Decreased Erythrocyte Deformability Research Articles

Influence of diabetes and hypercholesterolemia on laboratory methods for hereditary spherocytosis diagnosis.

IntroductionHereditary spherocytosis (HS) is characterized by decreased erythrocyte deformability resulting in hemolytic anemia. This is a heterogeneous disease regarding underlying protein deficiency, disease severity, age at diagnosis and clinical course. Although largely considered as pediatric disease, HS could be initially diagnosed also in elder patients as a result of gallstones or splenomegaly fortuitous finding. Concurrently, common adulthood metabolic disorders like diabetes or dyslipidemia are also known to impair RBC rheology and deformability. Therefore, we aimed to investigate if these diseases affect the screening and diagnostic tools used for HS diagnosis.MethodsWe applied our workflow for HS diagnosis on 95 pathological samples: 29 patients with diabetes, 20 with hypercholesterolemia, 17 with dyslipidemia, 6 with hypertriglyceridemia, 23 with metabolic syndrome (MS). Thus, a total of 73 samples were analyzed by automated reticulocyte analysis, 52 by cryohemolysis test, and 41 by ektacytometry osmoscan analysis as we used two out of the three tests for each individual sample.ResultsApplying our screening algorithm based on automated reticulocyte indices, a total of 4 samples (4.2%): one sample (5%) from the diabetes group and three samples (16.7%) from the MS group, positioned into the HS zone. However, no significant difference was found between any of the pathological groups and the controls for the cryohemolysis test or the osmoscan.ConclusionWhile diabetes and hypercholesterolemia are pathologic conditions known to present with decreased erythrocyte deformability and disturbed rheology, their possible concomitant presence with HS would not interfere with the screening and confirmatory laboratory methods.

Assessment of erythrocyte morphology in patients with type 2 diabetes mellitus: a pilot study of electron microscopy-based analysis in relation to healthy controls

Background/aim The present study aimed to assess erythrocyte morphology in newly diagnosed type 2 diabetes mellitus patients using scanning electron microscopy.Materials and methods In total, 30 patients admitted to endocrine outpatient clinics were included in the study. The patients were divided into two groups according to their fasting blood glucose levels: type 2 diabetes mellitus (n = 15, fasting blood glucose levels ≥ 126 mg/dL) and control (n = 15, fasting blood glucose levels < 99 mg/dL). The patient’s demographic characteristics, haemoglobin A1c levels, and scanning electron microscopy findings regarding erythrocyte morphology were recorded.ResultsThere was no significant difference between the control and type 2 diabetes mellitus group in terms of the participants’ age (51.13 ± 8.53 vs. 50.33 ± 8.72 years, p = 0.8) and the male/female ratio (9/6 vs. 9/6). In the control group, discocytes were abundant, echinocytes were rare, and spherocytes were absent. On the other hand, discocytes were less common and echinocyte-shaped erythrocytes were more common in the type 2 diabetes mellitus group than in the control group. In addition, spherocytes were detected in the type 2 diabetes mellitus group. Moreover, the diameter of discocytes was significantly lower (p = 0.014), and blood glucose and haemoglobin A1c levels were significantly higher (p < 0.05 for both) in the type 2 diabetes mellitus group than in the control group. ConclusionOur findings indicate that high glucose levels in type 2 diabetes mellitus patients lead to significant alterations in erythrocyte morphology, including decreased erythrocyte deformability and the formation of echinocytes and spherocytes due to eryptosis. The possibility of decreased erythrocyte deformability due to excessive eryptosis may disturb microcirculation in newly diagnosed, treatment-naïve type 2 diabetes mellitus patients who do not have any complications.

The Role of Blood Viscosity in Infectious Diseases.

Blood viscosity is increased by elevated concentrations of acute phase reactants and hypergammaglobulinemia in inflammation. These increase blood viscosity by increasing plasma viscosity and fostering erythrocyte aggregation. Blood viscosity is also increased by decreased erythrocyte deformability, as occurs in malaria. Increased blood viscosity contributes to the association of acute infections with myocardial infarction (MI), venous thrombosis, and venous thromboembolism. It also increases vascular resistance, which decreases tissue perfusion and activates stretch receptors in the left ventricle, thereby initiating the systemic vascular resistance response. This compensates for the increased vascular resistance by vasodilation, lowering hematocrit, and decreasing intravascular volume. This physiological response causes the anemias associated with malaria, chronic inflammation, and other chronic diseases. Since tissue perfusion is inversely proportional to blood viscosity, anemia may be beneficial as it increases tissue perfusion when erythrocyte aggregating factors or erythrocytes with decreased deformability are present in the blood.

