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

Anemia in chronic renal failure causes a number of serious problems to the patient. As a result, it is imperative to make use of all rational options to alleviate it. The present study addresses the question, the answer to which is not yet known, whether or not the degree of anemia depends on the efficacy of continuous ambulatory peritoneal dialysis (CAPD) and, if so, what the importance of peritoneal clearance and residual renal function is. A significant correlation between the hematocrit (Hct) and the total weekly Kt/V index (tKt/V) (r = 0.61, p<0.01), total weekly creatinine clearance (tCLCR) (r = 0.50, p<0.05), and residual glomerular filtration rate (r = 0.43, p<0.05) was demonstrated in a group of 22 CAPD patients. Stepwise regression analysis showed that of all the variables monitored, Hct depends exclusively on tKt/V (p<0.01, r2 = 0.37). The value of Hct in a group of patients with a tKt/V <2.3 (n = 15) was 28.9+/-1.2% (arithmetic mean +/- SEM) while in a group with a tKt/V > or =2.3 (n = 7), it was 35.1+/-1.9% (p<0.01). On dividing tKt/V and tCLCR into their peritoneal and renal components, a significant correlation between Hct and renal Kt/V (r = 0.47, p<0.05) was found; stepwise regression analysis identified renal Kt/V (p<0.01) and peritoneal Kt/V (p<0.05), with R2 = 0.38 as major variables with an effect on Hct. The authors conclude the efficacy of blood purification is another factor affecting renal anemia in CAPD patients. The relationship between anemia and blood purification is best expressed using the Kt/V index. The Kt/V provided by one's own kidneys seems to be of greater importance for anemia than the Kt/V provided by peritoneal dialysis. The results provide the basis for prospective interventional studies.
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PMID:The anemia in continuous ambulatory peritoneal dialysis patients is related to Kt/V index. 995 Jan 81

Megakaryocytic differentiation of progenitor cells was investigated in nine patients with low-risk myelodysplastic syndromes (MDS) (eight refractor anemia [RA] and one RA with ringed sideroblasts [RARS] and five patients with high-risk MDS (two RA with excess of blasts [RAEB] and three RAEB in transformation [RAEB-T]). Bone marrow-derived CD34+ cells were enriched to a purity of 87% +/- 2% (mean +/- SEM) and assayed in short-term suspension cultures in the presence of 10 ng/mL of PEGylated recombinant human megakaryocyte (MK) growth and development factor (PEG-rHuMGDF) and in addition to 50 ng/mL stem cell factor and 10 ng/mL interleukin-3. Cells of the megakaryocytic lineage were identified by flow cytometric analysis of CD42b (GP1b) and mature MKs by morphologic criteria. Transcription of c-mpl receptor-specific mRNA in the CD34+ cells of these patients was investigated by full-length reverse transcriptase polymerase chain reaction of the p form of c-mpl as well as of the alternative splice product c-mpl k. CD34+ cells from seven healthy bone marrow donors served as controls. Differentiation along the MK pathway was stimulated in five patients with RA. C-mpl mRNA was expressed in the CD34+ cells in all cases. In three low-risk patients the capacity for in vitro MK growth was absent or minimal even though mRNA for c-mpl receptor was detected in the CD34+ cells of this group as well. In patients with high-risk MDS, PEG-rHuMGDF stimulated in vitro MK growth from CD34+ cells in only one of five cases. As in the patients with low-risk MDS, c-mpl mRNA for both c-mpl p and c-mpl k splicing products was detected. These results indicate that the in vitro response to stimulation with c-mpl ligand discriminates between two groups of patients with low-risk MDS and that the observed defect in megakaryocytic development is unrelated to the level of c-mpl expression in both low-risk and high-risk MDS.
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PMID:Characterization of defective megakaryocytic development in patients with myelodysplastic syndromes. 1008

Serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), and interferon-gamma (IFN-gamma) were estimated by conventional ELISA kits in 60, 42, and 58 Thai patients, respectively, with beta(o)-thalassemia HbE and found to be above the normal range in 13%, 21%, and 33% of the patients, respectively. Using high-sensitivity ELISA systems, an additional 10 beta(o)-thal/HbE patients were compared with 9 controls for concentrations of circulating TNF-alpha and IL-1beta, and 9 and 5 patients, respectively, but only 1 and none of the controls, respectively, showed values above the normal ranges. In patients with abnormally high IFN-gamma levels, basal hemoglobin values were significantly lower than in those with normal levels of the cytokine (mean +/- SEM: 6.03+/-0.24 vs. 7.08+/-0.18, p < 0.05), although circulating concentrations of soluble transferrin receptors (sTrF) and absolute reticulocyte counts were similar in the two groups. Patients with raised or normal levels of TNF-alpha, IL-1alpha, or IL-1beta had similar basal hemoglobin values. In a phagocytosis assay, monocytes of patients with raised serum levels of IFN-gamma showed significantly more attached or ingested IgG-coated red cells than those of patients with normal concentrations of the cytokine (mean +/- SEM: 192+/-22 vs. 140+/-14 per 100 monocytes, p < 0.05). Moreover, in 3 of 4 of the former patients, the number of attached or ingested IgG-coated red cells per 100 monocytes was above the 95% reference limit for the latter patients. The results suggest that IFN-gamma aggravates the anemia of beta(o)-thal/HbE by activating mononuclear phagocytes for destruction of red cells but not by inhibiting erythropoiesis. The elevated serum levels of TNF-alpha and IL-1 could contribute to complications of the disease, such as cachexia and thromboembolic phenomena.
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PMID:Serum levels of tumor necrosis factor-alpha, interleukin-1, and interferon-gamma in beta(o)-thalassemia/HbE and their clinical significance. 1009 Mar 95

Erythropoietin (EPO) is the main red cell growth factor and its release into the blood stream is stimulated by anemia and also by various kinds of hypoxia. We studied the blood EPO concentration in a population of 96 infants who died suddenly and compared their mean EPO levels to control infants. The normal values were low at birth and progressively increased during the first 2 years. In the sudden infant death (SID) group the EPO level was significantly higher (p = 0.001) for the entire population and particularly in the youngest group (0-2 months): 14.7 +/- 2.4 IU/l (mean +/- SEM) in SID group vs. 3.6 +/- 0.4 IU/l in control group (p < 0.001). Although we could not analyze the blood hemoglobin concentration after death, the anemia hypothesis was refuted by an assay of the percentage of fetal hemoglobin which was normal for age in the control and SID groups. Moreover, there was no significant difference in EPO levels between explained and unexplained deaths. We also observed an increase in the stress hormones, cortisol and beta-endorphin, in the entire SID group. These SID results suggest a profound and long-lasting hypoxia at least during terminal agony.
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PMID:Erythropoietin blood level is increased in sudden infant death. 1036 33

Novel erythropoiesis stimulating protein (NESP) is a hyperglycosylated analogue of recombinant human erythropoietin (Epoetin) which has an increased terminal half-life in animal models. The aim of this study was to extend these observations to humans. Using a double-blind, randomized, cross-over design, the single-dose pharmacokinetics of Epoetin alfa (100 U/kg) and an equivalent peptide mass of NESP were compared following intravenous bolus in 11 stable peritoneal dialysis patients. This was followed by an open-label study to determine the single-dose pharmacokinetics of an equivalent peptide mass of NESP by subcutaneous injection in six of these patients. The mean terminal half-life for intravenous NESP was threefold longer than for intravenous Epoetin (25.3 versus 8.5 h), a difference of 16.8 h (95% confidence interval, 9.4 to 24.2 h, P = 0.0008). The area under the serum concentration-time curve was significantly greater for NESP (291.0 +/- 7.6 ng x h per ml versus 131.9 +/- 8.3 ng x h per ml; mean +/- SEM; P < 0.0005), and clearance was significantly lower (1.6 +/- 0.3 ml/h per kg versus 4.0 +/- 0.3 ml/h per kg; mean +/- SEM; P < 0.0005). The volume of distribution was similar for NESP and Epoetin (52.4 +/- 2.0 ml/kg versus 48.7 +/-2.1 ml/kg; mean +/-SEM). The mean terminal half-life for subcutaneous NESP was 48.8 h. The peak concentration of subcutaneous NESP was approximately 10% of that following intravenous administration, and bioavailability was approximately 37% by the subcutaneous route. The longer half-life of NESP is likely to confer a clinical advantage over Epoetin by allowing less frequent dosing in patients treated for anemia.
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PMID:Pharmacokinetics of novel erythropoiesis stimulating protein compared with epoetin alfa in dialysis patients. 1054 Dec 99

