Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 31-year-old secundipara with eclampsia developed the HELLP syndrome after delivery. Clinically, along with very high blood pressure values (29.3/17.3 kPa) and eclamptic attacks, an intense pain in the upper abdomen and nausea were dominant. The patient also had severe thrombocytopenia (18 x 10(9)/L), hemolysis, and increased liver enzymes (SGOT up to 220 U/L and SGPT up to 100 U/L). An intensive therapy, including--together with usual interventions in serious EPH gestoses--also plasmapheresis, antithrombin III substitution, freshly frozen plasma, and transfusion of blood and thrombocytes, proved successful in achieving the normalization of the blood pressure, blood count and liver enzymes, as well as a clinical improvement, so that 18 days after delivery it was possible for the patient to go home, provided with necessary instructions.
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PMID:[The HELLP syndrome--a case report]. 174 83

On the basis of a literature review the extremely severe form of EPH gestosis--the HELLP syndrome is described. In the clinical manifestations of the syndrome a symptom triad predominates: haemolytic anaemia, raised values of hepatic enzymes and thrombocytopenia. The only causative treatment saving the life of the mother and fetus is possibly early termination of pregnancy and adequate supplementation of blood deficiency. The pathophysiology, clinical manifestations, differential diagnosis and treatment of the HELLP syndrome are discussed.
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PMID:[The HELLP syndrome as a severe complication of EPH gestosis]. 270 Oct 42

TRK-100, a stable PGI2 analogue structurally different from carbacyclines, was compared with other antiplatelet drugs for its effect on platelet functions using animal models. TRK-100 (10-300 nM) inhibited rat platelet aggregation induced by ADP (3 microM), collagen (12.5 micrograms/ml) and A23187 (10 microM), and its potency was about 1/3-1/7 that of PGI2. TRK-100 (0.3-3 mg/kg, p.o.) dose-dependently inhibited rabbit platelet adhesion (ED50: 2.2 mg/kg), and its effect lasted over at least 5 hr. In contrast, aspirin and ticlopidine (both at 300 mg/kg, p.o.) showed only a slight inhibition (4-7%). In the thrombocytopenia induced by collagen injection in rats, TRK-100 (3-300 micrograms/kg, i.v.; 0.1-3 mg/kg, p.o.) dose-dependently inhibited a decrease in platelet number, and its ED50 was 0.48-0.62 mg/kg orally and 13.7-16.4 micrograms/kg intravenously, while the inhibition by aspirin and ticlopidine (both at 1000 mg/kg, p.o.) was 40 and 37%, respectively. In the experimental thread thrombosis in rats. TRK-100 (0.03-3 mg/kg, p.o.) dose-dependently inhibited thrombus formation, and its ED50 was 0.46 mg/kg, being 21 and 87 times as potent as aspirin and ticlopidine, respectively. These results reveal that TRK-100 has a potent antiplatelet activity and is orally and intravenously effective for a variety of thrombosis models, suggesting that it may have a therapeutic value as an antithrombotic drug.
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PMID:Antithrombotic effect of TRK-100, a novel, stable PGI2 analogue. 355 83

Because intravascular fibrin deposition is found in the glomerular capillaries of patients who have died of eclampsia, it was long assumed that a chronic form of intravascular clotting represents the decisive cause of the condition. Fibrin deposition is also typically observed in the uteroplacental bloodstream. The occurrence of high levels of soluble fibrin and fibrin(ogen) degradation products, which in severe cases can also include fibrin oligomers, in combination with thrombocytopenia and factor VIII consumption were interpreted as additional evidence for the significance of intravascular clotting in the pathogenesis of EPH gestosis. The hemolysis of the microangiopathologic type, which occurs in severe cases, was attributed to the resulting impairment in microcirculation. Doubts regarding this theory arose when it was noted that the course of EPH gestosis is not altered by the use of heparin, and that even in severe cases of eclampsia with hemolysis and thrombocytopenia the plasmatic clotting system is involved only to a small extent and probably only secondarily. More recent investigations have yielded the first evidence of reduced prostacyclin synthesis in maternal and fetal vessels in patients with EPH gestosis. Since prostacyclins lower arterial resistance yet at the same time are strong inhibitors of thrombocyte aggregation, this prostacyclin deficiency could account for the hypertension and the occurrence of platelet thrombi in the placental bloodstream associated with EPH gestosis. The observation of a reduction in the number of thrombocytes as a consequence of increased platelet breakdown, which precedes a rise in the level of fibrin(ogen) degradation products, also points to the significance of an abnormal interrelation between platelets and endothelium. In addition to the plasmatic and thrombocytic hypercoagulability and impaired prostacyclin synthesis, hemoconcentration with increased microvascular permeability is also observed. Early detection of disturbances of the vessel wall and vessel contents may provide a means of prophylaxis.
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PMID:Recent aspects of hemostasis, hematology and hemorheology in preeclampsia-eclampsia. 637 2

The case of a 22-year-old primigravida in the 33rd week of pregnancy is presented, showing an uncommon form of EPH-gestosis which so far has been described very rarely in German literature. It is a case of pre-eclampsia with haemolytic anaemia, thrombocytopenia, increased liver values and beginning kidney failure. The key to the survival of mother and child lies in rapid delivery and an adequate substitution of erythrocytes and blood plasma. Symptomatics, differential diagnosis and therapy are discussed. Reference literature is given.
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PMID:[Pre-eclampsia with haemolytic anaemia, thrombocytopenia, liver and kidney involvement--an uncommon form of severe gestosis. A case report]. 655 58

