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)

Gastritis cystica polyposa (GCP) is a rare inflammatory disease of the gastric remnant that usually develops after partial gastrectomy. It is defined by the presence of polyps on anastomotic gastric mucosa and at histopathological examination, by the presence of mucosal and submucosal cysts with foveolar hyperplasia. The disease is characterized by the frequency of gastro-intestinal bleeding and possibility of carcinomatous association. We report seven cases of GCP collected over 5 years (1994-1999). Diagnosis was made 9 to 45 years after partial gastrectomy and Finsterer. The patients were 52 to 72 years old. Revealing symptoms were cardiac failure, cardiac ischemia, melena, severe anemia and epigastric pain. For one patient, GCP was discovered casually. Endoscopic examination showed in all patients; the presence of several polyps sized between 3 to 15 mm on the perianastomotic gastric remnant. Histology examination of the polyps showed microscopic features of GCP in all cases. In one patient, there was a mild glandular atrophy with extensive intestinal metaplasia and mild dysplasia. Helicobacter pylori was present only in this case.
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PMID:[Gastritis cystica polyposa: report of 7 cases and literature review]. 1638 3

Of all the pathologies that cause a critical reduction in oxygen supply to the tissues, atherosclerosis is undoubtedly the most frequent. At the coronary level, ischemia causes a critical imbalance in oxygen supply and demand to the myocardium. Protracting this condition induces necrosis since, when the heart surpasses certain limits, it is incapable of modulating its metabolism in relation to the availability of energy substrates. Recently, internists and cardiologists have been examining the role of anemia as a cause or cofactor in the development of myocardial ischemia. The drop in circulating erythrocyte mass and consequent drops in hemoglobin and hematocrit represent obstacles to oxygen transport and delivery to tissues. Tachycardia secondary to anemia leads to a shorter diastolic phase and reduction in arterial pressure, phenomena which are particularly prominent in acute anemia. Such changes can result in serious repercussions for people suffering from coronary disease, leading often to documentable myocardial damages. On the other hand, in chronic anemia the compensation phenomenom--represented by an increase in heart rate, cardiac output, ventricular volume and contractility--requires integrity of the cardiac apparatus, thus explaining the very serious repercussions of the anemic state for cardiac patients. Recently, the possibility of preventing and treating anemia-induced or anemia-exacerbated ischemia has been confirmed in the literature, albeit not unequivocably, demonstrating that this topic deserves particular attention.
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PMID:[Anemia and myocardial ischemia: relationships and interferences]. 1670 Apr 23

New, critically important data have been recently generated about the response to hypoxia. This response can be schematized in three main systems or functions, ie, detectional or oxygen sensing, regulatory, which controls gene expression and effector. The principal organizer of the regulatory branch is a specific transcription factor, the hypoxia-inducible factor 1 (HIF-1). In the presence of oxygen, the alpha subunit of HIF-1 (HIF-1alpha) is modified by hydroxylases, that represent the central point of the oxygen sensing mechanism. This type of hydroxylation induces HIF-1alpha catabolism by the proteosome. On the contrary, in hypoxia, or in the presence of certain growth factors that increase HIF-1alpha synthesis, HIF-1alpha translocates to the nucleus, where it binds HIF-1beta, and thence acts on transcription of genes carrying hypoxia responsive elements (HRE) on their promoters. These genes regulate the synthesis of an ample series of proteins, which span from respiratory enzymes and transporters to hormones regulating circulation and erythropoiesis. The role of HIF-1alpha is not restricted to the mere induction of adaptation to decreased oxygen: instead, it significantly participates in cell repairing mechanisms. A simple list of some of the stimulatory or inhibitory alterations of pathophysiological importance involving the HIF-1 system, would include: chronic lung disease, smoking adaptation, anemia/hemorrhage, ischemia/reperfusion, growth, vascularization and cell resistance of tumors, preeclampsia and intrauterine growth retardation, retinal hyper o hypovascularization, drug intoxications, bowel inflammatory disease and wound repair. This list illustrates by itself the importance of the mechanism herein reviewed.
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PMID:[Response to hypoxia. A systemic mechanism based on the control of gene expression]. 1671 69