This study sought to determine the maximum tolerable limit of anemia for the brain during halothane anesthesia. Using a multiparameter sensor, we continuously monitored brain tissue oxygen tension (PO2), carbon dioxide tension (PCO2), and pH during profound hemodilution and subsequent transfusion. Twelve New Zealand White rabbits were anesthetized, intubated, and mechanically ventilated at a fraction of inspired oxygen (FiO2) of 21% to produce an arterial carbon dioxide tension (PaCO2) of 35 to 40 mm Hg. The femoral artery was cannulated to continuously monitor arterial blood pressure and to intermittently measure arterial blood gases. The electroencephalogram (EEG) was recorded throughout the course of the study. A fiberoptic sensor was inserted into the brain for the continuous measurement of brain PO2, PCO2, pH, and temperature. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. Severe anemia was induced by repeatedly withdrawing 50-mL aliquots of blood and infusing an equal volume of 6% hetastarch. This procedure was performed four times for each rabbit. After the forth blood draw and fluid infusion, a total of 60 mL of packed red blood cells were transfused. Upon completion of the hemodilution, the hemoglobin concentration was 2.4 +/- 0.3 g/dL (mean +/- SEM). Brain tissue PO2 decreased from 27 +/- 3 mm Hg to a minimum of 12 +/- 2 mm Hg. Brain tissue pH also decreased from 7.22 +/- 0.03 to 7.12 +/- 0.05 and returned to the baseline value with transfusion. Brain PCO2 did not change significantly during the experiment. Cerebral blood flow increased from 37 +/- 3 to 66 +/- 15 mL x 100 g(-1) x min(-1) during hemodilution and returned to baseline after infusion of red blood cells. There was some loss of EEG amplitude and the calculated cerebral metabolic rate (CMRO2) decreased from 4.3 +/- 0.6 to 1.9 +/- 0.3 mL x 100 g(-1) x min(-1) at the most profound level of anemia. This is the first report of which the authors are aware of continuous monitoring of brain tissue pH, PCO2, and PO2 during profound hemodilution and transfusion. Hemodilution results in a decrease in brain tissue PO2. Increases in CBF and oxygen extraction can only partially compensate for the decreased oxygen carrying capacity of the blood. Decreases in brain tissue PO2, pH, CMRO2, and a loss of EEG amplitude suggest that the maximum tolerable limit of hemodilution was achieved in this study.
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PMID:Effects of profound anemia on brain tissue oxygen tension, carbon dioxide tension, and pH in rabbits. 1114 76

Anemia management in hemodialysis patients continues to evolve, and recently, greater emphasis has been placed on the wider use of intravenous iron to maintain adequate iron levels. This survey provides scarcely available yet potentially useful information on the clinical treatment of anemia in a large cohort of hemodialysis patients. The erythropoietin and iron administration details and pertinent laboratory measurements from 1,639 patients were analyzed for the month of December, 1998. A standardized protocol had been used in that erythropoietin was begun at a total weekly dose of 150 U/kg IV or 100 U/kg subcutaneously and was then adjusted to maintain a hematocrit (Hct) of 33-36%. Iron supplements, oral, IV, or both, were administered to maintain percent transferrin saturation (TSAT) at 20-30% and/or a serum ferritin of 100-500 ng/ml. No intravenous iron was administered if the ferritin was more than 500 ng/ml. Although 82% of patients were on iron supplementation and, among them, 58% were on IV iron, the percentage of patients with TSAT >20, i.e., bioavailable iron, was only 51%. The serum ferritin was high at 498 +/- 10 ng/ml (mean +/- SEM) and 88% and 10% of patients had serum ferritin >100 and >1,000 ng/ml, respectively, suggestive of sequestration of part of the infused iron. Erythropoietin was administered to 96% of patients, 99.5% by IV route. The latter was consistent with the US dialysis population at large but in variance with DOQI preference for the subcutaneous route. The target Hct range of 33-36 was found in 33%, with a mean Hct of 34.0 +/- 0.12. When the data were reanalyzed by excluding patients who had not been receiving erythropoietin and had not been on dialysis for at least 3 months, the percentage of patients achieving the target Hct increased to 37%. Paired analysis of 875 patients present in 1996 and 1998 showed that, although there was a marked increase in the use of IV iron, the improvement in anemia was modest, and there was evidence for increased iron accumulation. In summary, this 1998 survey on the clinical practice of anemia management in a large hemodialysis population indicates that there is a marked increase in need-based IV iron usage that was associated with modest improvement in anemia and evidence for increased iron storage. A maintenance iron dosing protocol with smaller doses of iron, such as 25 mg of iron dextran per hemodialysis, may make bioavailable iron continuously present for erythropoiesis, yet may reduce the chance for iron catalyzed lipid peroxidation and tissue iron deposition.
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PMID:Anemia and iron target realization in 1998: clinical management of anemia in 1,639 patients on hemodialysis. 1157 28