Nitrite may serve as a combination partner and a biomarker for the anti-cancer activity of RRx-001.

RRx-001 is an anti-cancer immunotherapeutic that increases the sensitivity of drug resistant tumors via multiple mechanisms which involve binding to hemoglobin and enhancing nitrite reductase activity of deoxyhemoglobin. In the present study, the effect of clinically used doses of RRx-001 on erythrocyte deformability was examined. A dose dependent effect of RRx-001 (1-1000 micro molar) on erythrocyte deformability was measured by ektacytometer under hypoxia (n =8). Low dose RRx-001 (20 micro molar) in the presence of ODQ (1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one), L-NAME (L-NG-Nitroarginine methyl ester) or nitrite were examined both in normoxia and hypoxia. Intracellular nitric oxide (NO) levels were measured fluorometrically with DAF-FM-DA. Higher doses of RRx-001 (100, 1000 micro molar) significantly decreased erythrocyte deformability under hypoxia (p <0.01; p <0.05, respectively). RRx-001 (20 micro molar), alone or in combination with ODQ or L-NAME, did not change deformability. However, RRx-001 and nitrite caused an increase in deformability (p <0.01) under hypoxia. RRx-001 induced NO production was more pronounced in the presence of nitrite (p <0.05). Co-administration of RRx-001 and nitrite under hypoxic conditions results in a significant increase in erythrocyte deformability that is related to increased NO production. We suggest that measurement of serum nitrite level in RRx-001 treated cancer patients should be routinely undertaken and supplemented if levels are low for maximal activity.

Hereditary spherocytosis and allied disorders

Hereditary spherocytosis and allied disorders

Microfluidic assemblies designed for assessment of drug effects on deformability of human erythrocytes

Extreme deformability of human erythrocytes is a prerequisite for their ability to squeeze through narrow capillaries of the blood microcirculation system. Various drugs can modify this deformability and consequently provoke circulation problems. We demonstrate that microfluidic assemblies are very convenient platforms for in vitro study of the associated processes. Two types of microfluidic channels were designed to quantitatively investigate modifications of erythrocyte deformability induced by hydrogen peroxide, ethanol and pentoxifylline based on transit velocity measurements. With a high sensitivity our microfluidic assemblies show that hydrogen peroxide decreases erythrocyte deformability in a dose-dependent manner. Then, results on ethanol resolve a biphasic nature of this reactant on the deformability of single erythrocyte cells. Results on pentoxifylline provide evidence that, similar to ethanol, also this medical drug has a double-sided effect on the erythrocyte deformability, i.e. increasing the deformability at low concentrations, while decreasing it at higher ones. Taken together, our microfluidic designs propose a potent measurement method for the erythrocyte deformability, as well as providing a perspective to evaluate effects of drugs on it.

Timolol effects on erythrocyte deformability and nitric oxide metabolism.

