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)

Human recombinant erythropoietin (r-huEPO) is very effective in the treatment of anemia of hemodialyzed patients. We describe 4 patients who developed symptoms of central nervous dysfunction during r-huEPO therapy. Three exhibited typical hypertensive encephalopathy, whereas signs of cerebral ischemia were found in the fourth. The increase in blood viscosity with r-huEPO treatment, leading to a rise in peripheral vascular resistance and blood pressure especially in previously hypertensive patients, may be of importance in the pathogenesis of these cerebrovascular incidents; preexistent arteriosclerosis is an possible additional risk factor.
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PMID:[Cerebrovascular incidents in 4 hemodialysis patients treated with erythropoietin]. 318 75

This project was concerned with the clinical knowledge reported by general practitioners in relation to the diagnosis and management of seven common clinical conditions: acute otitis media, jaundice, iron-deficiency anaemia, transient cerebral vascular insufficiency, infectious mononucleosis, pulmonary infarction, and carcinoma of the prostate. Postal questionnaires were sent to three groups of doctors: a constant group of experienced general practitioners who were or had been trainers, randomly selected groups of 200 general practitioners, and small groups of consultants who were specialists in each condition. The last two groups were changed for each of the chosen clinical conditions; the constant group remained the same throughout. The study was not concerned with the attitudes and skills of general practitioners or consultants, and no attempt has been made to analyse the process of clinical problem-solving. The differences between the constant group and random group of general practitioners were minor. Consultants received questionnaires identical to those sent to general practitioners and were asked to answer them as they would expect a competent general practitioner to do; their answers suggested a more direct approach to the problem concerned than those given by general practitioners. The information obtained has implications for education for general practice and educational audit programmes. Areas for further research are suggested.
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PMID:Clinical knowledge and education for general practice. 615 93

In a medical out-patient clinic, over a period of several years, atrial myxoma was diagnosed in four patients with ages ranging between 32 and 69 years. With the exception of one patient referred for assessment of ventricular premature beats, presentation was not primarily attributable to cardiac causes. In all patients, there was a latency period of years between the onset of symptoms and establishment of the diagnosis. The history of patients with atrial myxoma includes symptoms such as dizziness, syncope, transient cerebral ischemia, weight loss and malaise. The differential diagnosis may encompass consideration of neoplastic disease since laboratory findings can reveal evidence of an inflammatory reaction, accelerated sedimentation rate, anemia, abnormal electrophoresis, hypoproteinemia as well as elevated alkaline phosphatase. One patient had undergone numerous examinations to rule out the presence of malignant disease. Symptoms related to the cardiovascular system include exertional dyspnea, premature beats, tachyarrhythmias and nonspecific chest pain. Auscultatory findings are consistent with those of mitral stenosis. M-mode and two-dimensional echocardiography established the diagnosis in all patients and confirmed the usefullness of this examination technique in the assessment of patients in a general medical clinic.
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PMID:[Atrial myxoma in the patients of a general and internal medicine outpatient clinic]. 666 80

Twenty-five patients receiving chronic hemodialysis were studied with systematic cervical auscultation and periorbital Doppler tests to determine the incidence of cervical bruits and their significance. Eighteen (72%) of the patients had bruits. All of the bruits heard in this study were loudest in the supraclavicular fossa, and in no patient was a bruit heard along the carotid arteries without a louder bruit of similar characteristics more proximally. No patient with a bruit in the area of the carotid bifurcation had an abnormal ipsilateral periorbital Doppler examination, and none had symptoms of cerebral ischemia. There was no evidence in these patients that the bruits were related to occlusive arterial disease. It is concluded that most cervical bruits in patients receiving hemodialysis are the result of a hyperdynamic circulatory state associated with anemia and arteriovenous fistulae.
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PMID:Cervical bruits in hemodialysis patients. 721 77

