Development Of Anemia In Patients Research Articles

ERYTHROPOIETIN SYNTESIS IN PATIENTS WITH CHRONIC HEART FAILURE DEPENDING ON COMORBID PATHOLOGY

Introduction. Decreased production of erythropoietin by the kidneys plays crucial role in the development of anemia in patients with chronic heart failure, especially on the background of comorbid diabetes mellitus type 2. In diabetic patients due to early damage of the kidney vessels and following erythropoietin deficiency anemia develops much earlier than clinically significant decrease of glomerular filtration rate.
 The aim of the study was to find out possible dependence of changes in the erythropoietinsynthesizing function of the kidneys on the degree of severity of anemic hypoxia in elderly and senile patients with chronic heart failure, including those with comorbid type 2 diabetes mellitus.
 Materials and methods. 120 patients with chronic heart failure of ischemic origin, type 2 diabetes mellitus and mild and moderate anemia were examined. Control group comprised 12 people with chronic heart failure without comorbid pathology. The examined groups were comparable in terms of gender and age, differing in the presence of comorbid diabetes mellitus and degree of severity of anemic syndrome. The level of erythropoietin in blood serum was determined by standard enzymelinked immunosorbent assay.
 Results. Type 2 diabetes mellitus in patients with chronic heart failure results in a significant decrease in erythropoietin production by 25 % compared to the control group (p<0,05). Comorbid to heart failure anemia leads to an increase in the level of erythropoietin by 74,4 % (р<0,05), and in the case of chronic heart failure and type 2 diabetes mellitus on the background of concomitant anemia – only by 39,5 % (р<0,05). As the severity of anemia in patients with chronic heart failure without diabetes progresses, the severity of the compensatory response of the kidneys to chronic anemic hypoxia is significantly higher than in patients with heart failure and comorbid type 2 diabetes.
 Conclusions. Diabetic nephropathy in patients with chronic heart failure and comorbid anemia leads to a significant deterioration of the erythropoietin-synthesizing function of the kidneys, complicating the course of both main and comorbid diseases.

Factors for the development of anemia in patients with newly introduced olaparib: A retrospective case-control study.

Anemia is the most common dose-limiting toxicity of olaparib. However, few studies have analyzed the clinical features of olaparib-induced anemia. This study investigated the clinical features of olaparib-induced anemia. Additionally, the role of folate or vitamin B12 in olaparib-induced anemia was examined. This retrospective case-control study included patients who received olaparib at Mie University Hospital between January 2018 and December 2020. Data were collected between initiation of olaparib and discontinuation of olaparib or till December 2021. We investigated the development of grade ≥ 3 anemia during olaparib administration for at least 1 year. We examined patients with grade ≥ 3 anemia considering the mean corpuscular volume (MCV), its association with gastrointestinal events and cumulative dose of carboplatin. For the sub-study analysis, data on patients treated with olaparib for ovarian or endometrial cancer were collected to evaluate the Common Terminology Criteria for Adverse Events (CTCAE) or monthly changes in folate or vitamin B12 levels from baseline to 3 months after olaparib initiation. These data were collected between initiation of olaparib and discontinuation of olaparib or till November 2022. Patients with no data on folic acid or vitamin B12 levels were excluded from the sub-study. In the main study, 40 patients were included. Eighteen patients (45%) developed grade ≥ 3 anemia, and all patients discontinued treatment (94%) or reduced olaparib dose (67%) after developing anemia. Among the patients with grade ≥ 3 anemia, 9 (50%) exhibited macrocytic anemia and 15 (83%) had previously received carboplatin. The incidence of grade ≥ 2 dysgeusia was significantly higher in patients with grade ≥ 3 anemia (P = .034). Moreover, the cumulative dose of previously administered carboplatin was higher in patients who had 3 episodes of anemia (P = .102). In sub-study, 12 had data on folic acid and vitamin B12 levels. Sub-study analysis showed that none fulfilled the criteria for deficiency of folate or vitamin B12, while 3 developed grade 3 anemia. This study revealed that olaparib-induced anemia frequently occurs as macrocytic and normocytic erythroblastic anemia without folate or vitamin B12 deficiencies. A high cumulative dose of previously administered carboplatin and dysgeusia may be associated with olaparib-induced anemia.