Timolol maleate is a compound used in treatment for reducing increased intra-ocular pressure by limiting aqueous humor production. Decreased erythrocyte deformability (ED), increased activity of erythrocyte acetylcholinesterase (AChE), increased values of nitrosoglutathione (GSNO) and nitic oxide (NO) and decreased plasma levels of NO metabolites, were described in primary open angle glaucoma patients. In healthy human red blood cells (RBCs), timolol is an inhibitor of AChE and induces NO efflux and GSNO efflux from that blood component in lower concentration than those obtained in presence of the natural AChE substrate, acetylcholine (ACh). The signal transduction pathway in RBCs described for NO in dependence of AChE-ACh active complex involves Gi protein, protein tyrosine kinase (PTK like Syk and p53/56Lyn), protein tyrosine phosphatase (PTP) and adenylyl cyclase (AC).The aim of this in vitro study was to verify the effect of timolol maleate in ED, NO efflux and NO derivatives molecules (NOx) like nitrite (NO2-), nitrate (NO3-, peroxynitrite (-ONOO) and GSNO under the presence of PTK, PTP, AC and guanylyl cyclase (GC) enzyme proteins inhibitors.Blood samples from healthy donors were each one divided and were performed aliquots in absence (control aliquots) and presence of timolol or timolol plus each inhibitor and Gi protein uncoupling. No significant differences in erythrocyte NO efflux, GSNO, peroxynitrite, nitrite and nitrate concentrations in response to timolol when compared with the untreated blood samples aliquots were obtained.It was observed an increase in erythrocyte deformability at high shear stresses induced by the simultaneous presence of timolol and band 3 protein dephosphorylation by PTK syk inhibitor. No significant differences where verified in peroxynitrite levels in the blood aliquots in presence of timolol plus each enzyme inhibitor and Gi protein uncoupling in relation to the control aliquots. No variation of GSNO concentration occurs under the presence of timolol and AMGT (PTK lyn inhibitor) besides the significant higher values observed with each one of the other inhibitors. Nitrate concentration increases significantly in all aliquots with timolol plus each one of the inhibitors. The same was observe with nitrite levels with exception of the aliquots with timolol plus AMGT or timolol plus Gi protein uncoupling showing no significant values in relation to the control aliquots.Besides the changes in NO derivative molecules and NO efflux from RBCs obtained in this study with blood samples of healthy donors under the effect of timolol plus each inhibitor of the proteins participants in NO signal transduction mechanism, further analogue studies must be promoted with blood samples of patients with glaucoma or any other inflammatory vascular disease.

Effects of indomethacin on erythrocyte nitric oxide metabolism and erythrocyte deformability

Increased erythrocyte filtration index (decreased erythrocyte deformability; ED) was observed in patients with Behcet disease. When patients with Behcet took indomethacin, decreased values of erythrocyte acetylcholinesterase enzyme activity were obtained. An inverse association between nitric oxide (NO) efflux from erythrocytes and ED values was verified in blood samples of patients with vascular inflammatory diseases. The aim of this in vitro study was to verify the effect of indomethacin on ED, NO efflux, nitrite nitrate, peroxynitrite and nitroso- glutathione (GSNO) in the presence of protein tyrosine kinase (PTK Syk), protein tyrosine phosphatase (PTP), adenylyl cyclase (AC) and phosphatidylinositol 3 kinase (PI3K) enzyme inhibitors respectively Syk inhibitor, calpeptin, MDL and wortmannin (WORT). Blood samples from ten healthy donors were divided and aliquots were performed in absence (control aliquot) and presence of indomethacin or indomethacin plus each one of the inhibitors. Further ED and NO efflux and its metabolites were evaluated by the usual methodology. A significant increase in ED values was noted in the presence of indomethacin plus WORT. No significant differences where verified in NO efflux from erythrocytes in all blood aliquots. Significantly increase in GSNO concentration in the presence of indomethacin plus calpeptin, MDL or Wort were observed. Nitrate and peroxynitrite concentrations increased or decreased significantly respectively in all aliquots in relation to the control one. The nitrite levels increased in the aliquots with indomethacin and indomethacin plus MDL, or indomethacin plus Syk. In conclusion indomethacin act as antioxidant decreasing peroxynitrite, not changing NO efflux values and increasing nitrate levels independent of band 3 phosphorylation degree or cyclic adenosine monophosphate (cAMP) concentration. Indomethacin mobilizes nitrite and GSNO in dependant of band 3 phosphorylation degree and cAMP. Indomethacin did not change erythrocyte deformability, unless in combination with wortmannin which increased it.

Effect of Levosimendan and Nigella Sativa on Erythrocyte Deformability During Myocardial Ischaemia-Reperfusion Injury in Rats

