Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the clinical and laboratory features of eight children (median age, 20 months; range, 13 months to 11 years) with acute megakaryocytic leukemia (M7) and compared the findings with those reported in the literature. The diagnosis was supported by ultrastructural examination for platelet peroxidase or immunophenotyping for glycoprotein IIb/IIIa or the von Willebrand factor protein. Two patients had Down's syndrome. Initial findings included anemia (in all patients), thrombocytopenia (in six), myelofibrosis (in three), lytic bone lesions (in two), and pronounced leukocytosis (in one). Stem cell culture studies of peripheral blood specimens revealed an aberrant phenotype of the megakaryocytes in one patient and reversal to a normal pattern after successful therapy. Remission was achieved in seven of the eight patients after aggressive chemotherapy, and four patients remained in remission 27 to 57 months after diagnosis. Three of these four patients underwent allogeneic bone marrow transplantation. M7 leukemia is not infrequent in children younger than 3 years of age, especially in those with Down's syndrome. The availability of monoclonal antibodies specific to restricted antigens of the megakaryocytic lineage has made the diagnosis of M7 leukemia both possible and practical.
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PMID:Acute megakaryocytic leukemia (M7) in children. 259 24

A 43-yr-old Japanese woman presented with mild anemia, leukocytosis and splenomegaly in May 1984. Splenomegaly and anemia gradually progressed. Sixteen years later, in October 2000, she developed inguinal lymphadenopathy. Biopsy of the lymph node revealed infiltration of blasts, megakaryocytes, fibroblasts and myeloid cells. Large blasts with basophilic cytoplasm with cytoplasmic projections appeared in the peripheral blood. These blasts were negative in peroxidase stain, positive in acid phosphatase and weakly positive in periodic acid-Schiff stain. Immunohistochemical staining with monoclonal antibodies revealed that these blasts were positive with anti-CD41 (glycoprotein IIb/IIIa) and negative with other monoclonal antibodies. So diagnosis of granulocytic sarcoma in megakaryoblastic transformation from chronic idiopathic myelofibrosis was made. A cytogenetic study revealed that bone marrow cells were 46,XX del(13)(q?) initially and additional abnormalities including der(5,5,11)(q11;q13)ins(5;?)(q11;?) were found when she developed megakaryoblastic transformation. Granulocytic sarcoma of megakaryoblastic transformation from chronic idiopathic myelofibrosis is a rare event. Immunophenotyping with monoclonal antibody for CD41(glycoprotein IIb/IIIa) confirmed the diagnosis.
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PMID:Granulocytic sarcoma of megakaryoblastic differentiation in the lymph nodes terminating as acute megakaryoblastic leukemia in a case of chronic idiopathic myelofibrosis persisting for 16 years. 1173 54

A 64-yr-old Japanese man presented with mild anemia, leukocytosis, and thrombocytosis in November 1999. A diagnosis of chronic myeloid leukemia was made with a positive Ph chromosome, and interferon alpha treatment was started, 6 million units a day. Two years later, in October 2001, the patient developed leukocytosis, an increased LDH level, and large blasts with basophilic cytoplasm with cytoplasmic projections appeared in the peripheral blood. Bone marrow aspiration revealed increased blasts (59.6%). These blasts were negative on peroxidase stain, positive on acid phosphatase, and weakly positive on alpha naphthyl butyrate esterase stain and periodic acid-Schiff stain. Immunohistochemical staining with monoclonal antibodies revealed that these blasts were strongly positive with anti-CD41 (glycoprotein IIb/IIIa), weakly positive with CD7, CD33, and CD34, and negative with other monoclonal antibodies. A diagnosis of megakaryoblastic transformation from chronic myeloid leukemia was therefore made. Two-color fluorescence in situ hybridization (FISH) for portions of the major-bcr and abl genes from bone marrow cells revealed two fused signals in 90.6% and one fused signal in 5.8% of 106 cells. A cytogenetic study revealed that bone marrow cells were 69, XYY, +6, -7, +8, -9, t(9;22)(q34;q11), +11, +13, -15, -16, dic(17;18)(p11;p11), -18, +19, +21, der(22)t(9;22) in six of nine examined cells. These findings confirmed that these megakaryoblasts originated from megakaryocytes of the chronic myeloid leukemia clone.
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PMID:Double Ph-positive megakaryoblastic transformation of chronic myeloid leukemia. 1236 19

