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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various vitamins and minerals play roles in HIV infection. There is evidence that a number of HIV+ patients suffer from deficiencies in vitamins B12, B6, A, and D; folate, zinc and selenium; and carotenoids such as beta-carotene, betacryptoxanthin, and lutein. Vitamin B12 deficiency can result in peripheral neuropathy, encephalopathy, cognitive dysfunction and anemia. Lowered levels of vitamins B6 and A can lead to impaired immune function and, in the latter, an increased rate of perinatal transmission. Low levels of vitamin D have been linked to weight loss and wasting. Folate deficiencies are related to anemia, and low levels of zinc and/or selenium have been linked to impaired immune function. Information on the carotenoids, which have been found to be associated with cellular immune function, is mostly derived from recent research. Studies have shown that the levels of carotenoids are decreased in HIV+ people even in the early stages of infection, but the greatest deficiencies appeared in patients with the most advanced disease. Other clinical trials seem to indicate that administration of beta-carotene improves immune function, causing an increase in CD4 counts over baseline levels. Clinical trials conducted in response to all of these deficiencies have found multivitamin supplementation to be beneficial. Therefore, it is recommended that all HIV-infected patients receive a multivitamin supplement to assist in reversing the damage caused by these vitamin and mineral deficiencies.
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PMID:Update on vitamins, minerals, and the carotenoids. 1136 98

Folic acid (folate) levels were measured in the serum of patients with various neurological diseases in Japan. Thirty-six patients showed decreased serum folate levels among 343 consecutive neurological patients (10.5%). Folate administration (15 mg/d) to folate-deficient patients improved neurological symptoms in 24 of 36 cases (67%). Serum folate levels were significantly lower in female than in male folate-deficient patients. Folate-deficient patients showed predominantly axonal neuropathy, which responded to folate supplementation more markedly. Male patients more frequently exhibited neuropathy, especially demyelinating and motor-dominant neuropathy, than females. Anemia was correlated with male sex and low serum folate levels. Male patients were more responsive than females to folate treatment. More male patients had taken excess alcohol or received gastrectomies than females. Neurological symptoms were more frequently improved by folate supplementation in patients with neuropathy than exclusive encephalopathy. Serum folate levels were lower in patients with encephalopathy, especially those with dementia, while folate therapy was more effective in neurological patients without dementia. Dysgeusia and anemia improved in all patients after folate administration. Neurological patients with malabsorption or treated with continuous drip infusion were resistant to folate therapy. Since folate-responsive neuroencepahlopathies are not rare among patients with neurological diseases in Japan, the serum folate level would serve as a valuable indicator for folate supplement therapy.
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PMID:Folic acid-responsive neurological diseases in Japan. 1157 72

Hyperphosphataemia in haemodialysis patients is associated with secondary hyperparathyroidism and more importantly with an increased cardiovascular mortality in dialysed patients. Removal of phosphate during dialysis is less than net intestinal uptake. This imbalance results in a positive phosphate balance. To control serum phosphate concentration oral phosphate binders have to be taken to reduce net intestinal uptake. The use of classical phosphate binders such as calcium carbonate, calcium acetate and aluminium-containing phosphate binders is limited by their side effects. Hypercalcaemia aggravates vascular calcification and cardiovascular risk. Aluminium intoxication causes aluminium osteopathy, anaemia and encephalopathy. Therefore, the development of calcium- and aluminium free phosphate binders has become a challenge to clinical nephrology. Polyallylamine hydrochloride (sevelamer) is one of the new alternative compounds which has been shown to effectively bind phosphate in dialysis patients. A promising approach in the development of alternative phophate binders are trivalent-iron (Fe(III)) containing phosphate binders. They were not only successfully tested in experimental animals but have also been shown to reduce urinary phosphate excretion and serum phosphate concentrations in patients with preterminal failure and those on maintenance haemodialysis. This review outlines the experimental and clinical data on Fe-III based phosphate binders providing evidence that they will be as effective and safe as phosphate binders without the major side effects of classical phosphate-binding compounds.
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PMID:Compounds in development to combat hyperphosphataemia. 1177 14

