Current Issue : January - March Volume : 2012 Issue Number : 1 Articles : 9 Articles
Background: Using blood lactate monitoring for risk assessment in the critically ill patient remains controversial.\r\nSome of the discrepancy is due to uncertainty regarding the appropriate reference interval, and whether to\r\nperform a single lactate measurement as a screening method at admission to the hospital, or serial lactate\r\nmeasurements. Furthermore there is no consensus whether the sample should be drawn from arterial, peripheral\r\nvenous, or capillary blood. The aim of this review was:\r\n1) To examine whether blood lactate levels are predictive for in-hospital mortality in patients in the acute setting, i.\r\ne. patients assessed pre-hospitally, in the trauma centre, emergency department, or intensive care unit.\r\n2) To examine the agreement between arterial, peripheral venous, and capillary blood lactate levels in patients in\r\nthe acute setting.\r\nMethods: We performed a systematic search using PubMed, Cochrane Central Register of Controlled Trials,\r\nCochrane Database of Systematic Reviews, and CINAHL up to April 2011. 66 articles were considered potentially\r\nrelevant and evaluated in full text, of these ultimately 33 articles were selected.\r\nResults and Conclusion: The literature reviewed supported blood lactate monitoring as being useful for risk\r\nassessment in patients admitted acutely to hospital, and especially the trend, achieved by serial lactate sampling, is\r\nvaluable in predicting in-hospital mortality. All patients with a lactate at admission above 2.5 mM should be closely\r\nmonitored for signs of deterioration, but patients with even lower lactate levels should be considered for serial\r\nlactate monitoring. The correlation between lactate levels in arterial and venous blood was found to be acceptable,\r\nand venous sampling should therefore be encouraged, as the risk and inconvenience for this procedure is minimal\r\nfor the patient. The relevance of lactate guided therapy has to be supported by more studies....
Background: Interpreting the erythroid lineage in populations with high frequency of a+ thalassemia allele is\r\nchallenging due to the high prevalence of a+ thalassemia homozygotes. For such populations, separate reference\r\nvalues for normal and a+ thalassemia homozygotes are needed.\r\nMethods: We studied the erythroid lineage in 1,079 citizens of United Arab Emirates (UAE). Subjects with abnormal\r\nhemoglobin (39), iron deficiency (136) or erroneous entries (8) were excluded. MCV distribution in the remaining\r\nindividuals (896) was visibly bimodal. Statistical mixture analysis with Normix program was used to separate\r\nsubpopulations with normal and small red cells. Hardy-Weinberg equation was used to estimate genotype\r\nfrequencies.\r\nResults: MCV of 78.0 fl separated phenotype-derived normal homozygotes (715) from phenotype-derived a+\r\nthalassemia homozygotes (181). The erythrocyte indices were significantly different between the two groups (p <\r\n0.0001). The overall prevalence of phenotype-derived a+ thalassemia homozygotes (-a/-a) was 0.20 and markedly\r\nvaried among tribes, 0 to 0.31 (Mean = 0.15). The frequency of phenotype-derived a+ thalassemia allele was 0.44;\r\nwhen accounting for tribal population structure and inbreeding, the calculated frequency was 0.34. These values\r\nwere very similar to those found in the same population by genotyping and other phenotyping methods. The\r\nerythrocyte reference values for phenotype-derived normal homozygotes in Emiratis closely overlapped with those\r\nfor Caucasians and normal homozygotes defined by genotyping. The reference values for phenotype-derived a+\r\nthalassemia homozygotes in Emiratis also closely overlapped with those for a+ thalassemia homozygotes defined\r\nby genotyping.\r\nConclusion: In populations with frequent a+ thalassemia mutations, two sets of erythrocyte reference values could\r\nbe determined without genotyping....
Introduction. Patients with �Ÿ-thalassemia intermedia have a higher incidence of thromboembolic events compared to the general\r\npopulation. Previous studies have shown that patients with sickle cell disease, who are also prone to ischemic events, have higher\r\nintracranial arterial blood flow velocities measured by transcranial Doppler sonography (TCD). The aim of this study is to evaluate\r\nintracranial arterial flow velocities in patients with �Ÿ-thalassemia intermedia and compare the results with those found in healthy\r\nsubjects. Methods. Sixty-four patients with �Ÿ-thalassemia intermedia and 30 healthy subjects underwent transcranial Doppler\r\nsonography. Results. Significantly higher flow velocities were found in intracranial arteries of patients compared to controls (P =\r\n0.001). Previously splenectomized patients with thrombocytosis showed higher flow velocities than nonsplenectomized patients\r\nwithout thrombosis. Conclusion. The increased flow velocities in patients with �Ÿ-thalassemia intermedia may point to a higher risk\r\nof ischemic events. Preventive measures such as blood transfusion or antiplatelet treatment may be beneficial in these patients....
