of renal osteodystrophy in children on CAPD. 362 2

Fifty-seven patients with refractory acute leukemia were treated with high-dose cytosine arabinoside to establish the maximum tolerated dose and duration and to determine the antileukemic activity. The maximum tolerated regimen was found to be 3 g/sq m every 12 hr for 6 days. At this dose, nonhematologic toxicity was limited to conjunctivitis in approximately half of the patients, and liver toxicity (transient elevations in transaminase, alkaline phosphatase, or bilirubin) was frequently observed, but neither was dose-limiting. Extending the duration of treatment to 8 days resulted in excessive diarrhea and skin toxicity (painful erythema with bullae), while increasing the dose to 4.5 g/sq m q. 12 hr for 6 days resulted in severe cerebellar toxicity. Myelosuppression was severe, but was not related to the intensity of treatment; granulocyte recovery occurred a median of 28 days (range 22-40 days) after initiating therapy, and platelet recovery occurred after a median of 25 days (range 16-41 days). Antileukemic activity was evaluable in the 46 patients who survived at least 3 wk. Complete remissions were obtained in 1 of 6 patients with chronic myelogenous leukemia (CML) in accelerated phase and 1 of 3 acute lymphoblastic leukemia (ALL) patients. A more detailed analysis of response was possible for the 37 evaluable patients with acute nonlymphoblastic leukemia: 70% of these patients responded, with 51% complete remissions. The median unmaintained response was 4 mo (range 2-26+ mo). The complete response rate was higher in patients who received at least 12 doses of high-dose cytosine arabinoside compared to shorter regimens [17/28 (61%) versus 2/9 (22%), p less than 0.05]. Resistance to cytosine arabinoside in conventional doses was documented in 11 patients, 5 of whom responded (2 complete remissions) to high-dose regimens. We conclude that high-dose cytosine arabinoside in the maximally tolerated regimen of 3 g/sq m every 12 hr for 6 days has substantial antileukemic activity in patients refractory to standard therapy. Durable unmaintained remissions can be achieved, even in patients who fail to respond to cytosine arabinoside in conventional doses.
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PMID:High-dose cytosine arabinoside therapy for refractory leukemia. 622 74

In a retrospective study clinical and hepatotoxic side effects caused by Tigason treatment are investigated. The material consists of data on 27 patients with normal liver function tests at the beginning of treatment. The clinical side effects encountered were: dryness of lips and mucous membranes (n = 14), diffuse hair loss (n = 5), epistaxis (n = 1) and conjunctivitis (n = 1). Abnormal liver function tests (glutamic oxaloacetic transaminase, glutamic pyruvic transaminase lactate dehydrogenase and alkaline phosphatase) were found in 7 patients: 3 developed slight transient elevation of parameter during treatment, 2 transient elevation of more parameters, normalizing despite continued therapy in 1 and in the other normalizing after discontinuation. Finally 2 patients developed persistent elevation of one or more parameters. In the last 2 patients liver biopsy showed changes of toxic hepatitis.
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PMID:Side effects due to RO 10-9359 (Tigason). A retrospective study. 711 42

Five Holstein heifers (approximately 8 months of age and weighing 225-275 kg) were inoculated subcutaneously with 1,000 TCID50 of rinderpest virus, virulent Kabete O strain. They become clinically ill 2 to 5 days post-inoculation, with fever (40 C to 41.5 C), conjunctivitis, and diarrhea. All were euthanatized when moribund at 6 days postinoculation. The following tissues were collected in formalin, embedded in paraffin, and subsequently subjected to histopathologic and immunohistochemical examination: tongue, buccal mucosa, soft palate, esophagus, rumen, abomasum, duodenum, jejunum with and without Peyer's patch, ileum, cecum, proximal colonic lymphoid patch, spiral colon, eyelid, gall bladder, spleen, tonsil, trachea, lungs, and numerous lymph nodes. Immunohistochemical examination was accomplished using a primary rabbit anti-rinderpest antibody, and either a peroxidase-diaminobenzidine or alkaline phosphatase-Vector Red detection substrate system. In the lymph nodes, spleen, and tonsil, depletion of lymphocytes from all areas was extensive, with antigen most prominent in persisting reticular cells throughout the tissues. In the intestine, necrotizing and ulcerative changes in the mucosa were extensive and widespread. Damage was most severe in areas overlying lymphoid patches. In both small and large intestine, antigen was distributed predominantly in epithelial cells, histiocytic cells in the lamina propria, and in remaining reticular cells of lymphoid patches. In oral mucosa, there were multiple ulcerations and numerous multinucleate syncytial cells, both containing and without antigen. Lungs and trachea had subtle yet consistent necrosis of epithelial cells, with antigen often distributed in a circumferential manner in epithelium of bronchioles.
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PMID:Distribution of antigen in cattle infected with rinderpest virus. 820 82

