Coexisting Iron Deficiency Research Articles

Diagnostic accuracy of mean corpuscular volume in detecting coexisting iron deficiency in patients of sickle cell disorders: A hospital-based study.

Co-existing iron deficiency in patients of sickle cell disease (SCD) and trait may worsen anemia, and adversely affect neuro-cognitive development and growth. Determining a cut-off below which Mean corpuscular Volume (MCV) can predict iron deficiency in SCD patients can preclude use of more expensive test serum ferritin. This study was conducted to determine the diagnostic accuracy of low MCV in detecting iron deficiency compared to serum ferritin levels in patients with SCD. 60 consecutive patients with SS or AS pattern on hemoglobin electrophoresis were enrolled. The index test (MCV) and the reference standard test (serum ferritin) were performed in a blind and independent manner. The measures of diagnostic accuracy were calculated and the precision of the point estimates were expressed by 95% confidence intervals. As MCV is a continuous variable, we also used multi-level likelihood ratios to compute diagnostic accuracy of MCV at several cut-points. The sensitivity of low MCV in detecting iron deficiency was 40.0% (95% CI-20.0-63.6), the specificity was 78.4% (95% CI-61.3-89.6) using serum ferritin as a reference standard. The sensitivity and specificity of predicting coexisting iron deficiency at this point was 60.9% (CI-38.6-80.3%) and 75.7% (CI-58.8-88.2%) respectively. The low sensitivity (40%) of microcytosis in detecting iron deficiency indicates that many cases will be missed if MCV alone is used to detect co-existing iron deficiency anemia in SCD patients. No single test is good enough to detect co-existing iron deficiency and a combination of tests might be useful.

Effect of Iron replacement therapy in Pregnant Beta Thalassemia Carrier Patients with Coexisting Iron Deficiency Anemia.

Iron deficiency anemia (IDA) and β -Thalassemia trait are two prevalent etiologies of microcytic hypochromic anemia. Pregnant women with IDA face significant risk of short-term and long-term complications for mother and newborns. The incidence of concurrent thalassaemia trait and iron deficiency was reported to be quite high but despite the high prevalence of these two conditions, the diagnosis is often underestimated and not properly managed.
 OBJECTIVE; The present study was conducted to evaluate impact of iron therapy in pregnant beta thalassemia minor patients with iron deficiency anemia.
 METHODS; Study Group constitutes 60 beta thalassemia trait pregnant women with iron deficiency anemia (IDA) with Hb less than 11g/dl, HbA2 levels >3.5% on HPLC and low serum ferritin (<30 ng/mL).After the initial investigations, participants received iron supplementation as 60 mg elemental iron three times daily for duration of 8 weeks. After completing therapy, complete blood count and serum ferritin were performed.
 RESULTS; Iron replacement therapy results in effective increment in hemoglobin, red cell indices and Serum ferritin.
 CONCLUSION; Pregnant women with beta-thalassemia minor combined with IDA can receive Iron replacement therapy for improvement in Hemoglobin effectively.

Low Serum Hepcidin Levels in Patients with Ulcerative Colitis - Implications for Treatment of Co-existent Iron-Deficiency Anemia.

Ulcerative colitis (UC) is often associated with anemia. Hepcidin, the central regulator of iron homeostasis, is known to be induced by inflammation and suppressed by anemia. It is not clear how hepcidin is affected in those with UC, when both inflammation and anemia may co-exist.Such knowledge may hold implications for treatment. Hematological and iron-related parameters, C-reactive protein (CRP), growth differentiation factor 15 (GDF-15) and erythroferrone (ERFE) (erythroid regulators of hepcidin) levels were estimated in blood from those with UC and in control subjects. Values for hematological and iron-related parameters showed evidence of iron-deficiency and resultant anemia, in patients with UC. The presence of UC was significantly associated with inflammation. Serum levels of ERFE, but not of GDF-15, were significantly higher in patients with UC than in control patients, while hepcidin levels were significantly lower. Serum hepcidin concentrations in patients with UC correlated positively with serum iron, ferritin and GDF-15, and negatively with serum ERFE. The iron status and serum hepcidin levels in UC patients with co-existent anemia were significantly lower and serum ERFE values significantly higher than in those with UC without anemia. The effect of anemia on hepcidin predominated over that of inflammation in patients with UC, resulting in suppressed hepcidin levels. This effect is possibly mediated through erythroferrone. We suggest that a serum hepcidin-guided approach may be useful to guide use of oral iron supplements to treat co-existent iron-deficiency anemia in patients with UC and other chronic inflammatory diseases.

