anemia of chronic disease

The article presents modern data on the etiology, pathogenesis, diagnosis, prevention and treatment of iron deficiency anemia (IDA) and anemia of chronic disease, as well as their combination on the eve of and during pregnancy. The emphasis is made on the role of iron deficiency of any etiology in the development of obstetric and perinatal complications, especially its impact on the central nervous system formation and further psychophysical child development. Need for prevention of iron deficiency states in risk groups which includes all women of reproductive age who have menstruation is shown based on evidence-based medicine data. Effectiveness and safety of modern drugs containing iron in oral and parenteral forms has analyzed. The paper presents data on the safety and effectiveness of an innovative form of ferric iron in the form of liposomal iron, which differs in the mechanism of action, digestibility and the absence of side effects typical for this group of drugs.

According to various authors the frequency of IDA in pregnant women ranges up to 80%, in puerperas up to 40%. It is unimpossible to stop IDA without iron supplementation only with an iron-rich diet. Two main groups of iron preparations are used to correct iron deficiency differing in the valence of iron atoms – bivalent iron salts and trivalent complexes. These drugs differ in the tolerability and bioavailability of atomic iron. Liposomal iron is a new drug for treatment of iron deficiency and IDA today; it has an innovative way of iron delivery to the body. Liposomal iron has advantages for the prevention of anemia in patients with anemia of chronic disease or its combination with IDA (inflammatory bowel diseases, obesity, after resection of the stomach and intestines, etc.). An innovative form of liposomal iron in Ukraine is represented by a dietary supplement Ferroview containing 30 mg of elemental iron, that is corresponds to the average prophylactic dose recommended in WHO documents

The cause of the anemia associated with chronic, intermittent, asymptomatic, low-level parasitemia in children in malaria-endemic endemic areas is not well understood. Nitric oxide (NO) decreases erythropoiesis, and it is likely an important mediator of anemia of chronic disease. Production of NO is decreased in acute uncomplicated and cerebral malaria, but it is increased in asymptomatic Tanzanian children (with or without parasitemia). We hypothesized that chronic overproduction of NO in these asymptomatic children contributes to the anemia associated with subclinical/subpatent malaria. In 44 fasting, asymptomatic, malaria-exposed, Tanzanian children, NO production (measured using fasting urine NOx excretion) was inversely associated with hemoglobin concentration (P = 0.03, controlling for age and gender). Using multiple linear regression, hemoglobin concentration was negatively associated with parasitemia (P = 0.005). After controlling for age and parasitemia, NO was no longer an...

Correspondence and Reprint requests : Dr Sunita Sharma, D-10/ Sector 27, Noida (UP)-201301, India. [DOI-10.1007/s12098-009-0302-z] [Received April 10, 2009; Accepted August 19, 2009] ... Evaluation of Serum Transferrin Receptor and sTfR Ferritin

Various human disorders are associated with misdistribution of iron within or across cells. Friedreich ataxia (FRDA), a deficiency in the mitochondrial iron-chaperone frataxin, results in defective use of iron and its misdistribution between mitochondria and cytosol. We assessed the possibility of functionally correcting the cellular properties affected by frataxin deficiency with a siderophore capable of relocating iron and facilitating its metabolic use. Adding the chelator deferiprone at clinical concentrations to inducibly frataxin-deficient HEK-293 cells resulted in chelation of mitochondrial labile iron involved in oxidative stress and in reactivation of iron-depleted aconitase. These led to (1) restoration of impaired mitochondrial membrane and redox potentials, (2) increased adenosine triphosphate production and oxygen consumption, and (3) attenuation of mitochondrial DNA damage and reversal of hypersensitivity to staurosporine-induced apoptosis. Permeant chelators of higher...