Objective: Ischaemia-reperfusion (IR) injury is a chain of events put in place by tissue ischaemia. Reperfusion following the cellular damage causes an active inflammatory response. Erythrocyte deformability and plasma viscosity play a critical role in tissue and organ perfusion. In this study we aimed to evaluate the effect of levosimendan and nigella sativa on erythrocyte deformability during myocardial IR injury in rats. Methods: Twenty-four Wistar albino rats were included in the study. The animals were randomly divided into four experimental groups. The coronary arteries of rats in Group C (control group) were not occluded or reperfused. Myocardial IR was performed by ligating the left anterior descending coronary artery for 30 min, followed by 2 h of reperfusion in the IR (IR), IR-levosimendan (24µg/kg) (IRL) group and IR-nigella sativa (0.2 mL/kg) (IRNS) group. Erythrocyte suspensions formed with a PBS buffer solution containing 5% htc were used to measure the deformability. Results: As a result compared to control group, IR increased the relative resistance, a marker of erythrocyte deformability, significantly (p<0.05). There were significant differences between the groups according to the comparisons with ANOVA test (p<0.0001). The results obtained after corrections with Bonferroni test were as follows: Comparisons of the IRL and IRNS groups revealed similar results (p=0.764). The values of the IR group were significantly higher than those of the control, IRNS and IRL groups (p<0.0001, p=0.001, p=0.003, respectively). Conclusion: Rats with IR injury had decreased erythrocyte deformability. This injury might cause more problems in microcirculation. Levosimendan and nigella sativa may be useful in reducing the adverse effects of this type of injury.

Perspective: interesterified triglycerides, the recent increase in deaths from heart disease, and elevated blood viscosity.

The authors hypothesize that consumption of interesterified fats may be the cause of the continuous increase in cardiovascular deaths in the United States which began in 2011. Interesterification is a method of producing solid fats from vegetable oil and began to supplant partial hydrogenation for this purpose upon recognition of the danger of trans fats to cardiovascular health. Long, straight carbon chains, as are present in saturated and trans fatty acids, decrease the fluidity of the erythrocyte cell membrane, which decreases erythrocyte deformability and increases blood viscosity. This decrease in cell membrane fluidity is caused by increased van der Waals interactions, which also solidify dietary fats. Elevated blood viscosity is favored as the pathogenic mechanism by which trans fats increase cardiovascular mortality because changes in lipoprotein levels do not account for all the mortality attributable to their consumption. The rapid changes in cardiovascular mortality noted with the introduction and withdrawal of trans fats from the food supply are reviewed. The evidence implicating elevated blood viscosity in cardiovascular disease is also reviewed. Data regarding the production and consumption of interesterified fats in the US should be released in order to determine if there is an association with the observed increase in cardiovascular deaths.

The Effect of Sepsis on the Erythrocyte.

Sepsis induces a wide range of effects on the red blood cell (RBC). Some of the effects including altered metabolism and decreased 2,3-bisphosphoglycerate are preventable with appropriate treatment, whereas others, including decreased erythrocyte deformability and redistribution of membrane phospholipids, appear to be permanent, and factors in RBC clearance. Here, we review the effects of sepsis on the erythrocyte, including changes in RBC volume, metabolism and hemoglobin’s affinity for oxygen, morphology, RBC deformability (an early indicator of sepsis), antioxidant status, intracellular Ca2+ homeostasis, membrane proteins, membrane phospholipid redistribution, clearance and RBC O2-dependent adenosine triphosphate efflux (an RBC hypoxia signaling mechanism involved in microvascular autoregulation). We also consider the causes of these effects by host mediated oxidant stress and bacterial virulence factors. Additionally, we consider the altered erythrocyte microenvironment due to sepsis induced microvascular dysregulation and speculate on the possible effects of RBC autoxidation. In future, a better understanding of the mechanisms involved in sepsis induced erythrocyte pathophysiology and clearance may guide improved sepsis treatments. Evidence that small molecule antioxidants protect the erythrocyte from loss of deformability, and more importantly improve septic patient outcome suggest further research in this area is warranted. While not generally considered a critical factor in sepsis, erythrocytes (and especially a smaller subpopulation) appear to be highly susceptible to sepsis induced injury, provide an early warning signal of sepsis and are a factor in the microvascular dysfunction that has been associated with organ dysfunction.