Chronic kidney disease and anemia: updated management issues

Anemia is common in patients with chronic kidney diseases (CKD). It is a common complication of advanced CKD. Its prevalence in CKD stage 5 populations is over 50%. The hormone “erythropoetin” (EPO) secreted by the kidneys is essential in the maintenance of adequate hemoglobin in human body. Scientific Presentation BJM Vol. 34 No. 2(1) Suppliment 2023 177 Apart from failure of EPO secretion, many other factors including chronic inflammation, uremic bone marrow suppression, hyperparathyroidism, poor absorption of substrates from the uremic gastrointestinal tract etc. contribute to development of anemia in patients living with advanced kidney failure and dialysis. Iron deficiency state due to absolute or relative iron deficiency is common in CKD population. Furthermore, nutritional anemia is common in general population in our part of the world. Majority of this is also a result of iron deficiency. Replenishing iron stores in the body is the first strategy in the management of this condition. Besides the use of iron, deficiencies of other substrates like vitamin B12 should also be taken into account while managing anemia in CKD. Ferric citrate can be used as an hematinic and phosphate binder as well. Blood transfusion was invariable treatment strategy in the remote past. Though oral and parenteral iron and other hematinics are routinely used in the management of CKD, various erythropoesis stimulating agents (ESAs) used as injectable solutions lead the current therapeutic strategy in the treatment of anemia in patients with end stage renal disease (ESRD) and renal replacement therapies. More recently newer agents, the prolylhydroxylase inhibitors (PHI) like roxadustat which act as hypoxic ischemic factor (HIF) stabilizers have been more appealing to the patients and the clinicians. In contrast to the parenteral administration of ESAs, these new agents can be administered orally. While anemia is common, ideal treatment for anemia in CKD is still unsolved riddle and demands further research. Bangladesh J Medicine 2023; Vol. 34, No. 2(1) Supplement: 177-178

Severe iron-deficiency anaemia in a patient with heart failure: A case report and review of the literature

Background: Anaemia of different etiologies, but also iron deficiency without anaemia, worse symptoms and prognosis of patients with heart failure or coronary artery disease. Development of anemia in patients with chronic heart failure is multifactorial, one of most important mechanism being chronic inflammatory activation that impairs iron metabolism.

Erythropoietin Resistance Development in Hemodialysis Patients: The Role of Oxidative Stress.

Oxidative stress (OS) is considered a significant risk factor for the development of anemia in patients treated by regular hemodialysis (HD). Moreover, OS represents a risk factor for the development of erythropoietin (EPO) resistance in these patients. The aim of this study was to examine the role of OS regarding EPO resistance development in patients treated by regular HD. 96 patients treated with standard HD and on-line hemodiafiltration were included in this study. The patients were treated with short-acting and long-acting EPOs for anemia. The concentration of superoxide anion radical, hydrogen peroxide, thiobarbituric acid reactive substances, and nitric oxide in the form of nitrites and the activity of catalase, superoxide dismutase and reduced glutathione were measured in patients' blood spectrophotometrically. Standard biochemical analysis, inflammatory markers, nutritional status, HD parameters, and erythropoietin resistance index were also determined. Patients with resistance to short-acting EPO had significantly lower concentration of hemoglobin in the blood and hematocrit value, a significantly higher serum ferritin concentration, and significantly lower catalase activity in erythrocytes than patients without EPO resistance. Patients with resistance to long-acting EPO have a significantly lower hemoglobin concentration in the blood, hematocrit values, and serum concentration of prealbumin and vitamin D, as well as significantly higher concentration of C-reactive protein, superoxide anion, and hydrogen peroxide concentration than those without resistance. OS significantly contributes to EPO resistance development. OS, higher ferritin and CRP levels, lower hemoglobin, hematocrit and prealbumin levels, and vitamin D deficiency represent significant risk factors for EPO resistance development in HD patients.

A common symptom of anemia in diabetic nephropathy

In the progression of diabetic nephropathy, considerable attention is paid to the development of anemia. A significant reason for the development of anemia in patients with diabetes mellitus (DM) with diabetic nephropathy is a decrease in the production of erythropoietin in the per tubular cells of the proximal enthrone. Anemia predominates in patients with diabetic nephropathy, it is associated with cardiovascular disease, retinopathy. Anemia begins to develop long before the violation of the filtration function of the kidneys.