Peripheral Blood Erythrocyte Parameters in Β-Thalassemia Minor with Coexistent Iron Deficiency: Comparisons between Iron-Deficient and -Sufficient Carriers

Changes in erythrocyte parameters are well known in both β-thalassemia minor (BTM) and iron deficiency (ID) when either is present alone; however, to our knowledge, there has been no study showing the changes when the two conditions coexist. We herein assessed erythrocyte parameters in BTM with coexistent ID. The BTM cases were divided into two groups based on ferritin levels as ID+ and ID−; the ID+ group was then further divided based on hemoglobin (Hb) levels as iron-deficient carriers with (IDA+) and without (IDA−) anemia. When compared to the ID− group, all parameters were significantly different in the IDA+ group except mean corpuscular volume (MCV) and red blood cells (RBC). All parameters except RBC were significantly different between the IDA+ and IDA− groups. Hb, hematocrit (Hct), MCV, and mean corpuscular hemoglobin (MCH) levels in the IDA− group were found to be lower than in the ID− group. Changes in erythrocyte parameters in iron-deficient carriers are critical in screening for BT, particularly for correct formulation of mathematical algorithms utilized by artificial intelligence programs.

Coexisting Iron Deficiency Anemia and Thalassemia Traits in Infants: Implication for an Anemia Screening Program.

To study the prevalence of anemia among healthy infants, and outcomes of giving a therapeutic trial of iron to anemic infants in thalassemia-endemic area. A cross sectional study was conducted in 6-9-month-old, full-term healthy infants who attended the well child clinics at 2 tertiary care centers in southern Thailand. Complete blood count and serum ferritin were performed in every infant, and hemoglobin typing was performed only in anemic cases. All anemic infants were given a therapeutic trial of iron and categorized into either; iron responder (hemoglobin increased ≥ 1 g/dL) or iron non-responder (hemoglobin increased <1 g/dL) groups after one month of the therapeutic trial. Mean levels of hematological parameters, including the Mentzer index, were compared within the groups. A total of 620 infants were included in the study. From this, 230 infants (37%) were anemic for which iron deficiency contributed for 80% of the etiology. The iron responder group showed significant improvement in hematological parameters after a trial of iron, while there was no improvement in the iron non-responder group. Among iron responders, there were 31 out of 186 infants (16.6%) who had coexisting abnormal hemoglobin typing, and their post-treatment complete blood count still showed a mean corpuscular volume < 70, with a Mentzer index < 13. Iron deficiency remains a major cause of anemia among infants, and a therapeutic trial of iron is beneficial in this age group, even though thalassemia trait/hemoglobinopathy can co-exist.

Comorbid laboratory abnormalities in female pattern hair loss patients

Background: Female pattern hair loss (FPHL) is the main cause of alopecia in women and has a debilitating impact on the quality of life. However, certain comorbid conditions causing hair loss are often masked by FPHL and may remain undetected. Hence, it is imperative to identify them to administer appropriate treatment. The necessity of laboratory tests to evaluate these comorbidities in patients with FPHL has not been established. Objectives: This study aimed to identify the frequency of comorbid abnormalities detected by laboratory tests in patients with FPHL. Methods: Routine laboratory test results of patients with FPHL, who visit our hair clinic for the first time, were retrospectively collected and analyzed. These tests assessed the serum testosterone, thyroid-stimulating hormone, free thyroxin, zinc and ferritin levels, hemoglobin, as well as antinuclear antibody (ANA), and rapid plasma reagin test results. The correlation between age and hair loss severity and the frequency of comorbidities was evaluated using subgroup analysis. Results: Among the 356 patients with FPHL, coexisting zinc deficiency, iron depletion, and thyroid abnormalities were common and present in 41.7%, 39.7%, and 11.3% of them, respectively. The rate of concomitantly increased ANA titers was relatively low (4.4%), while that of syphilis and high serum testosterone levels was extremely low (0.3% and 0%, respectively). Younger patients (<50 years) with FPHL had a higher rate of coexisting iron deficiency than patients in the older age group. Conclusion: Testing for concomitant iron depletion, zinc deficiency, and thyroid disease is recommended in female patients with FPHL.