Since the discovery of hydrogen peroxide in 1819 it was known as a toxic agent for human organs. Due to the recent findings its role should be reevaluated. This review discusses the toxic and physiological roles of hydrogen peroxide and functions of enzyme catalase which is the main regulator of hydrogen peroxide metabolism. The concentration of hydrogen peroxide changes between 0,05 micromol/l and 117 micromol/l in exhaled breath condensate and in human fluids. Hydrogen peroxide is generated by physiological processes such as glycation, phagocytosis, cell metabolism and by pathological changes such as different tumors and side effects of some drugs. The main regulator of toxic concentration of hydrogen peroxide is the enzyme catalase while glutathione peroxidase and hemoglobin has a limited role in this process. Low concentration of hydrogen peroxide plays a role in degradation of some proteins, as a messenger in cell signaling and could contribute to apoptosis. The enzyme catalase, due to its structure and function, is very effective in destroying the toxic concentration of hydrogen peroxide without changing its low, physiologic concentration. Decrease in catalase due to anemia, decreased synthesis and especially to its inherited deficiency may be a risk factor in diabetes, cell damage due to ischemia, in uricase and ascorbic acid treatment as well as in sterilization with hydrogen peroxide. The hydrogen peroxide paradox means that its low concentration is vital for some physiological processes while its high concentration is toxic for human cells. The main regulator of hydrogen peroxide concentration is the enzyme catalase and its deficiency may be a risk factor for some pathological changes.
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PMID:[The hydrogen peroxide paradox]. 1678 44

Erythropoietin and its receptor, a cytokine hormone long-known for its pro-erythropoietic effect, has been found to be expressed on a variety of tissues, including the cardiovascular system. Recent experimental studies in the ischemia-reperfusion model have demonstrated that erythropoietin has a significant cardioprotective and pro-angiogenic effect. This effect is quantified by a reduction in the relative infarct and apoptosis area and improved recovery of mechanical function. Despite potentially detrimental effects, erythropoietin has been used extensively in the last decade for treatment of anemia associated with chronic renal failure, and it has been found to be a safe drug in humans. The potential role of erythropoietin in the treatment of ischemic heart disease in humans has yet to be demonstrated in preliminary clinical trials.
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PMID:[Erythropoietin as a protective agent in myocardial ischemia]. 1680 23

Thrombotic microangiopathy (TMA) is a rare but devastating disorder; it involves small vessels and is characterized by intravascular thrombi of aggregated platelets leading to thrombocytopenia and variable degrees of organ ischemia and anemia, which is due to erythrocyte fragmentation in microcirculation. Childhood cases with predominant renal involvement are referred as the hemolytic uremic syndrome (HUS), and adults with major central neurological involvement are labeled as thrombotic thrombocytopenia purpura (TTP). Endothelial damage due to toxins and/or lack of defense against complement activation have a central role. Recent discovery of the von Willebrand Factor cleaving protease (ADAMTS 13) has offered new insight into the pathogenesis of TMA. TMA is also a well-recognized serious complication of renal transplantation. Clinical features of intravascular hemolysis are not always found. It may occur as de novo or recurrent and the majority of de novo cases are related to cyclosporin therapy. Viral infections, severe renal ischemia and acute vascular rejection are less frequent causes. Recurrence is negligible in diarrhea-associated HUS in childhood, but non-diarrheal HUS recurs in majority of adults following renal transplantation. Renal transplantation is contraindicated in familial/relapsing recurrent forms of HUS.
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PMID:Review of thrombotic microangiopathy (TMA), and post-renal transplant TMA. 1690 37

Erythropoietin (EPO) is a hypoxia-inducible hormone required for erythroid differentiation. Expression of the EPO receptor is not restricted to hematopoietic cells and exhibits a multi-tissue distribution that includes neural cells, vascular endothelium and muscle progenitor cells. The ability for EPO to stimulate progenitor cell proliferation and prevent apoptosis is critical for maintenance of the erythroid lineage, but is also observed in neural and muscle progenitor cells. Mice lacking the EPO receptor die in utero due to severe anemia. However, even prior to lack of erythroid cell production in the embryo proper, these mice exhibit increased apoptosis in the brain as early as E10.5 and a reduction in the number of neural progenitor cells. Corresponding cultures of primary neural cells exhibit decreased neuron generation and increased sensitivity to reduced oxygen tension, and neurons do not survive after 24 h at low oxygen tension. In contrast, hypoxia induces EPO and EPO receptor in wild-type neuronal cells, and EPO enhances neuron survival at low oxygen tension. In vivo EPO is neuroprotective in adult animal models for brain ischemia. Induction of EPO and its receptor by hypoxia likely contributes to its neuroprotective activity and selective cell survival in the brain during hypoxic stress.
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PMID:Erythropoietin and normal brain development: receptor expression determines multi-tissue response. 1690 40