Erythropoietin Resistance in Hemodialysis Patients

Summary Anemia is defined as blood hemoglobin concentration of less than 120 g/l in women and less than 130 g/l in men. The main cause of the development of anemia in patients treated with regular hemodialysis is the lack of endogenous erythropoietin, and its main clinical consequences are: progressive decline in residual renal function, development of cardiovascular disorders, disorders of cognitive functions and a decrease in the quality of life of these patients. Despite the administration of an appropriate dose of erythropoietin, in 5-10% of patients treated with regular hemodialysis, there is resistance to erythropoietin activity. The main risk factors for the development of resistance to the effects of erythropoietin are: iron deficiency, microinflammation, deficiency of vitamin D, secondary hyperparathyroidism, deficiency of vitamin C, and inadequate hemodialysis. The main side effects of erythropoietin are: hypertension, thrombosis of the vascular approach to hemodialysis, and the red blood cell precursor aplasia in the bone marrow. Early detection and elimination of risk factors, optimization and indi-vidualization of hemodialysis prescription prevent the development of resistance to erythropoietin activity, enable the achievement of target blood hemoglobin, reduce the development of cardiovascular morbidity, and improve the quality of life of these patients.

ВЛИЯНИЕ МАГНИТНОЙ ОБРАБОТКИ КРОВИ НА НЕКОТОРЫЕ МЕХАНИЗМЫ КОРРЕКЦИИ АНЕМИИ У ПАЦИЕНТОВ С СЕПСИСОМ ПРИ ПРОВЕДЕНИИ ЭКСТРАКОРПОРАЛЬНОГО ОЧИЩЕНИЯ КРОВИ

Background. Anemia is rather common in patients with sepsis and is associated with depression of erythropoiesis by septic mediators.Aim. To study the effect of magnetic treatment of blood on the mechanisms of anemia correction in patients with sepsis.Material and methods. Laboratory parameters of 232 patients with sepsis were under analysis. Magnetic treatment of blood was carried out using the apparatus «HemoSPOK» (Magnomed, Belarus).Results. The use of magnetic blood treatment did not lead to the decrease in the number of erythrocytes (before treatment – 3.63 (3.0; 4.42)×1012/l, after – 3.47 (3.18; 3.62)×1012/l, p=0.916512) and hemoglobin level (before treatment – 109.5 (92.0; 129.0) g/l, after – 106.9 (91.0; 113.0) g/l, p=0.776105). The concentration of iron in blood increased from 5.83 (4.21; 7.13) to 10.0 (6.03; 13.80) μmol/l (p=0.027993). There was a simultaneous rise in ferritin from 210.3 ( 20.5; 311.6) to 545.1 (250.2; 813.2) ng/ml (p=0.027709).Conclusion: Magnetic treatment of blood prevents the development of anemia in patients with sepsis.

P191 RISING INCIDENCE OF IRON DEFICIENCY ANEMIA AND ASSOCIATED COST OF CARE IN HOSPITALIZED PATIENTS OF INFLAMMATORY BOWEL DISEASE IN USA: NATIONWIDE ANALYSIS 2002–2014

Extraintestinal complications are common in IBD, and are reported in more than 25% of patients. Anemia is one of the most common manifestations of IBD. One-third of patients with IBD have hemoglobin levels below 12 g/dL. Although ongoing blood loss from chronically inflamed intestinal mucosa and micronutrient deficiency (iron and B12) are the main mechanisms underlying the development of anemia in patients with IBD, chronic inflammation, hemolysis, and medication-induced myelosuppression may also play important roles. We analyzed the National Inpatient Sample (NIS) database for all subjects with discharge diagnosis of IBD (Ulcerative Colitis & Crohn’s disease) with or without iron deficiency anemia (IDA) as primary or secondary diagnosis via ICD 9 codes during the period from 2002–2014. All analyses were performed with the use of SAS (version 9.4). From 2002–2014 there were total 23834 discharges of Ulcerative Colitis (UC) patients and 31998 discharges of Crohn’s Disease (CD) patients with IDA, constituting 9.8% & 7.4% discharges respectively. There was a rising trend of IDA in percentage of discharged patients of IBD from 7.4% in 2002 to 9.2% in 2014. Over the years the median length of stay decreased for IBD patients with and without IDA, but still the length of stay was more in IBD patients with IDA vs without IDA. On Multivariate regression analysis Male gender, age above 50, Hispanic race, small hospital, congestive heart failure, malignancy and metastatic disease were significant predictors of IDA in IBD. This analysis demonstrates the burden of IDA in patients of IBD. In a patient population with the predisposition for anemia, like patients with IBD, early diagnosis and management of iron deficiency can promptly reduce hospital visits, improve quality of life, reduce loss of work, and, ultimately, lower health care costs.