Utility of sTFR/Ferritin index to differentiate iron deficiency anaemia and anaemia of chronic disease

Iron deficiency is a common condition that is usually diagnosed using conventional laboratory tests of iron status, such as serum ferritin and transferrin saturation. However, both ferritin and transferrin proteins are markedly influenced by inflammation, behaving as acute-phase reactants and making it difficult to differentiate between iron-deficiency anemia (IDA) and anemia of chronic disease (ACD). To assess the utility of sTfR/ Log ferritin Index to differentiate Iron deficiency anaemia and Anaemia of chronic disease. A cross-sectional study was conducted in the Department of Medicine, Victoria hospital and Bowring and Lady Curzon hospital, Bangalore Medical College and Research institute, Bangalore. A total of 150 blood samples were evaluated, i.e., 50 samples from iron deficiency anaemia group and 50 samples from patients with anaemia of chronic disorders &amp; 50 samples from healthy normal individual. In present study, samples are age matched with mean age of control 45.66±10.23, ACD 50.68±18.03, IDA 48.14±18.47. Hb, MCV, MCHC &amp; MCH were decreased in both the groups. However, the decrease in Hb &amp; MCV was much more in IDA as compared to ACD. Microcytosis was seen in 92% cases of IDA while it was observed in only 11% cases of ACD. sTfR/ log ferritin index was &amp;#62;1.5 in 80% of IDA. 90% of ACD and control subjects had sTfR/log ferritin index &amp;#60;1.5. sTfR levels were significantly higher in IDA (7.7± 5.8) as compared to the ACD cases (1.6 ±0.89) (p&amp;#60;0.001). sTfR/Log ferritin index is significantly higher in patients with Iron deficiency anemia (9.34±10.25) as compared to ACD (0.76±0.52) (p&amp;#60;0.001). sTFR/Log ferritin index indices is very useful in differentiating pure IDA, ACD and ACD with coexisting iron deficiency, thus providing a non-invasive alternative to bone marrow iron.

Discrepancy of Glycosylated Haemoglobin and Fructosamine in Egyptian Patients with Prediabetes and Iron deficiency

Background: the controversies concerning the influence of iron deficiency on glycaemic control parameters in patients with prediabetes prompted us to conduct this research. Objective: Our aim was to get a delicate estimation of these changes that may alter the management plan in this clinical situation. Patients and methods: a case control study included 197 Egyptian patients with prediabetes; 113 patients with iron deficiency versus 84 patients without iron deficiency (control group) during the period (May 2019 - October 2019). History, physical examination and laboratory tests of fasting and postprandial plasma glucose (FPG and PPPG), glycosylated haemoglobin (HBA1c), fructosamine, serum creatinine, ALT, AST, CBC, ferritin, serum iron and total iron binding capacity (TIBC) were done. Results: HBA1c was significantly higher in the iron deficiency group than the control group with non-significant difference between the studied groups regarding FPG and PPPG. HBA1c level was positively correlated with fructosamine, exclusively in the healthy group indicating the lack of credibility of HBA1c in iron deficient subjects with prediabetes. HBA1C level was inversely correlated with serum iron level in both study groups. Conclusion: there is discordance in glycaemic control parameters in patients with prediabetes and iron deficiency. Diagnosis of deranged glucose homeostasis in patients with co-existent iron deficiency and prediabetes should not be with HBA1c solely.

Discrepancy of Glycosylated Haemoglobin and Fructosamine in Egyptian Patients with Prediabetes and Iron deficiency

Background: the controversies concerning the influence of iron deficiency on glycaemic control parameters in patients with prediabetes prompted us to conduct this research. Objective: Our aim was to get a delicate estimation of these changes that may alter the management plan in this clinical situation. Patients and methods: a case control study included 197 Egyptian patients with prediabetes; 113 patients with iron deficiency versus 84 patients without iron deficiency (control group) during the period (May 2019 - October 2019). History, physical examination and laboratory tests of fasting and postprandial plasma glucose (FPG and PPPG), glycosylated haemoglobin (HBA1c), fructosamine, serum creatinine, ALT, AST, CBC, ferritin, serum iron and total iron binding capacity (TIBC) were done. Results: HBA1c was significantly higher in the iron deficiency group than the control group with non-significant difference between the studied groups regarding FPG and PPPG. HBA1c level was positively correlated with fructosamine, exclusively in the healthy group indicating the lack of credibility of HBA1c in iron deficient subjects with prediabetes. HBA1C level was inversely correlated with serum iron level in both study groups. Conclusion: there is discordance in glycaemic control parameters in patients with prediabetes and iron deficiency. Diagnosis of deranged glucose homeostasis in patients with co-existent iron deficiency and prediabetes should not be with HBA1c solely.