The economics of bleeding complications and the role of antithrombotic therapies in percutaneous coronary intervention (PCI) are discussed. More than 1 million PCI procedures are performed annually in the United States, at a mean cost of hospitalization of approximately $9,000 and billions of dollars in total health care costs. Ischemic complications have been reduced to the point that bleeding has become the most common complication. Bleeding complications and transfusions are also among the most costly complications in PCI, accounting for an incremental cost of hospitalization after PCI that may exceed $10,000, due to increased length of stay and the use of additional resources such as ultrasound evaluation and surgical repair of the vascular site. Anemia and transfusions are also associated with increased morbidity and mortality, contributing to additional treatment costs beyond those directly attributable to correcting the bleeding complication. In the past decade, significant reductions in heparin dose and warfarin use were associated with reduced bleeding complications, but glycoprotein IIb/IIIa inhibitors have been shown to increase the clinical and economic costs of bleeding complications. The replacement of heparin with bivalirudin is associated with significant reductions in the costs of antithrombotic therapy and in complications. Reductions in bleeding complications have become a primary target for further improvements in both clinical and economic outcomes.
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PMID:Economic impact of bleeding complications and the role of antithrombotic therapies in percutaneous coronary intervention. 1290 78

In Europe, the use of interventional cardiology, including percutaneous coronary intervention (PCI), is increasing rapidly. The use of anticoagulation agents in PCI procedures is essential, but despite technical improvements, a significant associated bleeding risk still exists: more than 5% of patients are estimated to require transfusion, and around a further 13% experience minor bleeding. The methods used to detect and measure blood loss following PCI, however, vary widely between institutions and clinical trials. The risk of bleeding is influenced by therapeutic options and patient-specific characteristics, such as age, anemia and previous exposure to anticoagulants. Bleeding is associated with death, and also with less severe conditions such as thrombocytopenia, anemia, and hematoma, which have major impacts on patients' welfare and length of hospital stay, and on hospital budgets. Unfractionated heparin is the most widely used anticoagulant during PCI. Heparin, antiplatelet agents and other anticoagulants, however, have limitations that make it difficult to achieve a level of anticoagulation that prevents ischemic events without promoting bleeding. The use of low-molecular-weight heparin and the addition of glycoprotein IIb/IIIa inhibitors offer improved outcomes, but safer and more effective therapeutic agents are still required. New anticoagulants, including direct thrombin inhibitors such as bivalirudin, show similar levels of efficacy to heparin plus glycoprotein IIb/IIIa inhibitors, but with fewer hemorrhagic complications, and might advance clinical practice. This review evaluates the impact of PCI-related bleeding on patients' outcomes and hospital resources, examines methods for the detection and measurement of bleeding, and appraises the therapeutic options--particularly the newer agents--available to minimize hemorrhagic complications.
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PMID:Drug insight: bleeding after percutaneous coronary intervention-risks, measures and impact of anticoagulant treatment options. 1626 87