P191 RISING INCIDENCE OF IRON DEFICIENCY ANEMIA AND ASSOCIATED COST OF CARE IN HOSPITALIZED PATIENTS OF INFLAMMATORY BOWEL DISEASE IN USA: NATIONWIDE ANALYSIS 2002-2014

Extraintestinal complications are common in IBD, and are reported in more than 25% of patients. Anemia is one of the most common manifestations of IBD. One-third of patients with IBD have hemoglobin levels below 12 g/dL. Although ongoing blood loss from chronically inflamed intestinal mucosa and micronutrient deficiency (iron and B12) are the main mechanisms underlying the development of anemia in patients with IBD, chronic inflammation, hemolysis, and medication-induced myelosuppression may also play important roles. We analyzed the National Inpatient Sample (NIS) database for all subjects with discharge diagnosis of IBD (Ulcerative Colitis & Crohn’s disease) with or without iron deficiency anemia (IDA) as primary or secondary diagnosis via ICD 9 codes during the period from 2002-2014. All analyses were performed with the use of SAS (version 9.4). From 2002-2014 there were total 23834 discharges of Ulcerative Colitis (UC) patients and 31998 discharges of Crohn’s Disease (CD) patients with IDA, constituting 9.8% & 7.4% discharges respectively. There was a rising trend of IDA in percentage of discharged patients of IBD from 7.4% in 2002 to 9.2% in 2014. Over the years the median length of stay decreased for IBD patients with and without IDA, but still the length of stay was more in IBD patients with IDA vs without IDA. On Multivariate regression analysis Male gender, age above 50, Hispanic race, small hospital, congestive heart failure, malignancy and metastatic disease were significant predictors of IDA in IBD. This analysis demonstrates the burden of IDA in patients of IBD. In a patient population with the predisposition for anemia, like patients with IBD, early diagnosis and management of iron deficiency can promptly reduce hospital visits, improve quality of life, reduce loss of work, and, ultimately, lower health care costs.

High serum adiponectin is associated with anemia development in chronic kidney disease: The results from the KNOW-CKD study

BackgroundAdiponectin is an adipokine secreted by adipocytes. A low adiponectin level is a significant risk factor of diabetes mellitus and cardiovascular disease. Recent studies have shown that adiponectin is negatively associated with hematopoiesis and predicts the development of anemia in the general population. In chronic kidney disease (CKD) patients, circulating adiponectin level is paradoxically elevated and the role of adiponectin is complex. Therefore, we evaluated the relationship between adiponectin and anemia in these patients. MethodsThis prospective longitudinal study included 2113 patients from the KNOW-CKD study (KoreaN cohort study for Outcome in patients With CKD), after excluding 125 without data on adiponectin levels. Hemoglobin levels were measured yearly during a mean follow-up period of 23.7 months. Anemia was defined as hemoglobin levels of <13.0 and 12.0 g/dL for men and women, respectively. ResultsMean patient age was 53.6 ± 12.2 years, and 1289 (61%) were men. The mean estimated glomerular filtration rate (eGFR) was 50.4 ± 30.2 mL min−1 1.73 m−2. Serum adiponectin level was inversely associated with body mass index, eGFR, log-transformed C-reactive protein, and positively with Charlson comorbidity index, urine protein to creatinine ratio, and high density lipoprotein cholesterol. In addition, serum adiponectin level was also negatively correlated with hemoglobin level and reticulocyte production index in both men and women. In multivariable linear regression analysis after adjustment of multiple confounders, adiponectin was negatively associated with hemoglobin (men, β = −0.219, P < .001; women, β = −0.09, P = .025). Among 1227 patients without anemia at baseline, 307 newly developed anemia during the follow-up period. In multivariable Cox regression analysis after adjustment of confounders, high adiponectin level was significantly associated with an increased risk of incident anemia (per 1 µg/mL increase, hazard ratio, 1.02; 95% confidence interval 1.01–1.04; P = .001). ConclusionsA high serum adiponectin level is independently associated with a low hemoglobin level and predicts the development of anemia in patients with CKD. These findings reveal the potential role of adiponectin in CKD-related anemia.