English

BACKGROUND Immune Thrombocytopenic Purpura (ITP) is one of the most commonly encountered disease in paediatric practice. Thorough clinical and morphological study of peripheral blood and bone marrow is required for confirming ITP. Clinicomorphological aspects of paediatric ITP is a less studied topic especially in developing countries like India. The objective was to study the clinical and morphological profile of paediatric cases of ITP. METHODS This is a 5-year record based retrospective study conducted in a paediatric tertiary health care centre in Kerala, South India. Data of all paediatric cases diagnosed as ITP including clinical presentation, clinical findings, blood counts, peripheral blood morphology, bone marrow morphology, and treatment response was collected and entered in SPSS software version 16.0 and analysed. For assessing correlation, chi-square test was used. RESULTS The age of children ranged from 3 months to 15 years. H/o viral fever was noted in 53 % cases. Cases which had moderate and severe thrombocytopenia were 74 % and 21 % respectively. Isolated thrombocytopenia was the most common peripheral blood picture observed with few cases showing coexisting eosinophilia and anaemia. All cases showed megakaryocyte proliferation in marrow with 9 % cases showing coexisting iron deficiency anaemia. Majority of cases showed rapid response to steroid / IVIG therapy and the response had no correlation with grade of thrombocytopenia (p value &lt; 0.05). CONCLUSIONS Paediatric cases of ITP usually present following viral infections or vaccination, with worrisome bleeding episodes, petechiae, ecchymosis or purpura. KEYWORDS ITP, Paediatrics, Platelet Count, Thrombocytopenia, Vaccination

Microcytic anemia in children: parallel screening for iron deficiency and thalassemia provides a useful opportunity for thalassemia prevention in low- and middle-income countries

Microcytic anemia in children is commonly attributed to iron deficiency without attempting to find the cause. Inadequate investigations to exclude hemoglobinopathies lead to missed opportunities for identification of thalassemia carriers. Here we aim to describe the relative contribution of iron deficiency and thalassemia to microcytic anemia in children. This hospital-based prospective study was conducted at the Colombo North Teaching Hospital, Ragama, Sri Lanka. All newly diagnosed patients with microcytic anemia were recruited and data were collected using an interviewer-administered questionnaire. Full blood count, blood film, serum ferritin, c-reactive protein, quantification of hemoglobin sub-types and α-globin genotype were performed using 4 ml of venous blood. A total of 104 children (Male- 60.5%) were recruited. Iron deficiency was the cause for anemia in 49% whilst 16% and 10% had α- and β-thalassemia trait respectively. Seven (6.7%) children had co-existing iron deficiency and thalassemia trait while two coinherited α- and β-thalassemia trait. Children with β-thalassemia trait had significantly higher red cell count and lower mean corpuscular volume compared to children with iron deficiency. However, none of the red cell parameters were significantly different between children with α-thalassemia trait and iron deficiency. Iron deficiency contributes only to half of children with microcytic anemia; one-fourth had thalassemia trait. Co-existence of iron deficiency and thalassemia trait or co-inheritance of α- and β-thalassemia trait were found in 9%. Parallel investigation of children with microcytic anemia to diagnose iron deficiency and thalassemia provides an opportunity to identify thalassemia carriers which is beneficial for thalassemia prevention.

Growth-differentiation factor-15 expression in anemia of chronic disease and iron-deficiency anemia

BACKGROUND: Iron-deficiency anemia (IDA) is a common hematological disorder. Anemia of chronic disease (ACD) is mild-to-moderately severe anemia associated with chronic diseases. Growth-differentiation factor-15 (GDF-15) is a member of the transforming growth factor-β, produced by late-stage erythroid precursors in the bone marrow; it suppresses hepcidin expression during ineffective erythropoiesis. The aim of this study was to measure the level of the GDF-15 level in ACD and IDA and to evaluate its ability to differentiate between ACD and ACD with coexisting iron deficiency (mixed anemia).PATIENTS, MATERIALS AND METHODS: The present study including 87 persons “30 with IDA, 30 with ACD, and 27 controls.” The following investigations were done: complete blood count, erythrocyte sedimentation rate, iron profile (serum iron and total iron-binding capacity), C-reactive protein, ferritin, hepcidin, and GDF-15, depending on the results of these investigations, some patients of ACD group appear to be ACD with co-existing iron deficiency. The analysis of data was carried out using the Statistical Packages for the Social Sciences software version 24.RESULTS: The serum hepcidin was significantly lower in IDA, whereas the serum GDF-15 is comparable to that of the control group. The serum hepcidin and serum GDF-15 were significantly higher in (ACD and mixed anemia) group compared to the control group.CONCLUSION: GDF-15 is high in ACD group and comparable to the control in iron-deficiency group, and it is not a useful marker to differentiate between ACD and ACD with coexisting iron deficiency.