The relation across anemia, hemorrhagic complications, and mortality associated with percutaneous coronary intervention (PCI) is unclear. We reviewed the Randomized Evaluation in PCI Linking Angiomax to Reduced Clinical Events (REPLACE)-2 Trial, which compared bivalirudin plus provisional glycoprotein IIb/IIIa blockade with heparin plus planned glycoprotein IIb/IIIa blockade in patients undergoing urgent or elective PCI. Of the 6,010 patients randomized in REPLACE-2, 1,371 (23%) were anemic. Major bleeding was more common in anemic than in nonanemic patients (4.9% vs 2.8%, p = 0.0001). In anemic patients, treatment with bivalirudin (n = 678) resulted in a lower risk of major bleeding versus heparin plus glycoprotein IIb/IIIa blockade (n = 693, 3.5% vs 6.2%, p = 0.0221). Mortality was higher in anemic patients than in nonanemic patients at 30 days (0.9% vs 0.2%, p <0.0001), 6 months (2.6% vs 0.7%, p <0.0001), and 1 year (4.3% vs 1.5%, p <0.0001). There were no differences between anemic and nonanemic patients with regard to ischemic complications at 30 days. Although anemic patients had higher mortality rates, proportions of cardiovascular and noncardiovascular mortalities were equal in anemic and nonanemic patients. In conclusion, anemic patients undergoing PCI have an increased risk of mortality and major bleeding, but not of ischemic events, and the use of bivalirudin with provisional glycoprotein IIb/IIIa blockade decreases the risk of hemorrhagic complications compared with heparin plus planned glycoprotein IIb/IIIa blockade.
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PMID:Effect of anemia on hemorrhagic complications and mortality following percutaneous coronary intervention. 1753 72

Patients undergoing percutaneous coronary intervention (PCI) have a significant risk of hemorrhagic complications. Predictors of major hemorrhage and its relation to mortality in PCI are not well defined. Baseline and periprocedural predictors of major hemorrhage and its impact on mortality in patients undergoing elective or urgent PCI randomly assigned to heparin plus planned glycoprotein IIb/IIIa inhibitor (GPI) versus bivalirudin plus provisional GPIs in the REPLACE-2 Trial were determined. Of 6,001 patients, 3.2% experienced a major hemorrhage. Independent baseline predictors of major hemorrhage included advanced age, female gender, impaired creatinine clearance, and anemia. Independent periprocedural predictors of major hemorrhage included treatment with heparin plus GPI, increased procedural duration, provisional use of GPI, increased time to sheath removal, length of intensive care unit stay, and use of an intra-aortic balloon pump (all p <0.05). Mortality rates were higher in patients with than without major hemorrhage at 30 days (5.1% vs 0.2%), 6 months (6.7% vs 1.0%), and 1 year (8.7% vs 1.9%; p <0.001 for all). Furthermore, major hemorrhage was an independent predictor of 1-year mortality (odds ratio 2.66, 95% confidence interval 1.44 to 4.92, p = 0.002). In conclusion, in patients undergoing elective or urgent PCI, major hemorrhage was an independent predictor of 1-year mortality. A number of baseline and periprocedural factors independently predicted major hemorrhage, including treatment with heparin plus GPI.
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PMID:Predictors and impact of major hemorrhage on mortality following percutaneous coronary intervention from the REPLACE-2 Trial. 1795 Jul 91

Anemia has been shown to be an independent predictor of long-term mortality after percutaneous coronary intervention (PCI). African-Americans are known to have lower hemoglobin (Hgb) levels compared with Caucasians. The impact of anemia on long-term mortality in African-Americans undergoing PCI is unknown. We evaluated a total of 715 African-American patients (313 patients with anemia and 402 patients without anemia as defined by the World Health Organization [Hgb <13 g/dl for men and <12 g/dl for women]) using data from our bolus-only glycoprotein IIb/IIIa database. After a median follow-up of 3.2 years (interquartile range 2.4 to 3.8), there were a total of 72 (10%) deaths. Survival rate was 84% in the anemic group compared with 94% in the control group (hazard ratio [HR] 2.8, unadjusted p <0.001 by log-rank test). After adjustment for baseline clinical and procedural characteristics using a Cox proportional hazards model, Hgb as a dichotomous variable was a strong and independent predictor of all-cause mortality during the follow-up period (HR for death 2.0, 95% confidence interval 1.2 to 3.4, adjusted p = 0.012). Also, when Hgb was analyzed as a categorical variable having 3 groups with empirically determined cutoffs at <11.1, > or =11.1 to <12.7, and > or =12.7 g/dl, the effect remained significant (adjusted p = 0.008), with a HR of 2.3 for the group with lowest Hgb compared with the group with highest value (HR 2.6 for group with Hgb > or =11.1 to <12.7 compared with the group with the highest Hgb value). In conclusion, baseline Hgb is a strong and independent predictor of all-cause long-term mortality in African-Americans undergoing PCI.
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PMID:Effect of hemoglobin level on long-term all-cause mortality after percutaneous coronary intervention in African-Americans. 1936 93