Fibroblast Growth Factor 23 and Anemia in the Chronic Renal Insufficiency Cohort Study.

Anemia is an early complication of CKD that is associated with increased morbidity and mortality. Prior data show associations between abnormal mineral metabolism markers and decreased erythropoiesis. However, few studies have investigated elevated fibroblast growth factor 23 as a risk factor for the development of anemia in patients with CKD. We conducted a prospective cohort study of 3869 individuals with mild to severe CKD enrolled in the Chronic Renal Insufficiency Cohort Study between 2003 and 2008 and followed through 2013. We hypothesized that elevated baseline fibroblast growth factor 23 levels are associated with prevalent anemia, decline in hemoglobin over time, and development of incident anemia, defined as serum hemoglobin level <13 g/dl in men, serum hemoglobin level <12 g/dl in women, or use of erythropoietin stimulating agents. In the 1872 of 3869 individuals who had prevalent anemia at baseline, mean age was 58 (11) years old, and mean eGFR was 39 (13) ml/min per 1.73 m2. Higher levels of fibroblast growth factor 23 were significantly associated with prevalent anemia (odds ratio per 1-SD increase in natural log-transformed fibroblast growth factor 23, 1.39; 95% confidence interval, 1.26 to 1.52), decline in hemoglobin over 4 years, and risk of incident anemia (hazard ratio per 1-SD increase in natural log-transformed fibroblast growth factor 23, 1.13; 95% confidence interval, 1.04 to 1.24; quartile 4 versus quartile 1: hazard ratio, 1.59; 95% confidence interval, 1.19 to 2.11) independent of demographic characteristics, cardiovascular disease risk factors, CKD-specific factors, and other mineral metabolism markers. The results of our prospective analyses remained unchanged after additional adjustment for time-varying eGFR. Elevated fibroblast growth factor 23 is associated with prevalent anemia, change in hemoglobin over time, and development of anemia. Future studies are needed to elucidate the mechanisms for these associations.

Pathogenetic Characteristics of Anemia in Patients with Solid Tumors

Aim. To study the impact iron metabolism disturbances and cytokine levels on the development of anemia in patients with solid tumors. Materials &amp; Methods. The research included 42 patients with malignant neoplasms, including 24 patients with anemia (19 men and 5 women, median age 67.7 ± 10 years) and 18 patients without anemia (15 men, 3 women, median age 65.7 ± 14 years). Anemia was diagnosed according to the WHO criteria (in men: erythrocytes &lt; 4.0 &lt;sup&gt;x&lt;/sup&gt; 10&lt;sup&gt;12&lt;/sup&gt;/L, hemoglobin &lt; 130 g/L, hematocrit &lt; 39 %; in women: erythrocytes &lt; 3.8 &lt;sup&gt;x&lt;/sup&gt; 10&lt;sup&gt;12&lt;/sup&gt;/L, hemoglobin &lt; 120 g/L, hematocrit &lt; 36 %). Results. A comparative analysis of iron metabolism in patients with and without anemia was performed. The lower values of serum iron and transferrin saturation in patients with anemia were shown (p &lt; 0.05). The total iron-binding capacity, the levels of ferritin, transferrin, C-reactive protein, indirect bilirubin were similar between groups (p &gt; 0,05). Higher levels of interleukins 6 and 10 (IL-6 and IL-10) were observed in patients with anemia (p &lt; 0.05). For IL-6, correlations were observed with levels of erythrocytes (r = -0,58), hemoglobin (r = -0,57), hematocrit (r = -0,52), and leukocytes (r = 0,42). The levels of IL-10 slightly correlated with the levels of erythrocytes, leukocytes, platelets, MCV, and MCH (r &lt; 0.3). For IL-10, correlations were established with levels of MCHC (r = -0,71), hemoglobin (r = -0,64) and hematocrit (r = -0,32). Correlations between the levels IL-6, IL-6 and hemoglobin, erythrocytes and several color indices may indicate their influence on the development of anemia in patients with malignant neoplasms. Conclusion. A functional iron deficiency in patients with anemia was found. Several causes of anemia development and significant role of interleukins in anemia pathogenesis were also discovered.