A boy born healthy, developed gastrointestinal symptoms (diarrhea, vomiting, ulcerative stomatitis) and megaloblastic anaemia with thrombocytopenia and neutropenia at the age of five weeks. Serum levels of folate and cobalamin were normal, but there was cobalamin-mal absorption. In his serum apo-TC2 was not detectable and immunoreactive total TC2 was very low (10% of normal values). Cultured skin fibroblasts failed to secrete functioning TC2. Pharmacological amounts of parenteral Cyanocobalamin, administered regularly, led to hematological remission and normal development. Interruption of therapy was followed by relapse within a few weeks. A coexisting hypogammaglobulinemia did not respond to cobalamin therapy at the selected dose level. A family investigation of serum TC2 concentrations and the genetic TC2 variants in 7 persons of three generations yielded evidence of autosomal-recessive inheritance of a silent TC2 allele (TC2 QLFL SEA-like). Three persons with heterozygous deficiency were asymptomatic.
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PMID:[Inherited transcobalamin-II-deficiency: clinical, genetic studies and diagnosis using cultured fibroblasts]. 666 2

Pregnant women with either Type B EPH gestosis or gestosis alone were treated with low dose aspirin if thrombocytopenia were present (platelet counts below 75,000) or had platelet aggregation studies if their platelet counts were above 75,000. Platelet aggregation was usually decreased and aspirin therapy appeared to improve platelet counts. However, it appears that platelet abnormalities are only a secondary defect in the "gestosis" process as correction of their thrombocytopenia did not correct their hypovolemia.
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PMID:Diagnosis and treatment of pregnancy induced platelet dysfunction. 687 76

Five cases of pregnant woman with symptoms of right upper quadrant pain, hemoconcentration, liver dysfunction, and thrombocytopenia are presented as representative of impending gestosis. Plasma volume expansion achieved by either bed rest or intravenous albumin administration appeared to be effective therapy. It is presumed that impending gestosis represents an early form of severe toxemia (edema/proteinuria/hypertension [EPH[ gestosis).
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PMID:Impending gestosis. 731 42

2B1 is a bispecific murine monoclonal antibody (BsMAb) with specificity for the c-erbB-2 and Fc gamma RIII extracellular domains. This BsMAb promotes the targeted lysis of malignant cells overexpressing the c-erbB-2 gene product of the HER2/neu proto-oncogene by human natural killer cells and mononuclear phagocytes expressing the Fc gamma RIII A isoform. In a Phase I clinical trial of 2B1, 15 patients with c-erbB-2-overexpressing tumors were treated with 1 h i.v. infusions of 2B1 on days 1, 4, 5, 6, 7, and 8 of a single course of treatment. Three patients were treated with daily doses of 1.0 mg/m2, while six patients each were treated with 2.5 mg/m2 and 5.0 mg/m2, respectively. The principal non-dose-limiting transient toxicities were fevers, rigors, nausea, vomiting, and leukopenia. Thrombocytopenia was dose limiting at the 5.0 mg/m2 dose level in two patients who had received extensive prior myelosuppressive chemotherapy. Murine antibody was detectable in serum following 2B1 administration, and its bispecific binding properties were retained. The pharmacokinetics of this murine antibody were variable and best described by nonlinear kinetics with an average t 1/2 of 20 h. Murine antibody bound extensively to all neutrophils and to a proportion of monocytes and lymphocytes. The initial 2B1 treatment induced more than 100-fold increases in circulating levels of tumor necrosis factor-alpha, interleukin 6, and interleukin 8 and lesser rises in granulocyte-monocyte colony-stimulating factor and IFN-gamma. Brisk human anti-mouse antibody responses were induced in 14 of 15 patients. Several minor clinical responses were observed, with reductions in the thickness of chest wall disease in one patient with disseminated breast cancer. Resolution of pleural effusions and ascites, respectively, were noted in two patients with metastatic colon cancer, and one of two liver metastases resolved in a patient with metastatic colon cancer. Treatment with 2B1 BsMAb has potent immunological consequences. The maximum tolerated dose and Phase II daily dose for patients with extensive prior myelosuppressive chemotherapy was 2.5 mg/m2. Continued dose escalation is required to identify the maximally tolerated dose for patients who have been less heavily pretreated.
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PMID:Phase I trial of 2B1, a bispecific monoclonal antibody targeting c-erbB-2 and Fc gamma RIII. 755 34

In a significant proportion of patients with acute myeloid leukemia (AML), a series of hematological alterations--including refractory anemia, neutropenia, thrombocytopenia, abnormal iron metabolism, and elevated levels of blast cells both in peripheral blood and bone marrow--are observed before the diagnosis of AML is made. This preleukemic state has called the attention of several investigators around the world, since it represents a way to study the origin and progression of leukemia in man. During the past 5 years, major advances in the molecular and cellular biology of this disease have been achieved. It is now known that preleukemia is a clonal disorder that arises from a malignant transformation at the level of primitive pluripotent hemopoietic stem cells. The hemopoietic progenitors in preleukemic patients have abnormal responses to hemopoietic regulators, thus, they do not seem to follow the controlled proliferation observed in the hemopoietic system under normal conditions. The mechanisms of cell differentiation and maturation are also altered, leading to the production of immature (blast) cells, instead of the development of fully mature erythrocytes, granulocytes, platelets and lymphocytes. Several oncogenes, such as C-FMS and RAS, have been found to be structurally altered in a significant proportion of preleukemic patients, suggesting that they may be involved in the pathogenesis of the disease. In spite of the advances made during the last few years, major questions regarding the biology of this hematological disorder are still unanswered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human preleukemia: cellular, molecular and clinical aspects. 811 54


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