The aim of this study was to assess the impact of baseline anemia on the outcomes of patients with ST elevation myocardial infarctions who underwent primary percutaneous coronary intervention in relation to contemporary adjunctive antithrombotic therapy and gender. In the Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial, patients were randomized to bivalirudin alone or to unfractionated heparin plus a glycoprotein IIb/IIIa inhibitor before primary percutaneous coronary intervention. Outcomes were assessed at 30 days and 1 year according to anemia and gender. Baseline anemia was present in 331 of 3,153 patients (10.5%). Patients with versus without baseline anemia had a more than twofold increase in major bleeding at 30 days (13.5% vs 6.7%, p <0.0001) and at 1 year (14.8% vs 7.2%, p <0.0001), an association that on multivariate analysis was independent of gender. Mortality was significantly higher in men with versus without baseline anemia (4.6% vs 1.8% at 30 days, p = 0.003; 8.9% vs 3.0% at 1 year, p <0.0001) but not in women (5.3% vs 3.6% at 30 days, p = 0.42; 7.5% vs 5.9% at 1 year, p = 0.54). On multivariate analysis, anemia independently predicted 1-year all-cause mortality in men but not in women. Bivalirudin compared with unfractionated heparin plus a glycoprotein IIb/IIIa inhibitor resulted in twofold lower rates of all-cause and cardiac mortality and major bleeding in patients without but not in those with baseline anemia. In conclusion, baseline anemia was associated with increased major bleeding and death in patients with ST elevation myocardial infarctions who underwent primary PCI but was a stronger predictor of early and late mortality in men than in women. Paradoxically, in this post hoc analysis, the reductions in major bleeding and mortality in ST elevation myocardial infarction afforded by bivalirudin occurred primarily in patients without baseline anemia.
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PMID:Impact of anemia on clinical outcomes of patients with ST-segment elevation myocardial infarction in relation to gender and adjunctive antithrombotic therapy (from the HORIZONS-AMI trial). 2045 83

A 17-year-old Peruvian Paso mare was evaluated for bilateral epistaxis that had been present for at least 3 years. The mare had mild anemia, platelet count within the reference interval, unremarkable coagulation times, and a negative Coggins test. On endoscopic examination, structural abnormalities were not observed in the nasal cavities, pharynx, larynx, trachea, or either guttural pouch, but petechiation was noted in the nasal mucosa. Additional tests revealed prolonged cutaneous bleeding time, normal concentration of von Willebrand factor antigen, an abnormal clot retraction test, and failure of plalelet aggregation in response to agonists, suggesting a functional disorder of platelets. Genetic analysis indicated the horse was homozygous for a 10-base-pair deletion that included the last 3 base pairs of exon 11 and the first 7 base pairs of intron 11 of the gene encoding glycoprotein IIb. The diagnosis was Glanzmann thrombasthenia (GT) caused by a structural defect in glycoprotein IIb. GT is an autosomal recessive disorder caused by a defect in the glycoprotein IIb-IIIa complex on platelet surfaces. Separate genes encode each glycoprotein, and mutations in either gene can result in GT. This case of GT is unique given the age of the mare at the time of diagnosis. We conclude that GT, although an inherited disorder, should be considered in horses with suspected dysfunctional platelets, regardless of age.
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PMID:Glanzmann thrombasthenia in a 17-year-old Peruvian Paso mare. 2129 83


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