Background: Dyskeratosis congenita (DC) is a progressive, multi-system, inherited disorder of telomere biology\r\nwith high risks of morbidity and mortality from bone marrow failure, hematologic malignancy, solid tumors and\r\npulmonary fibrosis. Hematopoietic stem cell transplantation (HSCT) can cure the bone marrow failure, but it does\r\nnot eliminate the risks of other complications, for which life-long surveillance is required. Pulmonary fibrosis is a\r\nprogressive and lethal complication of DC.\r\nCase presentation: In this report, we describe a patient with DC who developed pulmonary fibrosis seven years\r\nafter HSCT for severe aplastic anemia, and was successfully treated with bilateral lung transplantation. We also\r\nperformed a systematic literature review to understand the burden of pulmonary disease in patients with DC who\r\ndid or did not receive an HSCT. Including our patient, we identified 49 DC patients with pulmonary disease (12\r\nafter HSCT and 37 without HSCT), and 509 with no reported pulmonary complications.\r\nConclusion: Our current case and literature review indicate that pulmonary morbidity is one of the major\r\ncontributors to poor quality of life and reduced long-term survival in DC. We suggest that lung transplantation be\r\nconsidered for patients with DC who develop pulmonary fibrosis with no concurrent evidence of multi-organ\r\nfailure....
Background: Recommendations given for intravenous iron treatment are typically not supported by a high level\r\nof evidence. This meta-analysis addressed this by summarising the available date from clinical trials of ferric\r\ncarboxymaltose using clinical trial reports and published reports.\r\nMethods: Clinical trial reports were supplemented by electronic literature searches comparing ferric\r\ncarboxymaltose with active comparators or placebo. Various outcomes were sought for efficacy (attainment of\r\nnormal haemoglobin (Hb), increase of Hb by a defined amount, for example), together with measures of harm,\r\nincluding serious adverse events and deaths.\r\nResults: Fourteen studies were identified with 2,348 randomised patients exposed to ferric carboxymaltose, 832 to\r\noral iron, 762 to placebo, and 384 to intravenous iron sucrose. Additional data were available from cohort studies.\r\nIntravenous ferric carboxymaltose was given up to the calculated iron deficit (up to 1,000 mg in one week) for iron\r\ndeficiency anaemia secondary to chronic kidney disease, blood loss in obstetric and gynaecological conditions,\r\ngastrointestinal disease, and other conditions like heart failure. The most common comparator was oral iron, and\r\ntrials lasted 1 to 24 weeks. Intravenous ferric carboxymaltose improved mean Hb, serum ferritin, and transferrin\r\nsaturation levels; the mean end-of-trial increase over oral iron was, for Hb 4.8 (95% confidence interval 3.3 to 6.3)\r\ng/L, for ferritin 163 (153 to 173) �µg/L, and for transferrin saturation 5.3% (3.7 to 6.8%). Ferric carboxymaltose was\r\nsignificantly better than comparator in achievement of target Hb increase (number needed to treat (NNT) 6.8; 5.3\r\nto 9.7) and target Hb NNT (5.9; 4.7 to 8.1). Serious adverse events and deaths were similar in incidence in ferric\r\ncarboxymaltose and comparators; rates of constipation, diarrhoea, and nausea or vomiting were lower than with\r\noral iron.\r\nConclusions: This review examined the available trials of intravenous ferric carboxymaltose using details from\r\npublished papers and unpublished clinical trial reports. It increases the evidence available to support\r\nrecommendations given for intravenous iron treatment, but there are limited trial data comparing different\r\nintravenous iron preparations....
Coadministration of azoles and vincristine has been shown to increase vincristine neurotoxic effects due to the inhibition of\r\ncytochrome P450 (CYP) isoform 3A4, for which vincristine is a substrate. Despite the absence of any casual relationship between\r\nseizure and coadministration of azoles, few case reports of vincristine-induced seizure have been documented after coadministration\r\nof fluconazole or posaconazole in children. In this paper we are reporting the first young female adult who experienced generalized\r\nseizure after coadministration of posaconazole and vincristine. The 19-year-old female was diagnosed with acute lymphoblastic\r\nleukemia. She started induction phase of Berlin Frankfurt Muenster protocol along with posaconazole 200 mg three times\r\ndaily as prophylactic antifungal therapy. Five days after the third vincristine dose, she developed generalized seizure accompanied\r\nby high blood pressure and SIADH. Her neurological exam/CT scan did not show any abnormality. In conclusion, this study\r\nreports a novel finding in the sense that all previous case reports pertaining to posaconazole-vincristine-induced seizure in\r\nliterature involved children. Physicians should be made aware of this rare possible outcome to closely monitor their patients and\r\ntake appropriate measures to prevent such possible adverse effect....
