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)

At the time of placentation, the conceptus surrounds itself with a trophoblastic layer where the villous tree develops and the uteroplacental circulation takes place. Analysis of the modalities of maternal blood entrance demonstrated a physiological hypoxia ending with the first trimester of pregnancy. Moreover, cultures of first trimester villous explants have shown the role of oxygen in extravillous cytotrophoblast proliferation, decidual invasion and spiral artery remodeling. Oxygen appears to be a key factor controlling the mechanism of placentation by regulating the transcription of several genes, such as VEGF (vascular endothelial growth factor), leptin, etc. These genes are turned on or off as a function of oxygen partial pressure via an oxygen sensor. Oxygen is now considered to be implicated in the development of several pathologies of pregnancy. It is involved at different steps in the cascade of events leading to preeclampsia. Positive correlations have been observed between oxygen partial pressure and abnormal development of the villous tree in intrauterine growth retardation, and in maternal anemia or pregnancy in altitude.
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PMID:[The human placenta and its pathologies: focus on oxygen]. 1464 82

Except rare instances of allogeneic stem cell transplantation, treatment of idiopathic myelofibrosis (IMF) is only palliative and based on cytostatic treatment (hydroxyurea and anagrelide), androgen therapy, steroids and splenectomy. Thalidomide is an anti-angiogenic and immunomodulatory drug with a wide spectrum of activities, which are not clearly understood. Current data suggest that the action of thalidomide is related to several different mechanisms, including suppression of tumor necrosis factor, effects on basic fibroblast growth factor, vascular endothelial growth factor, interleukins and interferons, downregulation of selected cell surface adhesion molecules, and changes in the lymphocyte subsets. We administered thalidomide to 16 patients with IMF (15 men, one women) who had transfusion-dependent anemia, thrombocytopenia or symptomatic splenomegaly. Median age was 59 yr (range: 52-78). Patients received thalidomide at an escalating dose from 100 to 400 mg/d (median 300 mg). The drug was discontinued in four patients because of progressive disease (two) or polyneuropathy (two). Other adverse effects were obstipation (10), fatigue (eight) and edema (two). Clinical response has now been observed for a median duration of 9 months (range: 3-20). Fifteen patients are evaluable. Anemia improved in six of 10 patients who were anemic. Platelet counts improved in five of seven patients with thrombocytopenia. Splenomegaly regressed in three of 13 patients. Lactate dehydrogenase (LDH) decreased in seven of 12 patients, but increased in four patients. LDH levels were not correlated with clinical response. In summary, thalidomide appears useful in the treatment of IMF.
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PMID:Thalidomide for the treatment of idiopathic myelofibrosis. 1496 63

This paper presents the role of erythropoietin application in diabetic patients with accompanying renal failure. The main cause of anemia in diabetics are: nephropathy, structural lesions of erythrocyte membrane and blood loss connected with diagnostic and therapeutic actions. There are publications which demonstrate that in patients with diabetes type 1 or 2 with accompanying nephropathy, anemia appears more frequently than in the group of patients with chronic renal failure caused by other factors. It is supposed, that the impaired erythropoietin synthesis in diabetics can be caused by autonomic neuropathy. Erythropoietin administration in case of diabetic nephropathy has a beneficial influence on fat metabolism, immune response and reduction of insuline resistance. Erythropoietin because of reduction of vascular endothelial growth factor synthesis blocks the development of diabetic retinopathy and macroangiopathy. Erythropoietin reduces the risk of the left-ventricular hypertrophy caused by anemia. Very important is that the erythropoietin resistance is lower in diabetics. Scientists who are adverse to erythropoietin administration in patients with diabetic nephropathy maintain, that it can lead to vascular complications and the deterioration of glycemia control.
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PMID:[Erythropoietin administration in diabetic patients]. 1497 47

Gene or cell doping is defined by the World Anti-Doping Agency (WADA) as "the non-therapeutic use of genes, genetic elements and/or cells that have the capacity to enhance athletic performance". New research in genetics and genomics will be used not only to diagnose and treat disease, but also to attempt to enhance human performance. In recent years, gene therapy has shown progress and positive results that have highlighted the potential misuse of this technology and the debate of 'gene doping'. Gene therapies developed for the treatment of diseases such as anaemia (the gene for erythropoietin), muscular dystrophy (the gene for insulin-like growth factor-1) and peripheral vascular diseases (the gene for vascular endothelial growth factor) are potential doping methods. With progress in gene technology, many other genes with this potential will be discovered. For this reason, it is important to develop timely legal regulations and to research the field of gene doping in order to develop methods of detection. To protect the health of athletes and to ensure equal competitive conditions, the International Olympic Committee, WADA and International Sports Federations have accepted performance-enhancing substances and methods as being doping, and have forbidden them. Nevertheless, the desire to win causes athletes to misuse these drugs and methods. This paper reviews the current status of gene doping and candidate performance enhancement genes, and also the use of gene therapy in sports medicine and ethics of genetic enhancement.
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PMID:Gene doping in sports. 1515 20