The structure of the intracranial veins and elastic-viscous properties of erythrocyte membranes in children with connective tissue dysplasia

Objective: To study the structure of intracranial veins and elastic-viscous properties of erythrocyte membranes in children with connective tissue dysplasia. Methods: Group 1 consisted of 60 children with signs of connective tissue dysplasia in age from 10 to 16 years. Group 2 consisted of 40 children. Magnetic resonance angiography was performed on the apparatus, equipped with a superconducting magnet system with field strength of 1.5 T. To examine the state of the cytoplasmic membrane of erythrocytes were used dry preparations of erythrocytes. The product was dried in air and then subjected to scanning, which was carried out using an atomic force microscope, equipped with non-contact silicon probe, resonance frequency and the radius of curvature of the cantilever. They used a semi-contact technique. Quantification of membrane elasticity was carried out by calculating the Young's Modulus (E, MPa). Results are expressed as median, quartiles 25 and 75, M (25%; 75%). Differences were considered significant at the achieved level of significance p < 0.05. Results: In group 1 hypoplasia of the right transverse sinus occurred in 5% of cases, arteriovenous malformations– in 5% of cases, hypoplasia of the left sigmoid sinus – in 5% of cases, hypoplasia of the left internal jugular vein - in 10.5% of cases. In group 2 the development of intracranial venous anomalies have been identified. Patients of group 1 Young's modulus was equal to 182.68 (132.43; 232.94) MPa, in the comparison group - 111.48 (38.35; 184.61) MPa. The Young's modulus was significantly higher in children with connective tissue dysplasia (p < 0.05). Conclusion: For children with severe dysplasia of the connective tissue characterized by congenital malformations of intracranial veins, which in itself can be a predictor of cerebrovascular pathology. In children with connective tissue dysplasia a higher Young's modulus erythrocyte membrane in infants than control group, suggesting decreased erythrocyte deformability when passing through the microvasculature.

Microcirculation and blood rheology abnormalities in chronic heart failure.

Generalized restricted blood flow is hallmark of CHF of any etiology, but the extent of microcirculation restriction and the role of intrinsic blood properties in heart failure remains unknown. The aim of this study was to estimate the microvascular blood flow and hemorheological properties in chronic heart failure to test the hypothesis that CHF patients have altered peripheral blood flow which contributes to the tissue perfusion disturbances. Cutaneous microvascular blood flow was estimated by Laser Doppler and Optical Tissue Oximetry techniques. Whole blood and plasma viscosity were measured by capillary viscometer, red blood cell aggregation was evaluated by direct microscopic method, erythrocyte deformability was assessed as elongation index in flow microchamber. Hematocrit-to-viscosity ratio was used as index of oxygen transport efficacy. Depression of the regulatory mechanisms of microvascular blood flow as well as decreased tissue perfusion indicated the restricted blood flow in microcirculatory network in CHF. Increased blood and plasma viscosity, enhanced red blood cell aggregation and decreased erythrocyte deformability were registered in CHF. Complex impairment of peripheral blood flow in CHF including restricted microcirculation, attenuated regulatory mechanisms and impaired hemorheological properties caused the reduced oxygen utilization contributing to symptoms and advance of heart failure.

Measurements of red cell deformability and hydration reflect HbF and HbA2 in blood from patients with sickle cell anemia

Decreased erythrocyte deformability, as measured by ektacytometry, may be associated with disease severity in sickle cell anemia (SCA). Heterogeneous populations of rigid and deformable cells in SCA blood result in distortions of diffraction pattern measurements that correlate with the concentration of hemoglobin S (HbS) and the percentage of irreversibly sickled cells. We hypothesize that red cell heterogeneity, as well as deformability, will also be influenced by the concentration of alternative hemoglobins such as fetal hemoglobin (HbF) and the adult variant, HbA2. To test this hypothesis, we investigate the relationship between diffraction pattern distortion, osmotic gradient ektacytometry parameters, and the hemoglobin composition of SCA blood. We observe a correlation between the extent of diffraction pattern distortions and percentage of HbF and HbA2. Osmotic gradient ektacytometry data indicate that minimum elongation in the hypotonic region is positively correlated with HbF, as is the osmolality at which it occurs. The osmolality at both minimum and maximum elongation is inversely correlated with HbS and HbA2. These data suggest that HbF may effectively improve surface-to-volume ratio and osmotic fragility in SCA erythrocytes. HbA2 may be relatively ineffective in improving these characteristics or cellular hydration at the levels found in this patient cohort.

Exposure of Stored Packed Erythrocytes to Nitric Oxide Prevents Transfusion-associated Pulmonary Hypertension.