Iron deficiency is an important public health problem. An understanding of anemia risk factors is essential to informed health\r\npolicies. We performed a cross-sectional study of 1,382 infants from the 2006 Brazilian National Survey on Demography and the\r\nHealth of Women and Children. Mild and moderate anemia was characterised by hemoglobin levels below 11.0 and 9.5 g/dL,\r\nrespectively. Rates for mild and moderate anemia were 25.9% and 9.9%, respectively. The logistic model included three risk factors\r\nfor mild anemiaââ?¬â?urban residence area (OR = 2.5; P = 0.004), fever in the past 2 weeks (OR = 2.4; P < 0.001), and age less than\r\n12 months (OR = 1.7; P = 0.024). Strategies to control infant anemia should include health promotion and nutritional education\r\nfor families from all socioeconomic levels. Lifestyle quality improvement based on adequate food consumption must be achieved\r\nby communities in all macroregions, and especially in urban areas....
Background: Several studies have shown that the pathophysiology of homozygous sickle cell anaemia (SCA)\r\nresults in a myriad of metabolic, nutritional, haematological and clinical effects that interact with other co-morbid\r\nfactors to determine the quality of life and life expectancy of afflicted patients. Because of its critical roles in\r\nnutrition and metabolism, inflammation, haematopoiesis and cellular immunity, this study determined the plasma\r\nlevels of leptin in steady and unsteady states of HbSS in Nigerian patients.\r\nMethods: A total of 51 SCA patients aged 5 - 35 years with 34 (61.8%) being females who were either on\r\nadmission or visiting four medical centres in Lagos, Nigeria together with 22 non-SCD controls aged 5 -30 years\r\ncomprising 12 (54.5%) females were enrolled after obtaining their informed consent and ethical approval. Patients\r\nwere further stratified into steady and unsteady cases of SCA based on clinical presentations, while blood samples\r\ncollected by venipuncture from each of the study participants were analyzed haematologically for full blood count\r\nand HbF level and microscopically for malaria, while plasma leptin was assayed using ELISA method. Body\r\ncomposition defined by weight, fat mass and body mass index (BMI) was determined using standard methods.\r\nData obtained for cases and controls were analyzed statistically.\r\nResults: Twenty - one patients had unsteady HbSS and elicited greater and significant (P < 0.05) reduction in fat\r\nmass, BMI, HbF and eosinophil count but elevated mean total leukocyte, count, level of irreversibly sickled cells and\r\nP. falciparum parasitaemia (4613.7 vs. 749.6 - 1078.4 parasites/uL), pyrexia rate (58.3 vs. 25.8%) when compared with\r\nsteady state patients or non-SCD controls. Compared to the control, significant decreases in plasma leptin before\r\nand after controlling for body fat that was worsened by crisis were observed among the SCD patients. Unlike the\r\nnon-SCD controls, leptin correlated non-significantly (P > 0.05) with all body composition indices measured in the\r\npatients except for fat mass in unsteady cases. Multivariate regression analysis identified ESR and RC as\r\nindependent predictor of low plasma leptin concentration in the SCA patients.\r\nConclusions: Base on these findings, we conclude that plasma level of leptin is further decreased in the unsteady\r\nstate of HbSS, shows poor correlation with adiposity and malarial infection but has inflammation and poor\r\nreticulocyte response as independent predictors among Nigerian patients....
We studied the nature of enucleated RBCs containing DNA remnants, Howell-Jolly (HJ) RBCs and reticulocytes (retics), that are\r\ncharacteristically present in the circulation of thalassemic patients, especially after splenectomy. Using flow cytometry methodology,\r\nwe measured oxidative status parameters of these cells in patients with �Ÿ-thalassemia. In each patient studied, these cells had\r\nhigher content of reactive oxygen species and exposed phosphatidylserine compared with their DNA-free counterparts. These results\r\nsuggest that oxidative stress in thalassemic developing erythroid precursors might, through DNA-breakage, generate HJ-retics\r\nand HJ-RBCs and that oxidative stress-induced externalization of phosphatidylserine is involved in the removal of these cells from\r\nthe circulation by the spleen, a mechanism similar to that of the removal of senescent RBCs....
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