Reduction In Erythrocyte Count Research Articles

Determination of the Toxic Dose of Experimental Lead Poisoning for Male Goats in Fallujah City, Iraq

This study aimed to induce lead poisoning experimentally in male goats to determine the toxic dose and investigate it is effects on hematological parameters, and the functions of the liver and kidney. The experiment was performed on 15 male goats, aged between 3 – 5 months with a mean weighing 13±0.65 kg. Goats were divided into five equal groups, the first represented the control group given tap water, while the other groups were given orally (by stomach tube) 70,100,200 and 400 mg/kg B.W. of lead acetate respectively, for 5 days. Blood was collected weekly for 4 weeks to estimate the concentrations of lead, hematological and biochemical analysis. The results indicated a significantly (P≤0.05) increase of lead(0.738±0.07ppm), only in goats which received 400 mg Pb/kg B.W of lead with symptoms included: depression, dullness, anemia, muscle twitching, staggering, and teeth grinding, with a significant reduction in erythrocyte count, packed cell volume, and hemoglobin 10.391±0.41*106/ml, 25.5±0.55%, and 8.30±0.19g/dl respectively, compared with the control ones. Also, increase in total white blood cell count to 9.098±0.08*103/ml, neutrophils 39.07±0.93%, monocytes 1.88±0.07%, and eosinophils 4.82±0.05%. The same group results showed significant elevations in the activities of liver enzymes; ALT 59.9±0.20u/l, AST 243±1.3u/l, in addition, the serum levels of creatinine and urea were also increased indicating renal frailer 1.96±0.05 mg/dl and 29.78±0.34 mg/dl respectively. In summary, this is the first study that proved the toxic dose of lead poisoning for male goats in Iraq and estimate their hazardous results on the hematological and chemobiological analyses on goats.

The Effects of Dextran on Postoperative Thrombosis and Hemodilution in Microvascular Head and Neck Reconstruction.

Free tissue transfer is an integral part of reconstructive head and neck surgery today. Although increased experience and refinements in techniques have minimized flap loss, pharmacological agents have been used to prevent thrombus formation and flap failures, despite their questionable effectiveness. The aim of this study is to investigate the use of dextran 40 in thrombosis prophylaxis, as well as its effects on blood coagulability and flap survival. This is a retrospective analysis of 176 free flaps performed at University Hospital Dubrava, Zagreb, Croatia, during a 4-year period. A comparison was made between 2 patient groups, based on their respective postoperative prophylaxis protocols. All patients were treated with low-molecular-weight heparin as deep vein thrombosis prevention, until patient mobilization. Group 1 was on dextran 40 protocol, whereas group 2 did not receive additional treatment. Primary outcome of the study was determined as flap loss rate, whereas secondary outcome was evaluated as the rate of thrombosis or hemorrhage. The hemodilution potential of dextran 40 was examined through blood count laboratory values. Total flap survival rate was 90.34%. There were 16 free flap losses and 1 partial loss overall. Anastomoses were re-explored in a total of 27 cases, of which 17 were salvaged. There were 29 events of hemorrhage or arterial or venous thrombosis: 17 in group 1 and 12 in group 2. A sum of 26 incidences of other postoperative complications was recorded, 13 in each group. Hemodilution status showed a statistically significant reduction in erythrocyte count and hemoglobin and hematocrit levels in the group receiving dextran 40, on postoperative days 1 and 3, but no such effect was observed on postoperative platelet count. Although dextran 40 has been shown to have a valuable effect on hemodilution, which is beneficial in microsurgery, it did not demonstrate better outcomes in terms of flap survival. Because it can cause serious systemic complications, it is better not to administer it routinely. However, its important influence on reduction in erythrocyte count and hemoglobin and hematocrit levels should be further investigated.

Mechanisms responsible for reduced erythropoiesis during androgen deprivation therapy in men with prostate cancer.