Transfusion of packed erythrocytes stored for a long duration is associated with increased pulmonary arterial pressure and vascular resistance. Prolonged storage decreases erythrocyte deformability, and older erythrocytes are rapidly removed from the circulation after transfusion. The authors studied whether treating stored packed ovine erythrocytes with NO before transfusion could prevent pulmonary vasoconstriction, enhance erythrocyte deformability, and prolong erythrocyte survival after transfusion. Ovine leukoreduced packed erythrocytes were treated before transfusion with either NO gas or a short-lived NO donor. Sheep were transfused with autologous packed erythrocytes, which were stored at 4°C for either 2 ("fresh blood") or 40 days ("stored blood"). Pulmonary and systemic hemodynamic parameters were monitored before, during, and after transfusion. Transfused erythrocytes were labeled with biotin to measure their circulating lifespan. Erythrocyte deformability was assessed before and after NO treatment using a microfluidic device. NO treatment improved the deformability of stored erythrocytes and increased the number of stored erythrocytes circulating at 1 and 24 h after transfusion. NO treatment prevented transfusion-associated pulmonary hypertension (mean pulmonary arterial pressure at 30 min of 21 ± 1 vs. 15 ± 1 mmHg in control and NO-treated packed erythrocytes, P < 0.0001). Washing stored packed erythrocytes before transfusion did not prevent pulmonary hypertension. NO treatment of stored packed erythrocytes before transfusion oxidizes cell-free oxyhemoglobin to methemoglobin, prevents subsequent NO scavenging in the pulmonary vasculature, and limits pulmonary hypertension. NO treatment increases erythrocyte deformability and erythrocyte survival after transfusion. NO treatment might provide a promising therapeutic approach to prevent pulmonary hypertension and extend erythrocyte survival.

Effects of lornoxicam and intravenous ibuprofen on erythrocyte deformability and hepatic and renal blood flow in rats.

BackgroundChange in blood supply is held responsible for anesthesia-related abnormal tissue and organ perfusion. Decreased erythrocyte deformability and increased aggregation may be detected after surgery performed under general anesthesia. It was shown that nonsteroidal anti-inflammatory drugs decrease erythrocyte deformability. Lornoxicam and/or intravenous (iv) ibuprofen are commonly preferred analgesic agents for postoperative pain management. In this study, we aimed to investigate the effects of lornoxicam (2 mg/kg, iv) and ibuprofen (30 mg/kg, iv) on erythrocyte deformability, as well as hepatic and renal blood flows, in male rats.MethodsEighteen male Wistar albino rats were randomly divided into three groups as follows: iv lornoxicam-treated group (Group L), iv ibuprofen-treated group (Group İ), and control group (Group C). Drug administration was carried out by the iv route in all groups except Group C. Hepatic and renal blood flows were studied by laser Doppler, and euthanasia was performed via intra-abdominal blood uptake. Erythrocyte deformability was measured using a constant-flow filtrometry system.ResultsLornoxicam and ibuprofen increased the relative resistance, which is an indicator of erythrocyte deformability, of rats (P=0.016). Comparison of the results from Group L and Group I revealed no statistically significant differences (P=0.694), although the erythrocyte deformability levels in Group L and Group I were statistically higher than the results observed in Group C (P=0.018 and P=0.008, respectively). Hepatic and renal blood flows were significantly lower than the same in Group C.ConclusionWe believe that lornoxicam and ibuprofen may lead to functional disorders related to renal and liver tissue perfusion secondary to both decreased blood flow and erythrocyte deformability. Further studies regarding these issues are thought to be essential.

Association of erythrocyte deformability with red blood cell distribution width in metabolic diseases and thalassemia trait.