Aluminium has recently been considered as a causative agent in dialysis encephalopathy, osteodystrophy, and anemia occuring in hemodialysis patients. The aim of this study is to prepare magnetic poly(2-hydroxyethylmethacrylate) (mPHEMA) adsorbent and to investigate it's useability for the removal of Al(III) ions from drinking and dialysis water. Magnetic PHEMA beads in a size range 80-120 microm were produced by a dispersion polymerization technique. Then Alizarin Red was covalenlty attached onto the mPHEMA beads. Al(III) adsorption from aqueous solutions was examined by batch system. mPHEMA beads were characterized by swelling tests, electron spin resonance (ESR), scanning electron microscopy (SEM), and elemental analysis. Important results obtained in this study are as follows: the swelling ratio of mPHEMA beads was 34%. The presence of magnetite in the polymeric structure was confirmed by ESR. The mPHEMA beads have a spherical shape and porous structure. Alizarin Red loading was 135.8 micromol g(-1) polymer. The maximum Al(III) adsorption was 722 micromol g(-1) polymer at pH 5.0. Non-specific Al(III) adsorption was about 23 micromol g(-1) polymer under the same conditions. High desorption ratios (98%) were achieved by using 0.1 M HNO3. It was possible to reuse the beads without significant loss of Al(III) adsorption capacity.
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PMID:Preparation of magnetic dye affinity adsorbent and its use in the removal of aluminium ions. 1185 78

Symptomatic arsenic poisoning is not often seen in occupational exposure settings. Attempted homicide and deliberate long-term poisoning have resulted in chronic toxicity. Skin pigmentation changes, palmar and plantar hyperkeratoses, gastrointestinal symptoms, anemia, and liver disease are common. Noncirrhotic portal hypertension with bleeding esophageal varices, splenomegaly, and hypersplenism may occur. A metallic taste, gastrointestinal disturbances, and Mee's lines may be seen. Bone marrow depression is common. 'Blackfoot disease' has been associated with arsenic-contaminated drinking water in Taiwan; Raynaud's phenomenon and acrocyanosis also may occur. Large numbers of persons in areas of India, Pakistan, and several other countries have been chronically poisoned from naturally occurring arsenic in ground water. Toxic delirium and encephalopathy can be present. CCA-treated wood (chromated copper arsenate) is not a health risk unless burned in fireplaces or woodstoves. Peripheral neuropathy may also occur. Workplace exposure or chronic ingestion of arsenic-contaminated water or arsenical medications is associated with development of skin, lung, and other cancers. Treatment may incklude the use of chelating agents such as dimercaprol (BAL), dimercaptosuccinic acid (DMSA), and dimercaptopanesulfonic acid (DMPS).
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PMID:Chronic arsenic poisoning. 1186 18

Fifth (erythema infectiosum) and sixth (roseola infantum) diseases are common rash illnesses of childhood that have long been recognized in clinical medicine. The discovery of the viruses that cause these illnesses has revealed relationships with other syndromes. Primary infection with the agent of erythema infectiosum, human parvovirus B19, is associated with transient aplastic crisis in hemolytic anemia, arthropathy in adults, chronic anemia in immunocompromised patients, and nonimmune fetal hydrops in pregnant women. The only documented illness associated with primary infection with human herpesvirus 6 is roseola or exanthema subitum in young children. However, reactivated infections in adults and immunocompromised patients may be associated with serious illness such as encephalitis/encephalopathy, and bone marrow suppression leading to transplant failure or graft-versus-host disease. Diagnostic studies for both viruses have been limited, although reliable serologic tests for human parvovirus B19 have recently become available. Diagnosis of human herpesvirus 6 remains problematic, because current tests cannot differentiate primary from reactivated disease. This is more of an issue for the putative relationship of these viruses to more chronic conditions, such as rheumatologic disease for human parvovirus B19 and multiple sclerosis for human herpesvirus 6. The relationship between the viruses and these conditions remains controversial, and better diagnostic tests and further information on viral pathogenesis for both viruses are required in order to make a reliable judgment in this regard.
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PMID:Fifth (human parvovirus) and sixth (herpesvirus 6) diseases. 1196 54