Liver hemangioma is the most common benign liver tumor. Giant hemangiomas can grow and give various clinical symptoms. We describe a case of rapid growth of liver hemangioma in a seventeen-year-old girl. She was treated with interferon alpha 2b for hepatitis C. About 12 months later she was admitted to the hospital with symptoms of large epigastric mass, anemia and thrombocytopenia. Ultrasound scan and computed tomography confirmed the clinical picture, suggesting giant liver hemangioma. During surgery large cavernous hemangioma deeply penetrating into normal liver parenchyma was found. In view of recent hepatitis C infection the resection procedure (left extended hemihepatectomy) was assessed as being dangerous for the patient's life. Ligation of the left branches of hepatic artery and portal vein reducing tumor blood supply was performed. The postoperative period was uneventful; the hemangioma in the left lobe had shrunk. Ultrasound and CT scans performed one and two years after surgery showed that the size of the hemangioma remained stable and the patient was asymptomatic. In this described case three potential factors stimulating the growth of hemangioma (puberty, hepatitis C infection and interferon treatment) are discussed. The potential role of vascular endothelial growth factor and fibroblast growth factor is raised.
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PMID:Rapid growth of liver hemangioma following interferon treatment for hepatitis C in a young woman. 1523 65

We present the case of a 33-year-old man with isolated splenic peliosis, a rare pathological condition characterized by blood filled cystic lesions. The patient presented with recurrent massive haemorrhagic ascites, which did not resolve, despite a splenectomy. He was found to have massively elevated levels of vascular endothelial growth factor (VEGF). The clinical course of the disease was prolonged. Repeated blood transfusions for recurrent anaemia were required, in addition to repeated aspiration of reaccumulating haemorrhagic ascites and pleural effusion. The clinical course was not in keeping with previously reported cases. We have described an atypical clinical presentation in a patient with isolated splenic peliosis associated with elevated VEGF concentrations. No previously known associations for the condition were found despite thorough investigations. Management of the patient has been symptomatic and palliative. We have reviewed the various reported associations of peliosis and discussed the possible role of VEGF in this patient's condition.
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PMID:Peliosis of the spleen with massive recurrent haemorrhagic ascites, despite splenectomy, and associated with elevated levels of vascular endothelial growth factor. 1561 52

The conventional treatment of myelofibrosis involves a wait-and-see approach for asymptomatic patients, oral chemotherapy for the hyperproliferative forms of the disease, androgens or erythropoietin for the anaemia, and splenectomy in selected patients. Low-dose thalidomide plus prednisone is a well-tolerated therapy for the anaemia and the thrombocytopenia of myelofibrosis, whereas imatinib has shown little efficacy. Allogeneic stem cell transplantation (allo-SCT) is the only curative therapy for myelofibrosis. Its standard modality has an associated mortality of about 30% and can be applied to younger patients with high-risk disease or resistant to conventional treatment. Reduced-intensity conditioning allo-SCT involves a low mortality and is a promising therapy for patients aged 45-70 years old with the above characteristics. Autologous SCT is a palliative therapy for patients resistant to conventional treatment who lack a suitable donor. The next candidates for the treatment of myelofibrosis are the thalidomide derivatives, the proteasome inhibitors, and vascular endothelial growth factor neutralizing antibodies.
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PMID:Modern management of myelofibrosis. 1572 78