Androgen deprivation therapy (ADT) is a mainstay of treatment for prostate cancer (PCa). As androgens stimulate erythropoiesis, ADT is associated with a reduction in hematocrit, which in turn contributes to fatigue and related morbidity. However, the mechanisms involved in ADT-induced reduction in erythropoiesis remain unclear. We conducted a 6-mo prospective cohort study and enrolled men with PCa about to undergo ADT (ADT-Group) and a control group of men who had previously undergone prostatectomy for localized PCa and were in remission (Non-ADT Group). All participants had normal testosterone levels at baseline. Fasting blood samples were collected at baseline, 12 wk, and 24 wk after initiation of ADT; samples were obtained at the same intervals from enrollment in the Non-ADT group. Blood count, iron studies, erythropoietin, erythroferrone, and hepcidin levels were measured. Seventy participants formed the analytical sample (31 ADT, 39 Non-ADT). ADT was associated with a significant reduction in erythrocyte count (estimated mean difference = -0.2×106 cells/µl, 95%CI = -0.3 to -0.1×106 cells/µl, P < 0.001), hematocrit (-1.9%, 95%CI = -2.7 to -1.1%, P < 0.001), and hemoglobin (-0.6 g/dl, 95%CI = -0.8 to -0.3 g/dl, P < 0.001). Serum hepcidin concentration increased in the ADT-group (18 ng/ml, P < 0.001); however, iron concentrations did not change (-1.1 µg/dl, P = 0.837). Ferritin levels increased in men on ADT (60 ng/ml, P < 0.001). Iron binding capacity, transferrin saturation, erythroferrone, and erythropoietin did not change. Nine men undergoing ADT developed new-onset anemia. In conclusion, reduced proliferation of marrow erythroid progenitors leads to ADT-induced reduction in erythropoiesis. Future studies should evaluate the role of selective androgen receptor modulators in the treatment of ADT-induced anemia.

Influence of blood donation on the incidence of plateau at $$ \dot{V}{\text{O}} $$ V ˙ O 2max

The purpose of this study was to examine the effects of reductions in blood volume and associated oxygen-carrying capacity on the incidence of plateau at $$\dot{V}{\text{O}}$$ 2max. Fifteen well-trained athletes (age 23.3 ± 4.5; mass 77.4 ± 13.1 kg, height 180.1 ± 6.0 cm) completed three incremental cycle tests to volitional exhaustion, of which the first was defined as familiarisation, with the remaining two trials forming the experimental conditions of pre- (UBL) and post-(BLE) blood donation (~450 cm3). The work rate for the incremental tests commenced at 100 W for 60 s followed by a ramp of 0.42 W s−1, with cadence being held constant at 80 rpm. Throughout all trials, $$\dot{V}{\text{O}}$$ 2 was determined on a breath-by-breath basis using a pre-calibrated metabolic cart. The criteria for plateau determination was a ∆ $$\dot{V}{\text{O}}$$ 2 ≤ 50 ml min−1 over the final two consecutive 30 s sampling periods. Despite a significant (P = 0.0028) 9.4 % reduction in haemoglobin concentration and 10.8 % (P = 0.016) reduction in erythrocyte count between UBL and BLE, there was no change in plateau incidence. However, significant differences were observed for both $$\dot{V}{\text{O}}$$ 2max (P = 0.0059) 51.3 ± 7.6 (UBL) 48.4 ± 7.9 ml kg−1 min−1 (BLE) and gas exchange threshold arrival time 383.4 ± 85.2 s (UBL) 349.2 ± 71.4 s (BLE) (P = 0.0028). These data suggest that plateau at $$\dot{V}{\text{O}}$$ 2max is unaffected by O2 availability lending support to the notion of the plateau being dependent on the anaerobic capacity and the classically orientated concept of $$\dot{V}{\text{O}}$$ 2max.

Hematological Profile and Martial Status in Rugby Players during Whole Body Cryostimulation

Cold-based therapies are commonly applied to alleviate pain symptoms secondary to inflammatory diseases, but also to treat injuries or overuse, as done in sports rehabilitation. Whole body cryotherapy, a relatively new form of cold therapy, consists of short whole-body exposure to extremely cold air (−110°C to −140°C). Cryostimulation is gaining wider acceptance as an effective part of physical therapy to accelerate muscle recovery in rugby players. The aim of this study was to evaluate the effect of repeated cryostimulation sessions on the hematological profile and martial status markers in professional rugby players. Twenty-seven professional rugby players received 2 daily cryostimulation treatments for 7 consecutive days. Blood samples were collected before and after administration of the cryotherapic protocol and hematological profiles were obtained. No changes in the leukocyte count or composition were seen. There was a decrease in the values for erythrocytes, hematocrit, hemoglobin and mean corpuscular hemoglobin content, and an increase in mean corpuscular volume and red cell distribution width. Platelet count and mean volume remained unchanged. Serum transferrin and ferritin decreased, while soluble transferrin receptor increased. Serum iron and transferrin saturation were unchanged, as was reticulocyte count, whereas the immature reticulocyte fraction decreased substantially. In conclusion, in this sample of professional rugby players, cryostimulation modified the hematological profile, with a reduction in erythrocyte count and hemoglobinization paralleled by a change in martial status markers.

Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia

BackgroundThe heritable haemoglobinopathy α+-thalassaemia is caused by the reduced synthesis of α-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for α+-thalassaemia have microcytosis and an increased erythrocyte count. α+-Thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with α+-thalassaemia homozygosity provide a haematological benefit during acute malaria.Methods and FindingsData from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by α+-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of ∼1.5 × 1012/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for α+-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 × 1012/l as a result of the reduced mean cell Hb in homozygous α+-thalassaemia. In addition, children homozygous for α+-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA. We estimated that the haematological profile in children homozygous for α+-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24–1.12, p = 0.09).ConclusionsThe increased erythrocyte count and microcytosis in children homozygous for α+-thalassaemia may contribute substantially to their protection against SMA. A lower concentration of Hb per erythrocyte and a larger population of erythrocytes may be a biologically advantageous strategy against the significant reduction in erythrocyte count that occurs during acute infection with the malaria parasite Plasmodium falciparum. This haematological profile may reduce the risk of anaemia by other Plasmodium species, as well as other causes of anaemia. Other host polymorphisms that induce an increased erythrocyte count and microcytosis may confer a similar advantage.

Inhibition of murine AIDS by a new azidothymidine homodinucleotide.

A new antiretroviral drug (azidothymidine homodinucleotide, AZTp2AZT), designed for the protection of macrophages against retroviral infection, was evaluated in a murine retrovirus-induced immunodeficiency model of AIDS (MAIDS) alone and in combination with oral azidothymidine (AZT). C57BL/6 mice were infected with the retroviral complex LP-BM5 and treated for 3 months by weekly administrations of 15 nmol of AZTp2AZT encapsulated into autologous erythrocytes for macrophage protection. AZTp2AZT treatment was found to reduce lymphoadenopathy (48%), splenomegaly (26%), and BM5d proviral DNA content in lymph nodes, spleen, and brain of 37%, 40%, and 36%, respectively, compared with untreated animals. AZT administration in drinking water (0.25 mg/ml) was more effective than administration of AZTp2AZT encapsulated into erythrocytes in reducing lymphoadenopathy, splenomegaly, gammaglobulinemia, and proviral DNA content in lymph nodes, but it caused a reduction in erythrocyte count and hematocrit levels. Although combined treatments do not provide additive responses in the several parameters investigated, they were found to be much more effective in reducing the proviral DNA content in brain (67%) than were monotherapies. Furthermore, no apparent signs of hematotoxicity were observed. Thus, macrophage delivery of antiviral drugs may contribute to brain protection from retroviral infections by mechanisms other than those exerted by oral AZT administration.

Negligible contribution of splenic erythropoiesis to recovery from anemia in rats.

The contribution of extramedullary erythropoiesis in the spleen during recovery from anemia was examined in rats. Six- and 18-week-old female Wistar rats were subjected to a total splenectomy or sham-splenectomy, and anemia was induced by bleeding the next day. Removing approximately 20% of the total volume of blood in the body resulted in a 9-26% reduction in erythrocyte count, hematocrit, and hemoglobin 3 days after bleeding, but the values returned to normal within 8 days of bleeding in young rats and within 14 days of bleeding in adult rats. Histology, image analysis, and differential cell counts revealed a marked increase in erythropoiesis in the spleen and femoral bone marrow in shamsplenectomy rats after bleeding; however, there were no statistical differences in hematology or bone marrow histology between the splenectomy and sham-splenectomy groups. These results indicate that the contribution of splenic erythropoiesis to the recovery from anemia was negligible in both young and adult rats.

Polychlorinated biphenyl-induced alteration of biologic parameters in the rat

Aroclor 1242, a commercial polychlorinated biphenyl (PCB) mixture, was administered ip to rats for 10 weeks. Principal findings included: loss of body weight; hepatic and renal damage, with some animals exhibiting renal papillary epithelial hyperplasia; slight reduction in erythrocyte count, diameter, and hemoglobin content, with an elevation in serum iron; diminished plasma corticosteroid and glucose concentrations; increased urinary excretion of protein, sugars, and coproporphyrin. The effect of PCBs on several hepatic microsomal enzymatic parameters was also evaluated. Maximal hydroxylation and N-demethylation activities were observed 3–10 days following a single ip injection (100 mg/kg). Each remained significantly higher than control values after 20 days, with hydroxylation activity still 150% of controls after 40 days. The minimal effective single dose for induction of hydroxylation activity was approximately 5 mg/kg. Induction of hydroxylation activity was found to be dose-dependent; however, a smaller degree of correlation was noted between N-demethylation activity and dose. Values for cytochromes P 450 and b 5 and NADPH-cytochrome c reductase activity were observed to roughly parallel hydroxylation and N-demethylation activities, the highest degree of correlation was manifest between enzymatic activity and cytochrome P 450 values.