Iron deficiency in stabled Dutch warmblood foals

Forty-three Dutch Warmblood foals were divided at random into 3 rearing groups immediately after birth: a box-rest group, a box-rest with exercise group, and a pasture group. All stabled foals (box-rest and exercise groups) were fed freshly cut grass harvested from the same pastures on which the pasture group foals were grazing. Blood samples were obtained monthly for CBC and biochemical analyses. At 1-3 months of age, the foals at pasture were active but the foals in the box-rest and exercise groups were listless. Mean hemoglobin concentrations, PCVs, blood iron concentrations, and saturation of total iron binding capacity were significantly lower (P < .05) in the box-rest group (11.3+/-1.2 g/dL, 33+/-3%, 123+/-67 microg/dL, and 18+/-9%) and the exercise group (11.6+/-1.5 g/dL, 34+/-4%, 101+/-61 microg/dL, and 15+/-10%) compared with the pasture group (14.0+/-0.8 g/dL, 42+/-3%, 212+/-67 microg/dL, and 32+/-10%). Oral supplementation of iron to all foals resulted in significant increases in the values of these variables in the box-rest group and exercise group at 4-5 months of age, and the stabled foals were as active as the foals at pasture. In the pasture group, no significant changes occurred. Management practices clearly influence the iron state in young growing foals from 1 to 3 months of age, and although not a frequent cause of anemia in the horse, an absolute deficit of body iron may occur in stabled foals fed freshly cut grass.     

Study on bone marrow angiogenic mediators and inhibitors in aplastic anemia

AIM: Through detecting bone marrow angiogenic mediators and inhibitors in aplastic anemia (AA) patients,the value of angionesis in AA pathogenesis was elucidated.METHODS: The patients were divided into severe AA group (SAA,8 patients),non severe AA group (NSAA,10 patients),and normal control group (7 persons),5 patients were observed before treating (group beginning) and getting improvement (group improving).The angiogenic mediators vascular endothelial growth factor (VEGF) and bFGF were detected by ELISA,angiogenic inhibitors IFN-γ and TSP were detected by ELISA and flow cytometry,respectively.RESULTS: The levels of VEGF were lower in SAA group and NSAA group than those in control group significantly (P<0.05),the levels of IFN-γ and TSP were higher than those in control group (P<0.05),especially in SAA group (P<0.01).Compared with group beginning,the level of VEGF was higher in group improving (P<0.05),the levels of IFN-γ,TSP were lower (P<0.05),there was no obviously difference between group beginning and group improving except IFN-γ.CONCLUSION: The dropping of angiogenic mediators and the rising of angiogenic inhibitors may be one reason of reducing the number of microvessel,which result in deficiency in supporting hemapoietic stem cells by bone marrow microenvironment.     

Iron Status of Cats with Chronic Kidney Disease

Background

Iron deficiency is a proposed mechanism for the anemia that occurs in cats with chronic kidney disease (CKD). Minimal research investigating the iron status of these cats has been performed.

Objective

To compare indicators of iron status in cats with CKD versus healthy cats and cats with nonrenal illness (NRI). To compare indicators of iron status in anemic versus nonanemic cats with CKD.

Animals

Thiry‐nine client or employee owned healthy cats, 40 cats with CKD and 34 cats with NRI included.

Methods

Exclusion criteria included prior iron or erythropoiesis stimulating agent administration, blood transfusion, or concurrent CKD and NRI. Complete blood counts, serum chemistries, serum iron concentrations, total iron binding capacity (TIBC), and ferritin concentrations were measured and percent transferrin saturation (TSAT) calculated on all cats. Data were analyzed using nonparametric statistical testing.

Results

No statistically significant differences were detected among groups for iron concentration (P = .50), ferritin concentration (P = .47), or TSAT (P = .19). TIBC was significantly lower in CKD (median 262 μg/dL; IQR 233–302; range 165–488) versus healthy cats (median 316 μg/dL; IQR 272–345, range 196–464); (P = .0030). When comparing anemic (hemoglobin <9.5 g/dL) versus nonanemic cats with CKD, TSAT was significantly lower (P = .033) in anemic (median 20.2%; IQR 17.8–34.5; range 17.6–35.9) compared to nonanemic (median 29.0%; IQR 25.5–44.1; range 11.5–94.4). No statistically significant differences found for ferritin concentration (P = .94), iron concentration (P = .21) or TIBC (P = .97).

Conclusions and Clinical Importance

These results indicate that an iron deficient state exists in anemic cats with CKD and is more likely functional rather than absolute.     