Increased red blood distribution width (RDW) in anemia is related to disturbances in the cellular surface/volume ratio, usually accompanied by morphological alterations, while it has been shown in inflammatory diseases that the activity of pro-inflammatory cytokines disturbing erythropoiesis increases RDW. Recently it has been reported that higher RDW is related with decreased erythrocyte deformability, and that it could be related with the association of RDW and increased risk of cardiovascular diseases. In order to analyze the influence of morphological alterations and proinflammatory status on the relationship between RDW and erythrocyte deformability, we analyzed erythrocyte deformability along with RDW and other hematological and biochemical parameters in 36 α-thalassemia, 20 β-thalassemia, 20 δβ-thalassemia trait carriers, 61 metabolic syndrome patients and 76 morbidly obese patients. RDW correlated inversely with erythrocyte deformability in minor β-thalassemia (r =-0.530, p < 0.05), and directly in both metabolic syndrome and morbidly obese patients (ρ= 0.270, p < 0.05 and ρ= 0.258, p < 0.05, respectively). Minor β-thalassemia is often accompanied by more marked cell-shaped perturbations than other thalassemia traits. This could be the reason for this negative association only in this setting. Higher anisocytosis seems to be associated with greater morphologic alterations (shape/volume), which reduce erythrocyte deformability. The proinflammatory profile in metabolic patients can be related to the positive association of RDW with erythrocyte deformability found in these patients. However, further research is needed to explain the mechanisms underlying this association.

Famine From Feast: Low Red Cell Vitamin C Levels in Diabetes

Famine From Feast: Low Red Cell Vitamin C Levels in Diabetes

Red blood cell distribution width and erythrocyte deformability in patients with acute myocardial infarction

Increased RDW has been found to be a marker of adverse outcomes in cardiovascular disease (CVD), although the exact mechanism remains unclear. Recently, several authors have found that higher RDW is associated with decreased erythrocyte deformability, which can impair blood flow through microcirculation, a fact which may explain the increased risk for CVD events associated with elevated RDW. The aim of the present study was to investigate the association between RDW and erythrocyte deformability in patients with acute myocardial infarction (AMI). The study group comprised 60 AMI patients and 72 gender- and age-matched controls, in whom erythrocyte deformability was determined by means of the elongation index (EI) in a Rheodyn SSD, along with haematological, biochemical and inflammatory parameters. Patients showed higher RDW (p = 0.012) and lower EI (p < 0.05) than controls. When anaemic patients were removed from the study, AMI showed still lower EI than controls (p < 0.05), but no differences in RDW were observed (p = 0.141). RDW correlated inversely with haematimetric indices (p < 0.001), but not with inflammatory and biochemical parameters (p > 0.05). EI correlated inversely with Hb, MCHC (p < 0.001) and directly with MCV (p < 0.05). EI also correlated inversely with glucose (p < 0.05) and directly with HDL-cholesterol (p < 0.05). The multivariate regression model showed that only MCV and Hb were independent predictors of RDW (beta coefficients: -0.383, -0.208; p < 0.001, p = 0.050, respectively). In addition, MCV, MCHC and hyperlipidaemia were independent predictors of EI (beta coefficients: 0.366, -0.533, -0.192; p < 0.001, p < 0.001, p = 0.019 respectively). In AMI patients, increased RDW is not related with EI, so this mechanism does not seem to be responsible for an increased CDV risk in these patients.

Association of altered hemorheology with oxidative stress and inflammation in metabolic syndrome

ObjectiveWe have shown increased whole blood viscosity (WBV), decreased erythrocyte deformability, and increased erythrocyte aggregation in metabolic syndrome (MetS) in our previous study. The objective of the study was to find out if the altered hemorheology shown in MetS in our previous study is associated with chronic inflammation and oxidative stress in the same subjects.MethodsOne hundred recruited participants were classified into three groups based on the number of the MetS components present following National Cholesterol Education Program, Adult Treatment Panel III definitions. WBV, erythrocyte aggregation, erythrocyte deformability, oxidative stress markers (erythrocyte reduced glutathione (GSH), superoxide dismutase (SOD), and urinary isoprostanes), inflammatory markers high-sensitivity C-reactive protein (hsCRP), and thrombotic marker D-dimer were measured. Data were analyzed by IBM SPSS 20 software.ResultsWe found a significant association of altered hemorheology with chronic inflammation and oxidative stress in MetS. There was a linear increase in the level of hsCRP and a linear decrease in the level of SOD and GSH across the quartiles of erythrocyte aggregation. Similarly, the thrombotic marker D-dimer showed a linear increase and oxidative stress marker GSH showed a linear decrease trend across the quartiles of WBV.DiscussionAlterations of hemorheology in MetS are probably due to the effect of chronic inflammation and oxidative stress. The negative effects of chronic inflammation and oxidative stress on the cardiovascular system could be due to the resulting altered hemorheology.