IRON METABOLISM, ERYTHROPOIESIS AND IMMUNE INFLAMMATION IN ANEMIC PATIENTS WITH CHRONIC HEART FAILURE IN THE PRESENCE OF DIABETIC NEPHROPATHY

The development of anemia in patients with chronic heart failure by the presence of diabeticnephropathy is characterized by erythropoietyc activity fall due to the low level of erythropoietinand functional iron deficiency, as a result of influence of pro-inflammatory cytokine level on hepcidinactivity, resulting in the disruption of the functional iron fund, deposited block of iron. The presenceof microalbuminaemia can be considered as a factor in formation of anemic syndrome due to loss oferythropoietin, transferrin, soluble transferring receptor as a part of protein’s pool in patients withchronic heart failure and diabetic nephropathy. The presence of anemia in patients with chronic heartfailure and diabetic nephropathy is associated with inadequate low central regulator of erythropoiesislevel in response to low hemoglobin concentrations on background of moderate decrease in glomerularfiltration rate.

Elevated Plasma Neutrophil Gelatinase-Associated Lipocalin Level as a Risk Factor for Anemia in Patients with Systemic Inflammation.

Studies on neutrophil gelatinase-associated lipocalin (NGAL) as an iron-regulatory protein are limited. This study investigated the relationships between plasma NGAL levels and indices of anemia in 187 patients with systemic inflammation. Plasma NGAL levels were significantly higher in patients with anemia versus in patients without anemia (185 ng/mL versus 98 ng/mL; P < 0.001). Serum iron levels were lower in patients with NGAL > 156 ng/mL than in those with NGAL ≤ 156 ng/mL (27.4 ± 25.3 µg/dL versus 58.1 ± 43.5 µg/dL; P < 0.001). In a receiver operating characteristic curve, the diagnostic ability of NGAL to identify anemia was superior to that of high-sensitivity C-reactive protein [0.712 (95% CI, 0.618–0.787) versus 0.649 (95% CI, 0.573–0.744); P < 0.01]. In a multivariate logistic regression analysis, the elevated NGAL level was significantly associated with the presence of anemia after adjusting for potential confounders [odds ratio, 1.30 (95% CI, 1.07–2.58); P = 0.010]. In conclusion, enhanced NGAL production may contribute to the development of anemia in patients with systemic inflammation.

Autoimmune Hemolytic Anemia in a Patient with Acute Myelomonocytic Leukemia

Autoimmune hemolytic anemia (AIHA) has been described in patients with lymphoid neoplasm with an etiologic relationship between the emergence of autoantibodies and lymphocyte dysfunction. Autoimmune disorders are less to develop in patients with other neoplasm like chronic myeloid leukemia, myelodysplastic syndrome or acute myeloid leukemia. Few reports have been documented the development of immune hemolytic anemia in patients with acute myeloid leukemia. We herein, present the case of de novo acute myelomonocytic leukemia associated with autoimmune hemolytic anemia. The patient has no previous medical history of anemia and Hb level at presentation was normal. She received chemotherapy containing Adriamycin plus Cytarabine. She showed marked improvement of anemia after steroid therapy with subsidence of all the clinical and laboratory manifestations of hemolysis when the patient went into remission. AIHA should be considered as one cause of anemia in

Hepcidin: a promising marker for differential diagnosis of anemia and macrophage activation syndrome in children with juvenile idiopathic arthritis