Serum Soluble Transferrin Receptor-Ferritin Indices in Diagnosing and Differentiating Iron Deficiency Anemia from Anemia of Chronic Disease among Patients with Chronic Kidney Disease

Background: Anemia is common in patients with chronic kidney disease (CKD) and this is generally anemia of chronic disease (ACD), but iron deficiency anemia (IDA) is also common. Soluble transferrin receptor (sTfR) is a useful marker for IDA. Present study was undertaken to assess the utility of sTfR as a marker of IDA and to differentiate ACD from IDA in selected group of Bangladeshi patients with CKD.&#x0D; Methods: This cross-sectional study was conducted in the Department of Nephrology, BSMMU, Dhaka, Bangladesh from January 2013 to December 2014. Patients with anemia admitted in Nephrology Department, whether on hemodialysis or not and Medicine Department of BSMMU were taken for study. The study population was further divided into two groups; Group A, patients (30) who were having IDA and Group B, patients (40) with ACD and a control group was also selected. Data were collected by face to face interview and laboratory investigations with a self-administered questionnaire.&#x0D; Results: The mean age of the patients in Group A and Group B were 38.40±13.23 and 34.85±10.52 years respectively and male-female ratio were 0.5:1 and 1:0.5. Mean sTfR level was higher (4.81± 1.64 μg/ml) in patients with IDA than (2.89±1.40 μg/ml) in patients with ACD (p &lt;0.0001). Mean ferritin level was 599.59± 449.15μg/L in ACD patients whereas 101.23±119.42 in IDA patients (p&lt;0.0001). Total iron binding capacity (TIBC) was more in ACD patients with sTfRe”3μg/ml as compared to ACD patients with sTfR&lt;3μg/ml. Transferrin saturation (TSAT) level was significantly decreased in ACD patients with sTfRe”3μg/ml as compared to ACD patients with sTfR&lt;3μg/ml. sTfR and ferritin indices between group A (IDA) and group B (ACD) shows mean sTfR:logSF level was significantly (P&lt;0.001) high in group A (2.71±1.13) in comparison to group B (1.08±0.54). Mean log sTFR:SF was also significantly higher (P&lt;0.05) in group A (0.001±0.0008) compared to group B (0.013±0.012).&#x0D; Conclusion: sTfR level has a comparable ability to serum ferritin in diagnosing IDA and ACD. However, sTfR and serum ferritin alone cannot definitely exclude coexisting iron deficiency in ACD. Log sTfR/ ferritin index has role in identifying development of iron deficiency in ACD whereas sTfR/ log SF ratio can differentiate pure IDA from ACD with or without iron deficiency. Thus, it is important to estimate both serum sTfR and sTfRferritin indices to be able to differentiate pure IDA, ACD and ACD with co-existing iron deficiency thus providing a non-invasive alternative to bone marrow iron.&#x0D; Birdem Med J 2019; 9(2): 151-156

Evaluating and Correcting Iron Deficit in Atypical Hemolytic Uremic Syndrome (HUS)