Anemia is a well-established infection-associated immunopathological feature of trypanosomiasis and the degree of the anemia is a reliable indicator of the severity of infection. Since infections with trypanosomes triggers a strong cytokine production and a type I immune response, the trypanosome-elicited anemia may be type I cytokine driven. This type of anemia termed anemia of chronic disease is characterized by an imbalance between erythrophagocytosis and erythropoiesis that is linked to a perturbed iron homeostasis including altered iron recycling by macrophages and iron sequestration. To further unravel the mechanisms underlying trypanosome-elicited anemia the expression profile of genes involved in erythrophagocytosis, uptake of iron-containing complexes and iron homeostasis was performed during the acute and chronic phase of experimental Trypanosoma brucei infections in a murine model. The results suggest that liver-associated erythrophagocytosis mediated by cytokine-activated macrophages (M1 cells) is the most likely main initiating event of aggressive anemia during the acute phase of infection. Persistence of strong type I cytokine production during the chronic phase of infection leads to hyper-activated M1 cells and a more progressive anemia. RT-PCR analysis of liver tissue demonstrates a strong increase of cell surface receptors involved in uptake of RBC and iron-containing compounds. For genes involved in iron processing we found an increase of ferroportin-1 (FPN-1), transferrin (Tf) and ceruloplasmin (CP) only in the acute phase, suggesting that export of iron is hampered in the chronic phase of infection. Our results suggest that in the chronic phase of trypanosomiasis, the iron-processing pathway is skewed towards iron sequestration, as evidenced by increased ferritin expression, while enhanced uptake of RBC/iron-containing compounds is maintained.

Background: The factors contributing to blood trans- fusions in patients with anemia of chronic disease are not well documented in the literature. We analyzed all blood transfusion events within a single oncology practice to determine if certain chemotherapy drugs, cancer types, or other factors necessitated more frequent transfusions. Patients and Methods: Out of 331 patients receiving chemotherapy, 103 (31%) patients

BACKGROUND: Hematological abnormalities are a common complication of HIV infection. These abnormalities increase as the disease advances. Bone marrow abnormalities occur in all stages of HIV infection. METHODS: Two hundred HIV infected individual were screened for hematological abnormalities from March 2007–March 2008. Absolute CD4 cell count analysis was carried out by flowcytometry. Depending on the results of the primary screening

BACKGROUND: Hematological abnormalities are a common complication of HIV infection. These abnormalities increase as the disease advances. Bone marrow abnormalities occur in all stages of HIV infection. METHODS: Two hundred HIV infected individual were screened for hematological abnormalities from March 2007–March 2008. Absolute CD4 cell count analysis was carried out by flowcytometry. Depending on the results of the primary screening

p38 mitogen-activated protein kinase (MAPK) activates a number of heat shock proteins (HSPs), including HSP27 and αB-crystallin, in response to stress. Activation of HSP27 or αB-crystallin is known to protect organs/cells by increasing the stability of actin microfilaments. Although our previous studies showed that 17β-estradiol (E2) improves cardiovascular function after trauma-hemorrhage, whether the salutary effects of E2 under those conditions are mediated via p38 MAPK remains unknown. Male rats (275–325 g body wt) were subjected to soft tissue trauma and hemorrhage (35–40 mmHg mean blood pressure for ∼90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were injected intravenously with vehicle, E2 (1 mg/kg body wt), E2 + the p38 MAPK inhibitor SB-203580 (2 mg/kg body wt), or SB-203580 alone, and various parameters were measured 2 h thereafter. Cardiac functions that were depressed after trauma-hemorrhage were returned to normal levels by E2 administratio...

We determined serum ferritin, C-reactive protein (CRP), fibrinogen, and the erythrocyte sedimentation rate (ESR) in 73 patients with anemia of chronic disease. Nomograms of CRP, ESR, or fibrinogen vs ferritin concentrations were constructed and used to estimate the iron store in bone marrow. Iron stores estimated from the nomograms were compared with the results of staining cytological bone marrow smears for iron, the reference method for evaluating iron in bone marrow. In contrast to the results of Witte et al. (Clin Chem 1985;31:1011; Am J Clin Pathol 1986;85:202-6 and 1988;90:85-7), we observed that nomograms of CRP, fibrinogen, or ESR (i.e., acute-phase reactants not influenced by changes in iron metabolism) vs ferritin are not suitable to correct for the acute-phase component of changes in ferritin concentrations. For ferritin concentrations less than 70 micrograms/L, we found that iron deficiency, as judged from bone marrow iron stain, apparently was always present.