PD 132301-2 is a substituted urea hypolipidemic and antiatherosclerotic agent that is a potent inhibitor of acyl-CoA:cholesterol acyltransferase (ACAT). To determine its subacute toxicity, PD 132301-2 was administered orally to beagle dogs at 0, 6, 12, 25, 50, 200, 400, or 800 mg/kg/day for 2 weeks. Clinico-pathologic evaluations were completed on all dogs. Liver and adrenal total and esterified cholesterol concentrations, adrenocorticotrophic hormone (ACTH) responsiveness, and adrenal ultrastructure were determined at 0, 6, 12, and 25 mg/kg. At 12 mg/kg or greater, salivation, epiphora, conjunctivitis, emesis, anorexia or decreased food consumption, and soft to mucoid feces and/or diarrhea were noted. Suppression of ACTH response occurred by Day 6 at all doses. Adrenocortical degeneration and/or necrosis in zona fasciculata and reticularis was seen at all doses; adrenal free and esterified cholesterol were normal at 6 mg/kg and decreased at 12 and 25 mg/kg. Increases in serum alanine aminotransferase (2- to 15-fold), aspartate aminotransferase (2- to 12-fold), and alkaline phosphatase (2- to 7-fold) were noted at 50 mg/kg or greater. Periportal hepatocellular hypertrophy and hypereosinophilia occurred at 50 mg/kg or greater; hepatic cholesterol values were not significantly affected by treatment. Dose-dependent ultrastructural alterations in adrenocortical cells included decreased numbers of mitochondria and smooth endoplasmic reticulum profiles, qualitative and quantitative changes in lipid globules, and increased numbers of autolysosomes. PD 132301-2 or one of its metabolites has potent adrenocorticolytic properties and limited hepatotoxic properties by mechanism(s) that are likely independent of systemic ACAT inhibition.
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PMID:Subacute toxicity of a novel inhibitor of acyl-CoA: cholesterol acyltransferase in beagle dogs. 838 21

Retinoids have been shown to be potent inhibitors of epithelial carcinogenesis. Recent evidence has demonstrated that retinoid actions are mediated through nuclear receptors, which are proteins encoded by the retinoic acid receptor and retinoid X receptor gene families. These receptors are activated by binding to specific retinoids; of the known naturally occurring retinoids, 9-cis retinoic acid is unique in its ability to bind to both receptor families. Because of its unique receptor-binding characteristics, 9-cis retinoic acid may have biological activity not possible with other retinoids. For this reason, we conducted a Phase I trial of 9-cis retinoic acid in adult patients with solid tumors. Twenty-two patients were treated twice daily with p.o. 9-cis retinoic acid at doses ranging from 20 mg/m2/day to 150 mg/m2/day. The patients had non-small cell lung cancer (n = 8), breast cancer (n = 5), colorectal cancer (n = 3), head and neck cancer (n = 2), nonmelanoma skin cancer (n = 2), or ovarian cancer (n = 2). The dose-limiting (WHO grade III) toxic effects, which occurred at the 150-mg/m2/day dose level, were headaches and diarrhea. Less severe (grades I and II) toxic effects included cheilitis, dry skin, conjunctivitis, fatigue, hypertriglyceridemia, alkaline phosphatase elevation, myalgia/arthralgia, and hypercalcemia. Of the 15 patients evaluable for tumor response, no objective responses were observed. Pharmacokinetic analysis revealed a reduction in peak 9-cis retinoic acid plasma levels with chronic administration. Based on this study, the recommended Phase II dose of 9-cis retinoic acid in adult patients with solid tumors is 100 mg/m2/day administered in a divided dose twice daily.
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PMID:Phase I trial of 9-cis retinoic acid in adults with solid tumors. 981 71