Introduction:Atypical hemolytic uremic syndrome (HUS), in the absence of Shiga toxin producing E. coli, is most often complement mediated and is associated with microangiopathic hemolytic anemia (MAHA). And while this association is well understood, it is less common to encounter concurrent pre-existing iron deficiency anemia. In such patients, apart from correcting anemia with supportive blood transfusions, the calculation and correction of iron deficit is a valuable but underutilized management strategy, and is highlighted in the presented case.Example case:A 33 year-old Hispanic female with no significant past medical history other than iron deficiency anemia with a baseline hemoglobin of 5.4 g/dL presented to the hospital for abnormal renal function seen on outside laboratory studies. She was found on admission to have a creatinine of 15.47, BUN of 94 (baselines unknown), LDH of 451, haptoglobin of 44, hemoglobin of 6.9 (MCV 87) and platelets of 107 x 10³/µL. Vital signs were stable. Peripheral smear revealed approximately 1 schistocyte/hpf. She complained of a recent but resolving upper respiratory infection and a 10 day history of new-onset blurry vision; she self-identified as a Jehovah's Witness. The patient was tentatively diagnosed with atypical HUS in light of MAHA, Cr >1.5, platelets>30 with only occasional schistocytes and no antecedent diarrheal illness. To definitely rule out pre-existing intrinsic renal disease and/or IgA nephropathy, however, the patient required a kidney biopsy, but was unable to undergo the procedure because of her anemia, thrombocytopenia and refusal to receive whole blood if needed. The patient's desired hemoglobin in order to undergo biopsy was set at 10 g/dL, and iron deficit was calculated as 677 mg. The patient was administered intravenous iron sucrose along accordingly along with epoetin, which resulted in gradual improvement in anemia during hospitalization. Decision to biopsy was deferred to her outpatient care provider.Discussion:Atypical HUS responds best to supportive care with blood transfusions and dialysis, if accompanying symptomatic uremia is present. Definitive therapy is with eculizumab. Patients who will not receive blood for religious purposes, however, present a challenge to providers in the acute setting of HUS, as gradual hemolysis can result in tissue hypoxia, hemodynamic instability and even death. Should patients have concurrent iron deficiency, however, even in the setting of active hemolysis, replacing iron can result in meaningful hemoglobin recovery. Iron deficit is calculated by the following equation: Body weight (in kg) x [target Hb - actual Hb] + depot iron (which is 500 mg if patient >35 kg).Iron deficit as a clinical tool is seldom discussed in the literature, with a particular paucity in studies pertaining to atypical HUS. One potential explanation for this absence is that atypical HUS is an already rare diagnosis, and is a disorder of peripheral red blood cell destruction rather than a disorder of decreased hemoglobin-to-oxygen binding, as is seen in iron deficiency. Regardless, the utility of iron replacement is evident in the presented case of atypical HUS, and should be explored further in larger scale retro- and prospective studies.Conclusions:While disease-directed therapy in atypical HUS (i.e. eculizumab) is required to effectively manage acute, complement-mediated hemolytic anemia and renal failure, correction of the calculated iron deficit in co-existing iron deficiency anemia, if present, can result in gradual but marked improvement in hemoglobin. Conversely, patients with atypical HUS who are actively hemolyzing with a normocytic anemia should still be evaluated for iron deficiency and undergo iron transfusions for any calculated deficit. DisclosuresNo relevant conflicts of interest to declare.

Role of Serum Transferrin Receptor in Diagnosing and Differentiating Iron Deficiency Anemia from Anemia of Chronic Disease in Patients with Chronic Kidney Disease

Background: Anemia is common in patients with chronic kidney disease (CKD) and this is generally anemia of chronic disease, but iron deficiency anemia (IDA) is also common. Soluble transferrin receptor (sTfR) is a useful marker for IDA. Present study was undertaken to assess the utility of sTfR as a marker of IDA in selected group of Bangladeshi patients with CKD.Methods: This cross-sectional study was conducted in the Department of Nephrology, BSMMU, Dhaka, Bangladesh from January 2013 to December 2014. Patients with anemia admitted in nephrology department whether on hemodialysis or not and medicine department of BSMMU were taken for study. The study population was further divided into two groups; Group A, patients who are having IDA and Group B, patients with ACD and a control group was also selected. Data were collected by face to face interview and laboratory investigations with a self-administered questionnaire.Results: The mean age of the patients in two study groups were 38.40±13.23 and 34.85±10.52 years respectively and male-female ratio were 0.5:1 and 1:0.5. Mean sTfR level was higher (4.81± 1.64 ?g/ml) in patients with IDA than (2.89±1.40 ?g/ml) in patients with ACD (p &lt;0.0001). In our study mean ferritin level was 599.59± 449.15?g/L in ACD patients whereas 101.23±119.42 in IDA patients (p&lt;0.0001). Total iron binding capacity (TIBC) was more in ACD patients with sTfRe”3?g/ml as compared to ACD patients with sTfR&lt;3?g/ml. Transferrin saturation (TSAT) level was significantly decreased in ACD patients with sTfR ?3?g/ml as compared to ACD patients with sTfR&lt;3?g/ml.Conclusion: sTfR has a comparable ability to S. ferritin in diagnosing IDA and ACD. However, sTfR and serum ferritin alone cannot definitely exclude co-existing iron deficiency in ACD. As sTfR is not affected by infection and/or inflammation, thus providing a non-invasive alternative to bone marrow study.Birdem Med J 2017; 7(2): 132-137

Hepcidin and iron parameters in children with anemia of chronic disease and iron deficiency anemia