Anemia amelioration by lactose infusion during trypanosomosis could be associated with erythrocytes membrane de-galactosylation

African trypanosomosis is a potentially fatal disease that is caused by extracellular parasitic protists known as African trypanosomes. These parasites inhabit the blood stream of their mammalian hosts and produce a number of pathological features, amongst which is anemia. Etiology of the anemia has been partly attributed to an autoimmunity-like mediated erythrophagocytosis of de-sialylated red blood cells (dsRBCs) by macrophages. Lactose infusion to infected animals has proven effective at delaying progression of the anemia. However, the mechanism of this anemia prevention is yet to be well characterized. Here, the hypothesis of a likely induced further modification of the dsRBCs was investigated. RBC membrane galactose (RBC m-GAL) and packed cell volume (PCV) were measured during the course of experimental trypanosomosis in mice infected with Trypanosoma congolense (stb 212). Intriguingly, while the membrane galactose on the RBCs of infected and lactose-treated mice (group D) decreased as a function of parasitemia, that of the lactose-untreated infected group (group C) remained relatively constant, as was recorded for the uninfected lactose-treated control (group B) animals. At the peak of infection, the respective cumulative percent decrease in PCV and membrane galactose were 30 and 185 for group D, and 84 and 13 for group C. From this observed inverse relationship between RBCs membrane galactose and PCV, it is logical to rationalize that the delay of anemia progression during trypanosomosis produced by lactose might have resulted from an induction of galactose depletion from dsRBCs, thereby preventing their recognition by the macrophages.     

鸡贫血因子病的血液病理学变化

本实验用鸡贫血病毒感染１日龄健康ＡＡ雏鸡，以未感染雏鸡为对照，在感染后７、１４、２８、３５、４２日龄检测其外周血液各种血细胞数量，血红蛋白含量，红细胞压积，红细胞平均体积，红细胞平均血红蛋白量、红细胞平均血红蛋白浓度；骨髓红系祖细胞、粒单系祖细胞（ＣＵＦ－ＧＭ）、基质成纤维祖细胞（ＣＦＵ－Ｆ）的增殖功能；血清因子和胞腺集落刺激因子（ＣＳＦ）对造血祖细胞增殖功能的影响；骨髓造血细胞分化功能；骨髓造血     

Recognition and classification of dysmyelopoiesis in the dog: a review

Dysmyelopoiesis is defined as a hematologic disorder characterized by the presence of cytopenias in the blood and dysplastic cells in one or more hematologic cell lines in the blood or bone marrow. The causes of dysmyelopoiesis include acquired mutations in hematopoietic stem cells (i.e., myelodysplastic syndromes [MDSs]), congenital defects in hematopoiesis, and dysmyelopoietic conditions associated with various disease processes, drug treatments, or toxin exposure. Two major subtypes of MDSs (i.e., MDS with refractory cytopenias and MDS with excess myeloblasts) have been described that differ in clinical presentation, response to treatment, and survival time. The most frequently occurring causes of secondary dysmyelopoiesis include immune-mediated hematologic diseases, lymphoid malignancies, and exposure to chemotherapeutic drugs. Differentiation of the various causes of dysmyelopoiesis is essential for establishing an appropriate therapeutic plan and for determining prognosis.     

Preliminary studies of serum acute-phase protein concentrations in hematologic and neoplastic diseases of the dog

Serum concentrations of acute-phase proteins (APPs): haptoglobin (Hp), ceruloplasmin (Cp), serum amyloid A (SAA), and C-reactive protein (CRP) were determined in healthy dogs (n = 15) and dogs with different diseases grouped as acute inflammation (I, n = 12), hematologic neoplasias (HT, including leukemia and lymphoma, n = 16), nonhematologic neoplasias (NHT, including epithelial, mesenchymal, and mixed, n = 20), and autoimmune hemolytic anemia (AIHA, n = 8). SAA and CRP were analyzed using commercially available enzyme-linked immunosorbent assay (ELISA) kits, and Hp and Cp were measured using colorimetric methods, all previously validated for use in dogs. Increased concentrations of all APPs were observed in all groups of diseased dogs, but statistical significance only was observed with Hp (I, P < .001; HT, P < .05), Cp (I, P < .05; AIHA, P < .01), and CRP (I, P < .001; HT, P < .001; AIHA, CRP P < .05). High variability in individual APPs within each group of diseases was found with no significant differences between leukemia and lymphoma as well as among different types of neoplasia. The AIHA group had smaller increases in Hp, SAA, and CRP but higher concentrations of Cp. When follow-up of individual cases was possible, a decrease in APPs generally was found in cases with favorable outcome. The results of this study suggest that neoplasia and hematologic diseases such as AIHA should be considered as possible causes of mild increases in APPs in dogs. Measurement of APPs may be helpful to assess clinical evolution and monitor treatment of these processes.