The aim of this study was to assess the pattern of adaptation to severe Haemodilution in pts with normal or stenotic carotid vessels. We enrolled 180 consecutive pts undergoing total hip replacement: 138 pts had echo-Doppler documented normal carotid arteries, 10 pts had kinking and 32 pts had monolateral or bilateral stenosis of internal carotid arteries (lesions, class of stenosis 1-49%). Haemoglobin values on the 4th day after surgery was 8.7 +/- 1.2 g/dl with no statistically significant differences in pts (patients) with carotid disorders versus normal pts. No pt showed clinical signs of cerebral ischemia or brain damage in the postoperative period. These results are consistent with experimental and clinical data showing that normovolaemic anaemia is well tolerated without disabling symptoms in pts with mild or moderate stenosis of carotid arteries.
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PMID:Asymptomatic carotid disorder and hemodilution: a perioperative study in major orthopaedic surgery. 764 42

Among the techniques of cerebral protection, the use of controlled arterial hypertension is based on the following arguments: 1) Cerebral ischaemia is the final common pathway of any insult to the brain, particularly through secondary lesions. Causes of secondary cerebral lesions include pressure under the brain retractors, temporary clipping, arterial hypotension, hypoxaemia, anaemia and hypercapnia. 2) In the brain, the critical lower value for cerebral blood flow is around 25 mL.100g-1.min-1, under which two types of ischaemic areas can be defined: the penlucida type where cerebral function is abolished, without permanent cerebral lesion and the penumbra type where cerebral tissue recovers only if flow is rapidly restored. In the latter case the duration of ischaemia is very important. 3) Cerebral blood flow is maintained stable within a large range of variations of mean arterial pressure through the autoregulation mechanisms, which is based on vasomotricity of the cerebral circulation, which implies major variations in cerebral blood volume. However, autoregulation needs several dozens of seconds to be achieved. Therefore, sudden variations in mean arterial pressure are associated with short lasting but major variations in cerebral blood volume. 4) In case of increased intracranial pressure, a decrease in cerebral perfusion pressure causes cerebral vasodilation through the autoregulation mechanism, with an increase in cerebral blood volume which will, in turn, increase intracranial pressure and thus decrease cerebral perfusion pressure, and so on. This is the vasodilatory cascade. The therapeutical increase in mean arterial pressure will correct this phenomenon and decrease intracranial pressure. This is called the vasoconstrictive cascade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Controlled hypertension and cerebral protection]. 767 93

The relationships between cerebral blood flow (CBF), cerebral metabolism (cerebral metabolic rate of oxygen, CMRO2) and cerebral oxygen extraction (arteriovenous difference of oxygen, AVDO2) are discussed, using the formula CMRO2 = CBF x AVDO2. Metabolic autoregulation, pressure autoregulation and viscosity autoregulation can all be explained by the strong tendency of the brain to keep AVDO2 constant. Monitoring of CBF, CMRO2 or AVDO2 very early after injury is impractical but the available data indicate that cerebral ischemia plays a considerable role at this stage. It can best be avoided by not "treating" arterial hypertension and not using too much hyperventilation, while generous use of mannitol is probably beneficial. Once in the ICU, treatment can most practically be guided by monitoring of jugular bulb venous oxygen saturation. If saturation drops below 50%, the reason for this must be found (high intracranial pressure, blood pressure not high enough, too vigorous hyperventilation, arterial hypoxia, anemia) and must be treated accordingly.
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PMID:Overview of monitoring of cerebral blood flow and metabolism after severe head injury. 808 32