BackgroundAnemia of chronic disease (ACD) and iron deficiency anemia (IDA) are the two most prevalent forms of anemia having interrelated characteristics. Hepcidin, a newly introduced biomarker for assessment of iron status, is a homeostatic regulator of iron metabolism. We investigated the role of hepcidin and other conventional iron parameters to assess iron status among children with ACD and IDA. We also identified children with ACD who developed iron deficiency (ID).MethodsThe study was undertaken in anemic children with 30 cases each of ACD and IDA along with 30 age and sex-matched controls. The ACD cases were subdivided into pure ACD and ACD with coexistent ID. All cases were subjected to following tests: complete blood count with peripheral smear, serum C-reactive protein, serum interleukin-6, iron studies, serum soluble transferrin receptor (sTfR), and serum hepcidin.ResultsThe mean serum hepcidin concentration was significantly increased in pure ACD patients (143.85±42.76 ng/mL) as compared to those in IDA patients (6.01±2.83 ng/mL, P < 0.001) and controls (24.96±9.09 ng/mL, P <0.001). Also, compared to pure ACD patients [normal sTfR levels (<3 µg/mL)], the serum hepcidin concentration was reduced significantly in ACD patients with ID [high sTfR levels (≥3 µg/mL)] with a mean of 10.0±2.97 ng/mL.ConclusionHepcidin measurement can provide a useful tool for differentiating ACD from IDA and also help to identify an iron deficiency in ACD patients. This might aid in the appropriate selection of therapy for these patients.

Prevalence of Iron Deficiency in Thalassemia Trait: A study in BSMMU, Dhaka

Background: Thalassemia is considered the most common genetic disorder worldwide and about 7% of world populations are carriers. A vast majority of such cases have iron deficiency.Objective: This study was undertaken to find out the pattern of iron status in thalassemia traits and thus to determine co-existing iron deficiency in them.Method: This cross sectional study was carried out in the Department of Hematology, BSMMU, Dhaka from January 2007 to December 2007. Adult anemic patients of hypochromic microcytic blood film attending outpatient department were screened for thalassemia on the basis of clinical history, physical findings and hemoglobin electrophoresis. A total of 50 anemic patients with carrier state of thalassemia was detected and selected for evaluation of iron profile.Results: Patients having iron deficiency detected by serum iron profile were compared with those without iron deficiency. The mean age in years of study subjects were 30.38 ± 9.79 years. Among the study population, 50% were male and 50% were female. Highest frequency of co-existent iron deficiency was found among the age of 21-30 years. Prevalence of iron deficiency was 30.2% among b-thalassemia trait. A statistically significant mean difference of Hb, MCV, MCH, MCHC, serum iron, TIBC, S. Ferritin, transferring saturation was found indicating study subjects without iron deficiency had higher level than with iron deficiency (p&lt;0.05).Conclusion: Clinical iron deficiency may occur in thalassemia trait/carriers of inherited hemoglobin disorders. The combined state should always be suspected and iron supplements are often needed to improve the status of anemia.Bangladesh J Medicine Jan 2014; 25 (1) : 13-16

Anemia of Chronic Disease in Rhenumatoid Arthritis And Its Realationship With Disease Activities

Anemia is a frequent cause of morbidity in patients with Rheumatoid Arthritis (RA) that reduces quality of life. This observational cross sectional study was carried out in Rheumatology OPD and Medicine Indoor of Bangabandhu Sheikh Mujib Medical University (BSMMU) from January 2009 to December 2010 to find out the frequency of Anemia of Chronic Disease (ACD) and relative frequency of pure ACD and ACD with coexistent Iron Deficiency Anemia (IDA) in RA and to describe the relationship between ACD and disease activity of RA patients. For this purpose a total of 130 RA patients were enrolled according to the inclusion and exclusion criteria of the study and divided into ACD group and non anemic group on the basis of hemoglobin level (11g/dl in females and &lt;12g/dl in males). ACD group of patients again divided into pure ACD and ACD with co-existent IDA subgroups on the basis of ratio of Soluble Transferrin Receptor (sTfR) to log ferritin (sTfR­F index).Patients with sTfR-F index value&lt;1 were classified as pure ACD and sTfR-F index value &gt;1 were classified as ACD with coexistent IDA. Disease activity were assessed by modified Disease Activity Score (DAS-28), Tender joint count, Swollen joint count, Morning stiffness in minutes, Health Assessment Questionnaire (HAQ) Erythrocyte Sedimentation Rate (ESR) in mm in 1st hour and Rheumatoid Factor (RF) positivity. Out of 130 patients, estimated frequency of ACD was 59%.Among the ACD patients, 16% were found to have pure ACD and 84% had both ACD and IDA. Disease activity parameters were compared between ACD group and non anemic group and then pure ACD and ACD with co­existent IDA subgroups of patients. We found significantly higher mean DAS-28 score ,tender joint count, swollen joint count, HAQ score and mean ESR in ACD group of patients as compared to non anemic RA patients. When differing levels of disease activity indices were compared, we also found significant difference between ACD and non anemic groups. Patients with pure ACD subgroups had significantly higher mean DAS-28, tender joint count, swollen joint count and HAQ score as compared to ACD with co-existent IDA subgroups of patients. When comparing differing levels of disease activity indices, no significant difference was observed between pure ACD and ACD with coexistent IDA patients with RA. This it can be said in conclusion that ACD is frequently encountered with high frequency of iron deficiency anemia among rheumatoid arthritis patents. RA patents with ACD tend to have severe disease than non anemic RA patents but pure ACD patints not necessarily had severe disease as compared to combined ACD and IDA. JCMCTA 2015 ; 26 (1) : 14-20