A 4-year-old Turkish girl was referred to our hospital with the findings of encephalopathy and pancytopenia. She had a history of severe abdominal cramps and gastrointestinal bleeding. A confused state, muscle pain and weakness, erythema-bullous and erythema-nodosum-like skin lesions, and alopecia were observed at her hospitalization. All of these symptoms resolved on follow-up. On laboratory investigation severe thrombocytopenia and leukopenia, mild anemia, a moderate increase in aspartate aminotransferase and alanine aminotransferase levels were detected. After reevaluating her medical history, it was learned that she had accidentally taken 1.3 to 1.5 mg/kg of colchicine 3 to 4 days before her first hospitalization. The possibility of misdiagnosis of colchicine intoxication should be borne in mind, and pediatricians must be aware of its toxic effects, especially in areas where patients with familial Mediterranean fever are present.
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PMID:Late diagnosis of severe colchicine intoxication. 1198 65

The need for reintubation within 24-72 h of planned extubation is a common event, occurring in 2-25% of extubated patients. Risk factors for extubation failure include being a medical, multidisciplinary or paediatric patient; age >70 years; a longer duration of mechanical ventilation; use of continuous intravenous sedation; and anaemia (haemoglobin <10 g/dl or haematocrit <30%) at the time of extubation. The pathophysiology of extubation failure can be distinct from that seen with weaning failure and includes upper airway obstruction, inadequate cough, excess respiratory secretions, encephalopathy, and cardiac dysfunction. Extubation failure prolongs the duration of mechanical ventilation, increases the length of ICU and hospital stay, increases the need for tracheostomy, and is associated with a higher hospital mortality. Great emphasis has been placed on accurately predicting extubation outcome because extubation delay is also associated with increased length of stay and mortality. Tests designed to assess for upper airway obstruction, secretion volume, and the effectiveness of cough seem most promising for improving the decision to extubate. Mortality increases with delays in reintubation for patients failing extubation. Timely identification of patients at elevated risk of extubation failure followed by rapid re-establishment of ventilatory support can improve outcome.
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PMID:Decision to extubate. 1202 99

Extubation failure, defined as the need for reinstitution of ventilatory support within 24 to 72 hours of planned endotracheal tube removal, occurs in 2 to 25% of extubated patients. The pathophysiologic causes of extubation failure include an imbalance between respiratory muscle capacity and work of breathing, upper airway obstruction, excess respiratory secretions, inadequate cough, encephalopathy, and cardiac dysfunction. Compared with patients who tolerate extubation, those who require reintubation have a higher incidence of hospital mortality, increased length of ICU and hospital stay, prolonged duration of mechanical ventilation, higher hospital costs, and an increased need for tracheostomy. Given the lack of proven treatments for extubation failure, clinicians must be aware of the factors that predict extubation outcome to improve clinical decision making. Risk factors for extubation failure include being a medical, multidisciplinary, or pediatric patient; age greater than 70 years; a longer duration of mechanical ventilation; continuous intravenous sedation; and anemia. Tests designed to assess for upper airway obstruction, secretion volume, and the effectiveness of cough can help to improve prediction of extubation failure. Rapid reinstitution of ventilatory support in patients who fail extubation may improve outcome.
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PMID:Extubation failure: magnitude of the problem, impact on outcomes, and prevention. 1254 31

The pathogenesis of fatal cerebral malaria (CM) is not well understood, in part because data from patients in whom a clinical diagnosis was established prior to death are rare. In a murine CM model, platelets accumulate in brain microvasculature, and antiplatelet therapy can improve outcome. We determined whether platelets are also found in cerebral vessels in human CM, and we performed immunohistopathology for platelet-specific glycoprotein, GPIIb-IIIa, on tissue from multiple brain sites in Malawian children whose fatal illness was severe malarial anemia, CM, or nonmalarial encephalopathy. Platelets were observed in 3 locations within microvessels: between malaria pigment and leukocytes, associated with malaria pigment, or alone. The mean surface area of platelet staining and the proportion of vessels showing platelet accumulation were significantly higher in patients with CM than in those without it. Platelet accumulation occurs in the microvasculature of patients with CM and may play a role in the pathogenesis of the disease.
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PMID:Platelet accumulation in brain microvessels in fatal pediatric cerebral malaria. 1255 30


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