Hepcidin is a 25-amino acid peptide, which is a key systemic regulator of iron metabolism. As considered, overproduction of hepcidin in the liver is controlled by high levels of proinflammatory cytokines. Is it known that interleukin-6 play a key role in the development of anemia in patients with juvenile idiopathic arthritis (JIA). However, IL-6 blockers itself may provoke the onset of Macrophage Activation Syndrome (MAS), manifesting, particularly, also with anemia. In view of the fact that macrophages involved in MAS express CD163 - a scavenger receptor that binds hemoglobin-haptoglobin complexes - and activate the pathways which are important for adaptation to oxidative stress induced by free iron, we can consider hepcidin as a welcome challenge to predict the development of MAS early in the course of the disease. During the study of 35 patients with JIA treated with biological disease-modifying drugs (tocilizumab and golimumab), direct relations between the level of hemoglobin and hepcidin were not found. However, it was found that the mean corpuscular hemoglobin level is associated with hepcidin concentration in patients with JIA. It was found that concentration of serum hepcidin may be used for early differential diagnosis of anemia and MAS in patients with JIA. High probability of evolution of anemia to MAS was found when concentration of hepcidin was &lt;140 ng/mL and ferritin &gt;160 g/L. The following combinations were associated with high probability of evolution of slight anemia to a severe form, but not to MAS: 1. hepcidin &gt;200 ng/mL and ferritin &lt;140 g/L; 2. hepcidin &gt;140 ng/mL and soluble transferrin receptor &lt;1.6 mg/L; 3. hepcidin &gt;140 ng/mL and total iron binding capacity &gt;46 mcmol/L. Misclassification should be assessed during further studies.

Malarial anemia: digestive vacuole of Plasmodium falciparum mediates complement deposition on bystander cells to provoke hemophagocytosis.

The digestive vacuole (DV) of Plasmodium falciparum, which is released into the bloodstream upon rupture of each parasitized red blood cell (RBC), was recently discovered to activate the alternative complement pathway. In the present work, we show that C3- and C5-convertases assembling on the parasitic organelle are able to provoke deposition of activated C3 and C5b-9 on non-infected bystander erythrocytes. Direct contact of DVs with cells is mandatory for the effect, and bystander complement deposition occurs focally, possibly at the sites of contact. Complement opsonization promotes protracted erythrophagocytosis by human macrophages, an effect that is magnified when ring-stage infected RBCs with reduced CD55 and CD59, or paroxysmal nocturnal hemoglobinuria (PNH)-RBCs lacking these complement inhibitors are employed as targets. Bystander attack can also directly induce lysis of PNH-RBCs. Direct evidence for complement activation and bystander attack mediated by DVs was obtained through immunohistochemical analyses of brain paraffin sections from autopsies of patients who had died of cerebral malaria. C3d and the assembled C5b-9 complex could be detected in all sections, colocalizing with and often extending locally beyond massive accumulations of DVs that were identified under polarized light. This is the first demonstration that a complement-activating particle can mediate opsonization of bystander cells to promote their antibody-independent phagocytosis. The phenomenon may act in concert with other pathomechanisms to promote the development of anemia in patients with severe malaria.

Role of hepcidin in the development of anemia in patients with rheumatoid arthritis

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Iron deficiency in children with early chronic kidney disease

Iron deficiency (ID) contributes to the development of anemia in patients with chronic kidney disease (CKD). The frequency of ID in children with early CKD has not previously been reported. This was a retrospective chart review of children with CKD stages 2 and 3 followed at the CKD clinic of Children's Hospital of Michigan. ID was defined as low ferritin and transferrin saturation <20%. Patients on iron supplements were considered as iron-deficient cases. There were 50 patients included in the study (72% male) with a mean age of 10.31 (±5.21). The mean glomerular filtration rate (GFR) was 55.4 ml/min/1.73 m(2) (±14.61). ID was present in 42% of patients, out of whom almost half (42.9%) presented with anemia. Females had a higher frequency of ID (64.3%). The frequency of ID with anemia increased from 4.3% to 29.6%, (p = 0.03) in stage 2 to stage 3 CKD, respectively. The frequency of ID without anemia also increased with progression of CKD from stage 2 to stage 3, however, the difference was not statistically significant. ID is frequent in patients with early CKD. Monitoring of iron tests and treatment of ID is important in this population of patients.