A total of 45 non-uremic dogs, with clinical signs indicating leishmaniosis, entered the study. Diagnosis was confirmed by indirect immunofluorescence assay (IFA) on serum and polymerase chain reaction (PCR) on bone marrow samples. The dogs were randomly allocated into Group A (n=37) that received allopurinol (10mg/kg B.W., per os, twice daily) for 4 consecutive months, and Group B (n=8) that were placebo-treated. Clinical signs were scored just before and at monthly intervals throughout the study period, in a blinded and independent fashion. Complete blood count, serum biochemistry profile, urinalysis, lymph node and bone marrow parasitology, IFA and enzyme-linked immunosorbent assay (ELISA) serology and bone marrow PCR were carried out at the beginning and at the end of the trial. A total of three Group A and one Group B dogs died of end stage kidney disease that developed during the trial. In Group A animals that endured the trial there was a significant improvement in the general body condition, conjunctivitis, peripheral lymphadenopathy, splenomegaly, masticatory muscle atrophy, ulcerative stomatitis, epistaxis, exfoliative dermatitis, cutaneous ulcerations, blepharitis and nasodigital hyperkeratosis. The same observation was made for anemia, lymphopenia, hyperproteinemia, hyperglobulinemia, hyperphosphatemia, increased alkaline phosphatase activity and the low albumin/globulin ratio. By contrast, no improvement of any kind was seen in Group B dogs. Lymph node and bone marrow parasite numbers were significantly decreased in Group A animals. In Group B, that occurred only in the lymph nodes. Apart from remission of clinical signs and restoration to normal of clinicopathological abnormalities, allopurinol did not eliminate Leishmania organisms, as the PCR result on bone marrow was still positive in all the dogs that finished the trial.
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PMID:A randomised, blinded, placebo-controlled clinical trial with allopurinol in canine leishmaniosis. 1142 83

A 54-year-old patient with primary cerebral lymphoma was treated with two 4-weekly cycles of high-dose intravenous cytarabine (12 g/m2) and methotrexate (3 g/m2). The administration of the first course proceeded without notable complications. Before the administration of methotrexate in the second cycle blood cell counts and chemistry showed no abnormalities except for slightly increased alkaline phosphatase and gamma-glutamyl-transpeptidase levels which was attributed to diphantoin comedication. The patient developed symptoms of acute renal failure 7 h after methotrexate infusion which resulted in a very high serum methotrexate level (39.84 micromol/l) at 20 h after infusion. Rescue therapy was intensified: the leucovorin dosage was increased (1,200 mg continuous i.v. infusion every 24 h) and combined with thymidine rescue therapy (8 g/m2 per day continuous i.v. infusion every 24 h). Urine alkalinization was increased and diphantoin therapy was stopped. Leucovorin eye drops and mouth washes were started 5 days after methotrexate administration to prevent conjunctivitis and mucositis as a result of high methotrexate levels (>2.4 micromol/l). In spite of the fact that serum methotrexate levels remained persistently higher than 0.1 micromol/l for 12 days, the patient experienced no further short-term systemic toxicity except for anaemia (grade 3 according to NCI Common Toxicity Criteria). After day 12 intensified rescue therapy and the frequency of alkalinization were decreased to standard procedures and stopped on day 19. It is concluded that i.v. administration with high-dose methotrexate can result in unpredictable acute toxicity. In our patient, acute methotrexate toxicity was treated successfully by intensification of classical leucovorin rescue therapy in combination with thymidine infusion. In addition, leucovorin mouth washes and eye drops may have prevented mucositis and conjunctivitis, respectively.
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PMID:Successful rescue with leucovorin and thymidine in a patient with high-dose methotrexate induced acute renal failure. 1145 8


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