The injured brain may be damaged by primary impact, secondary injury from secondary damage due to initiation of destructive inflammatory and biochemical cascades by the primary injury or secondary ischemic injury following secondary insults that initiate or augment these immunological and biochemical cascades. Cerebral ischemia will arise whenever delivery of oxygen and substrates to the brain fall below metabolic needs. Many factors lead to the development of secondary insults to the injured brain during initial resuscitation, transport, surgery, and subsequent intensive care. Continuous monitoring of cerebral oxygenation (jugular oximetry, brain tissue PO2) and cerebral blood flow velocity (transcranial Doppler ultrasonography) in patients with brain trauma reveals multiple episodes of transient hypoperfusion with an adverse relationship between incidence and outcome. Secondary brain insults arise through systemic or intracranial mechanisms that reduce cerebral blood flow from compromised CPP, vascular distortion or cerebrovascular narrowing or lower oxygen delivery from hypoxemia associated with airway obstruction, pulmonary pathology, or anemia. Secondary brain ischemia remains a common pathway to secondary brain damage in most critically ill neurosurgical patients. In the future prevention of secondary brain injury may well hinge on giving a cocktail of novel agents that modify destructive biochemical and inflammatory pathways, each having a potential therapeutic window possibly in a subgroup of patients. To date, phase 3 clinical trials of several agents including PEGSOD and tyrilizad mesylate have failed to show relevant efficacy after brain trauma or subarachnoid hemorrhage. The therapeutic role of calcium channel blockers in traumatic subarachnoid hemorrhage is currently under investigation following the results of subgroup metaanalysis. Several phase 3, NMDA receptor antagonist studies are underway in brain trauma with results expected soon. Although we know that secondary insults promote excitotoxic secondary brain damage there is currently no pharmacological intervention with proven efficacy and, therefore, detection and correction of secondary insults appear to offer the best therapeutic strategy. After brain trauma, systemic hypotension, compromised CPP, raised ICP, elevated temperature, hypoxemia, and jugular bulb venous desaturation are associated with poor prognosis. Clinical trials of moderate hypothermia following brain trauma are ongoing. Following adult brain trauma maintenance of CPP above at least 65 mmHg (probably > 40 mmHg in children below 8 years) seems important to improve outcome indicating the need for continuous ICP monitoring during intensive care of brain-injured patients.
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PMID:Mechanisms and prevention of secondary brain damage during intensive care. 970 38

Anemia is a common complication in cancer patients undergoing chemotherapy, and its severity depends on both the type of antineoplastic drugs and the clinical status of the patient. Breast cancer patients undergoing standard chemotherapy develop clinically significant anemia in up to 25% of cases. This percentage, moreover, increases up to 63% when more intensive chemotherapy regimens are used. The therapeutic use of erythropoietin in anemic patients, i.e., in patients with hemoglobin levels below 9-10.5 g/dl, is able to correct the anemic status in nearly 40%-80% of such patients, but it does not completely eliminate the need of blood transfusions: 20%-40% of patients need to be transfused despite the erythropoietin treatment. An alternative strategy for optimizing the erythropoietin treatment is its use in the prevention of anemia, i.e., in patients with normal hemoglobin values but at high risk of becoming anemic. In a phase III study, we evaluated the role of erythropoietin in the prevention of anemia in breast cancer patients undergoing dose-intensive chemotherapy. Clinically significant anemia occurred in 52% (95% CI = 33-69) of control patients and in no patient (95% CI = 0-14) in the erythopoietin arm (p =.00001). After six cycles of chemotherapy the mean hemoglobin decrease was 3.05 g/dl (± 1.0, 95% CI = 2.6-3.5) in the control arm and 0.8 g/dl (± 1.4, 95% CI = 0.3-1.4) in the erythropoietin arm. Moreover, 6.4% of control patients needed blood transfusion compared to no patients in the erythropoietin arm. Erythropoietin is active in both the treatment and the prevention of anemia in cancer patients undergoing chemotherapy. Due to its high economic cost, efforts should be made to identify subsets of patients in whom the preventive use could be cost-effective. Patients undergoing chemotherapy associated with a high risk of anemia could benefit from preventive use of erythropoietin in special circumstances, such as presence of risk of myocardial or cerebral ischemia, uncommon blood group, or religious beliefs hindering blood transfusions. Moreover, anemia prevention could be considered in patients at high risk of requiring blood transfusions, such as patients with low baseline value of hemoglobin or with a hemoglobin decrease of >/=2 g/dl after the first cycle of chemotherapy.
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PMID:Strategies for the Use of Epoetin Alfa in Breast Cancer Patients. 1038 21

The present investigation aimed to examine associations of anaemia with dementia. Analysis of community-dwelling, elderly subjects characterized for different dementias failed to confirm a previously reported association of anaemia with Alzheimer's disease (AD) but revealed instead a significant association with vascular dementia (VAD). Nearly 45% of VAD subjects were anaemic, compared with 17% of controls. Close to one-third of all subjects with haemoglobin levels > 0.5 g/dl below reference anaemia levels had VAD. Co-existing VAD may explain previous links between AD and anaemia. The association was independent of age, dementia severity and a range of other factors including vitamin B 12 and folate levels. Anaemia can exacerbate focal cerebral ischaemia and could precipitate or amplify VAD symptoms in elderly subjects with vasculopathy.
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PMID:Evidence for association of anaemia with vascular dementia. 1043 67


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