During pregnancy extravillous trophoblast invades maternal uterine tissues and remodels spiral arteries. Maternal anaemia and early onset pre-eclampsia are associated with perturbed trophoblast biology. We systematically compared numerical density, invasive depth and apoptosis rates of extravillous trophoblast in uterine tissues taken from hysterectomies following Caesarean section after normal pregnancies (n=4) or pregnancies complicated by pre-eclampsia (n=5) or anaemia (n=6). Full thickness sections of the placental bed were studied by immunohistochemistry using anti-active caspase 3, anti-cytokeratin 7, anti-lamin B, M30, Mib-1, anti-PARP, and by the TUNEL assay. In normal pregnancy extravillous trophoblast invaded 2.04+/-0.19 mm (mean+/-SEM ) from the endometrial-myometrial border into the myometrium; in pre-eclampsia 0.67+/-0.14 mm (P< 0.01), and in anaemia 3.84+/-0.21 mm (P< 0.001). The endometrial trophoblast density in normal pregnancy was 2.44+/-0.37 cells per 60,000 microm(3), in pre-eclampsia was 1.04+/-0.15 (P< 0.01), and in anaemia was 3.10+/-0.32. The rate of apoptotic extravillous trophoblast (M30-positive) in the endometrium in normal pregnancy was 7.17+/-1.46 per cent, in pre-eclampsia 4.4+/-0.71, and in anaemia 2.1+/-0.42 (P< 0.01). Maternal anaemia leads to general tissue hypoxia throughout gestation. Increased invasive depth could be explained by hypoxia-stimulated mitosis and decreased apoptosis of extravillous trophoblast. Reduced trophoblast invasion in pre-eclampsia cannot be explained by higher rates of apoptosis.
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PMID:Pre-eclampsia and maternal anaemia display reduced apoptosis and opposite invasive phenotypes of extravillous trophoblast. 1274 31

The role of maternal anemia in the development of postpartum depression (PPD) is unclear. PPD is a serious disorder that may negatively affect the physical and emotional health of a new mother and her infant. Although psychosocial factors that increase the risk of developing PPD are known, few studies have identified physiologic factors that predispose a woman to PPD. New mothers were visited at home on d 7, 14 and 28 after an uncomplicated labor and delivery. Hemoglobin (Hb) concentration was measured via finger-prick blood at each visit, and the women completed the Center for Epidemiological Studies-Depressive Symptomatology Scale (CES-D) on d 28. There was a negative correlation between Hb concentration on d 7 postpartum and depressive symptoms on d 28 (r = -4.26; P = 0.009). CES-D scores (means +/- SEM) on d 7 of women with normal Hb levels > 120 g/L (12 g/dL) were significantly lower (6.90 +/- 1.04) than those of women with Hb levels < or = 120 g/L (12 g/dL) [16.36 +/- 3.34; t(35) = -3.632, P = 0.001]. Thus, women suffering early postpartum anemia may be at increased risk of developing PPD.
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PMID:Low hemoglobin level is a risk factor for postpartum depression. 1465 62

The natural folate derivative, 5-methyltetrahydrofolate ([6S]-5-MTHF), could be an option for supplementation and fortification but its bioavailability remains unclear. This study compared the bioavailability of [6S]-5-MTHF with that of folic acid (FA) by measuring plasma folate responses after a single ingestion of equivalent doses of the two folate forms. In a double-blind, crossover study, 13 men (presaturated with FA) received in random order each of the following treatments administered orally at 1-wk intervals: 1) placebo capsule; 2) 500 micro g FA capsule; and 3) 500 micro g [6S]-5-MTHF capsule. Plasma total folate concentrations were measured before and up to 10 h after each treatment (n = 10 samples per treatment). Plasma folate concentrations increased significantly (compared with baseline) from 0.5 to 5 h after both folate treatments. The maximum plasma folate response did not differ between the two treatments (mean +/- SEM, 33.4 +/- 3.9 vs. 31.8 +/- 3.9 nmol/L, P = 0.7, for FA and [6S]-5-MTHF, respectively) and typically occurred in individuals between 0.5 and 3 h postprandially. The area under the plasma folate response curve was significantly greater after both folate treatments compared with placebo, and the response did not differ between the treatments. These results indicate that the short-term bioavailabilities of [6S]-5-MTHF and FA are equivalent. Supplementation with the natural folate derivative could have all the beneficial effects associated with FA, but without the potential disadvantage of masking the anemia of vitamin B-12 deficiency.
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PMID:The short-term bioavailabilities of [6S]-5-methyltetrahydrofolate and folic acid are equivalent in men. 1498 50


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