Until recently the major physiological function of erythropoietin (EPO) was thought to be the induction of erythropoiesis. However, a growing body of evidence indicates that EPO has tissue-protective properties and prevents ischemia induced tissue damage in several organs including the kidney. A pivotal intracellular pathway mediating the beneficial effects of EPO is the activation of Akt, i.e. serine/threonine protein kinase B. As a result, Akt phosphorylates the proapoptotic factor Bad, which in turn causes inhibition of programmed cell death (apoptosis). In the present article we review data on the non-hematological effects of recombinant human EPO (rHuEPO) in different experimental settings of acute and chronic kidney injury, and discuss clinical renoprotective strategies with rHuEPO or analogues substances that are not related to anemia correction.
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PMID:EPO: renoprotection beyond anemia correction. 1695 90

Transfusion of packed red blood cells in critically injured patients has been a lifesaving (although not completely benign) intervention for decades. The traumatically injured brain has been thought to be particularly susceptible to injury from anemia, due to the well-documented association of worsening mortality and functional outcome in the presence of hypotension and hypoxia, as well as the known vulnerability of many neuronal populations to ischemia. Red blood cell transfusion has been used in traumatic brain injury (TBI) to prevent cerebral ischemia by maximizing the oxygencarrying capacity of blood that is otherwise decreased by blood loss and dilution with crystalloid fluid replacement during resuscitation. Although many practitioners have commonly utilized hemoglobin (Hgb) or hematocrit thresholds for transfusion in these patients, the rationale for this practice has largely been centered on older studies in general critical care populations and animal evidence. Furthermore, in addition to an ideal " target " Hgb, many other questions remain about this clinical practice, such as the optimal duration of maintaining a specific Hgb level, and the ultimate effects of transfusion on neurological and functional outcome.
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PMID:The life-saving properties of blood: mitigating cerebral insult after traumatic brain injury. 1696 Feb 87

With the introduction of biomarkers like troponin I (cTnI), our ability to identify and quantify myocardial infarction in the postoperative period has been greatly enhanced. Even small elevations of cTnI should be considered as a myocardial infarction. Small increases in cTnI postoperatively have indeed been found to be associated with worse short and long-term outcomes, the higher the cTnI level the worse the outcome. Studies undertaken in the 1980s when postoperative myocardial infarction (PMI) was detected by means of electrocardiogram recordings every 12 hours following operation suggested that this complication occurred on the second or third postoperative day. More recent studies where postoperative myocardial necrosis has been detected by repeated troponin dosages have revealed that, in fact, postoperative myocardial infarction appears much earlier between 12 and 32 hour after the end of surgery. Two types of PMI were identified based on intense troponin surveillance. They stem from two different major pathophysiological mechanisms. One seems to be related to plaque-vulnerability, while the other may be due to the effects of prolonged ischemia. The postoperative period should be regarded as a vulnerable period' that acts synergistically with both plaque and patient vulnerabilities in the development of PMI. Monitoring troponin levels in the postoperative period following surgery enables the identification of patients with myocardial damage and the institution of early aggressive intervention (e.g., intensive beta blockers therapy, adequate analgesia, correction of anemia) in order to prevent the evolution of PMI during this golden period' that lasts about two days. In patients that are prone to develop PMI, and especially in those who are prone to develop PMI related to plaque rupture, prevention can be achieved by better preoperative identification of the vulnerable plaque, and by a better plaque stabilization, either metabolically (e.g., statins) or by actual coronary stenting. Further understanding of the mechanisms underlying PMI, as well as their early identification, may contribute to the reduction of the incidence of PMI and its associated morality in the future.
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PMID:Postoperative myocardial infarction: pathophysiology, new diagnostic criteria, prevention. 1723 64


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