Little is known about the vascular and metabolic adaptations that take place in the fetal heart to maintain cardiac function in response to increased load. Chronic fetal anemia has previously been shown to result in increased ventricular mass, increased myocardial vascularization, and increased myocardial expression of hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF). We therefore sought to determine whether chronic fetal anemia induces expression of HIF-1-regulated angiogenic factors and glycolytic enzymes in the fetal myocardium. Anemia was produced in chronically instrumented fetal sheep by daily isovolemic hemorrhage (80-100 ml) for either 3 (n = 4) or 7 days (n = 11) beginning at 134 days of gestation (term 145 days). Catheterized, nonbled twins served as controls. Isovolemic hemorrhage over 7 days resulted in decreased fetal hematocrit (37 +/- 1 to 20 +/- 1%) and arterial oxygen content (6.5 +/- 0.4 to 2.8 +/- 0.2 ml O2/dl). Myocardial blood flow and vascularization were significantly increased after 7 days of anemia. Myocardial HIF-1 protein expression and VEGF (left ventricular), VEGF receptor-1 (right ventricular), and VEGF receptor-2 (right ventricular, left ventricular) mRNA levels were elevated (P < 0.05) in 7-day anemic compared with control animals. Myocardial expressions of the glycolytic enzymes aldolase, lactate dehydrogenase A, phosphofructokinase (liver), and phosphoglycerol kinase were also significantly elevated after 7 days of anemia. Despite the absence of a significant increase in myocardial HIF-1alpha protein in 3-day anemic fetuses, expressions of VEGF, VEGF receptor-1, and the glycolytic enzymes were greater in 3-day compared with 7-day anemic animals. These data suggest that HIF-1 likely participates in the fetal myocardial response to anemia by coordinating an increase in gene expressions that promote capillary growth and anaerobic metabolism. However, factors other than HIF-1 also appear important in the regulation of these genes. We speculate that the return of mRNA levels of angiogenic and glycolytic enzymes toward control levels in the 7-day anemic fetus is explained by a significantly increased resting myocardial blood flow, resulting from coronary vascular growth and increased coronary conductance, and a return to a state of adequate oxygen and nutrient delivery, obviating the need for enhanced transcription of genes encoding angiogenic and glycolytic enzymes.
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PMID:Myocardial vascular and metabolic adaptations in chronically anemic fetal sheep. 1612 31

Cytokines have not been employed in clinical laboratory tests because of the many biological activities of individual cytokines and too complicated cytokine network. However, abnormal laboratory data and symptoms can be interpreted by blood cytokine levels. [Cytokines attributable to abnormal data and symptoms] For example, cytokines attributable to abnormal data and symptoms in rheumatoid arthritis are as follows: joint pain: TNFalpha, IL-1, IL-6, and IL-18; general fatigue and appetite loss: TNFalpha and IL-1; leukocytosis: G-CSF produced by IL-1-stimulated macrophages etc; thrombocytosis: megakaryocyte potentiating activity of IL-6; anemia: hepcidin up-regulated by IL-6, which inhibits iron absorption from the intestine, and IL-1, which decreases the blood iron level and promotes ferritin synthesis. [Differential diagnosis using blood cytokine levels] Blood cytokine levels are useful and important in the differential diagnosis of inflammatory disorders such as neutrophilia, eosinophilia, and especially in distinguishing tumoral fever from infectious fever in malignant lymphomas. [Disease/disorder-specific cytokines] In recent years, disease- or disorder specific cytokines have been identified, making cytokines more important in clinical use. For example, IL-18 for adult-onset Still disease; IFNgamma for hemophagocytic syndrome; IL-5 for allergic disorders; thrombopoietin for immune thrombocytopenic purpura; vascular endothelial growth factor for POEMS syndrome; PTH-rP for malignancy associated hypercalcemia. [Flow cytometric measurement of cytokines] Recently, a flow cytometric method has been developed in addition to ELISA. With this method, 30 cytokine concentrations can be measured simultaneously within four hours with a wide range of detection limit and high cost performance. Cytokines will be included in laboratory tests with this method.
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PMID:[Blood cytokine levels as a clinical laboratory test]. 1744 72

The correlation of erythropoietin (EPO) receptor levels with angiogenesis and progression in some cancers has suggested that EPO could acts directly as an angiogenic factor. The purpose of this study was to assess the effect of treatment with human recombinant erythropoietic (rHuEPO) agents in cancer patients with chemotherapy-induced anaemia on endoglin and vascular endothelial growth factor (VEGF) circulating levels as a possible marker of angiogenesis. Endoglin and VEGF were measured in serum samples from 25 cancer patients with chemotherapy-induced anemia before and after 3-4 weeks of treatment with rHuEPO. A group of 28 healthy voluntaries was used as control. VEGF serum levels were significantly higher in cancer patients than in controls. For endoglin, higher levels were observed without reaching statistical significance. No statistically significant differences in endoglin and VEGF serum levels were found between samples obtained before and after treatment with rHuEPO agents. In conclusion, our result do not support that rHuEpo treatment in anaemic cancer patients induce angiogenesis.
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PMID:Human recombinant erythropoietic agents do not induce changes in circulating levels of endoglin and vascular endothelial growth factor in anemic cancer patients. 1748 48


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