Minor hemoglobins other than A2 in iron deficiency.

To determine any difference in levels of minor hemoglobins, other than hemoglobin A2 (HbA2), in patients with iron deficiency. We divided ethylenediaminetetraacetic acid (EDTA)-anticoagulated blood specimens from 188 patients into 2 groups, of which 94 displayed a normal or high ferritin level and the remaining 94 had a low ferritin level. We correlated the red cell indices, hemoglobin levels, and ferritin levels with the percentage of various minor hemoglobins. The Student's t-test was used to assess the statistical significance of the difference between the mean concentrations of minor hemoglobins in the 2 groups. Only hemoglobin HbA1a had a positive correlation (0.33 in iron-deficient and 0.35 in iron-replete specimens) with serum ferritin concentration. Among the minor hemoglobins, HbA1a (P =.008) and HbA2 (P <.001) were significantly different between the 2 groups. HbA1a may be low in iron deficiency, independent of HbA2. This information may be used to predict coexistent iron deficiency in β-thalassemia traits, in which concomitant infection or inflammation leads to normal ferritin levels.

A New β0-Thalassemia Mutation (codon 102, AAC>ATCAC) in Coexistence with a Heterozygous P4.2 Nippon Gene

A new β-thalassemia (β-thal) frameshift mutation was found at codon 102 (AAC>ATCAC) in a 17-year-old Japanese male and his 14-year-old sister. Both demonstrated a more severe phenotype than the usual β-thal minor with mild hemolytic involvement. No mRNA derived from the thalassemic allele, or βTmRNA, was detected in the sequencing analysis of the whole mRNA (cDNA). However, the βTmRNA from the whole βmRNA was specifically amplified by amplification refractory mutation system (ARMS), and was actually found to be present. Furthermore, quantitative polymerase chain reaction (q-PCR) demonstrated a negligible amount of βTmRNA. Thus, their more severe phenotype was not caused by the “dominant type” β-thal in which a considerable amount of the βTmRNA would be expected. In fact, our proband had a total βmRNA level that was mostly normal. Thus, the cause of a β-thal phenotype by the frameshift mutation was ascribed to the reduced amount of mRNA. We further searched for the cause of their severe phenotype. However, factors that exacerbated the phenotype of β-thal, such as α-globin gene triplication, coexisting iron deficiency and infection were not found. Finally, we noticed that the red cell morphology revealed ovalocytosis and small numbers of stomatocytes that were seen in the hereditary spherocytosis (HS), especially by P4.2 mutations. The sequence of the P4.2 gene disclosed heterozygous P4.2 Nippon, or missense mutation at codon 142 (GCT>ACT) on exon 3, the most common mutation of Japanese HS. Frequent mutations of other membrane proteins, Band 3 and ankyrin that are common cause of HS in the Japanese population, other than P4.2, were not detected. When HS by P4.2 Nippon develops it is homozygous, and no P4.2 protein is observed in sodium dodecilsulphate-polyacrylamide gel electrophoresis (SDS-PAGE), while in our case the amount of the P4.2 was almost normal in the SDS-PAGE. However, there are several reports that revealed more severe phenotypes of β-thal by the coexisting abnormality of membrane protein. It is uncertain, but the presence of heterozygous P4.2 Nippon may be associated with the exacerbation of the phenotype of β-thal minor.