Iron overload is a common complication in patients with chronic renal failure treated with dialysis prior to the availability of recombinant human erythropoietin therapy. Iron overload was the result of hypoproliferative erythroid marrow function coupled with the need for frequent red blood cell transfusions to manage symptomatic anemia. The repetitive use of intravenous iron with or without the use of red blood cell transfusions also contributed to iron loading and was associated with iron deposition in liver parenchymal and reticuloendothelial cells. Here we report a 56-year-old female with end-stage renal failure who underwent kidney transplant twice and found to have iatrogenic iron overload with excess intravenous iron treated conservatively.

Introduction Severe IDA can cause many complications and impair the quality of life. Iron is an essential micronutrient required for catalysis, DNA synthesis, redox reactions and oxygen transport1. It is important for an early step in embryonic haematopoiesis, which is common for all developing blood cells. The link between IDA and leukopenia is not well recognized in the literature. Objectives To assess the prevalence and clinical significance of leukopenia in patients with IDA and effect of iron replacement and correction of anemia on the WBCs count. Materials and Methods We retrospectively reviewed the electronic medical records of all patients attended haematology clinic with the diagnosis of iron deficiency anemia (IDA) over 2 years in Hamad Medical Corporation, Qatar. All other causes of anemia and patients with systemic or chronic diseases were excluded. Age, nationality, BMI, Complete blood count and iron parameters were collected before and after treatment with IV iron therapy. Associated infections at the time of presentation (IDA and leukopenia) were noted including the course of the infection and response to treatment. Leukopenia was defined as WBCs count below 4000/microlitre. Statistical analysis was done using paired t test to compare variables after versus before iron therapy. Results Out of 1567 case of iron deficiency anemia, 80 case had leukopenia (5.105%) Their mean Leukocytes count was 3.35 +/- 0.48 ×103 before iron replacement. 7 patients had infections; 4 had upper respiratory tract infection, 1 urinary tract infection, 1 gastroenteritis, 1 lymphadenitis. Six of them received antibiotics and they had no complications. After iron therapy and correction of anemia the leukocyte count increased significantly to 4.38 +/- 1.82×103 (P < 0.05). There was no significant correlation between WBC count and iron parameters (Hb, TIBC, serum iron concentration). Discussion High level of erythropoietin in IDA is thought to cause down regulation of neutrophils in animal models. In our study leukopenia occurred in 5.1% of the big cohort with IDA. A previous study on 516 patients with IDA recorded leukopenia in 17.6% of them. Their cases with leukopenia occurred more in patients with severe anemia. The increase of WBC count with correction of anemia suggested a physiologic link between erythropoiesis and leukopoiesis. However, our study did not show correlation between WBC count and Hb or any of the iron parameters. In concert with our finding, a study in healthy children (n = 556) did not find associations between the measured iron markers and WBC In addition, the association between IDA and leukopenia did not significantly increase the risk of infections in our patients. The link between leukopenia and IDA needs to be addressed in more studies. Conclusions: The prevalence of leukopenia in this big cohort with IDA was 5.1%. This leukopenia was not associated with severe or complicated infections. There were no associations between the measured iron markers and white blood cell counts in healthy adults Figure Disclosures No relevant conflicts of interest to declare.

Introduction Iron deficiency anemia (IDA) is a major public health issue, with widespread prevalence and negative impact on health care system. IDA occurs when iron stores diminish to the level that disturbs erythropoiesis and causes anemia. Neutropenia is an abnormal reduction in the number of neutrophils. A little is known about the association between iron deficiency anemia and neutropenia. The aim of this study is to investigate the prevalence of neutropenia in a large cohort of adult patients with IDA and to find possible correlation between neutrophil levels with haemoglobin concentration and iron stores. We studied associated infections in this neutropenic group. Materials and Methods We retrospectively reviewed the electronic medical records of 1567 patients attended haematology clinic with the diagnosis of IDA ((haemoglobin level less than 12 gm/dl for women, less than 13 gm/dl for men) over the past 2 years in Hamad Medical Corporation, Qatar. Other causes of anemia and anemia associated with any systemic or endocrine disease were excluded. The values of complete blood count (CBC) and iron parameters were collected. Neutropenia was defined as neutrophils count to be less than 1.5x 109/L Results Sixty four patients of the 1567 cohort with IDA had neutropenia (4.084%) Their mean neutrophils count = 1.18 +/- 0.28x 109/L before iron replacement. Neutrophil count increased significantly to 2.33 +/- 1x 109/L after iron therapy (p< 0.05) . No significant correlation was detected between neutrophil count on the one hand and iron level, iron saturation, TIBC, Transferrin and ferritin level on the other hand. Eight out of the 64 patients with neutropenia had infection at the time of presentation; 5 upper respiratory tract infections, 1 gastroenteritis, 1 lymphadenitis, 1 urinary tract infections. Five of these patients received antibiotics, with no complications reported. Discussion In our cohort with IDA the prevalence of neutropenia was 4.08%. In all patients, the neutrophil count returned to normal after proper iron therapy. The effect of iron deficiency on neutrophils count is through its effect on haematopoiesis progenitors and bone marrow microenvironment which regulates the production of cell lineages. In addition, the high level of erythropoietin (observed in IDA) has been shown to down-regulate neutrophil production in animal models. In another relatively smaller study on 516 patients with IDA, neutropenia was found in 17.6% However, unlike in our study the neutrophil count was correlated with Hb level. On the other hand in 97 patients with unexplained neutropenia, IDA was found in 2.1% with correction of neutrophil count after correction of the anemia. In addition, the associated infection rate was low and was treated without complications. Our findings support a possible link between IDA and neutropenia evident by the improvement of neutrophils count after iron replacement, (1.18 vs 2.33x 109/). Conclusions: The finding of neutropenia is not uncommon in patients with IDA. This neutropenia markedly improved after iron replacement. Iron is essential for proper development and maintenance of the immune system in general and further studies are required to elaborate further in this unique association. Figure 1 Disclosures No relevant conflicts of interest to declare.

Introduction Iron deficiency anaemia (IDA) is one of the most common health problems worldwide, its prevalence is up to 1 in 5 of the general population. The diagnosis of absolute iron deficiency is easy unless the condition is masked by inflammatory conditions. All cases of iron deficiency should be assessed for treatment and underlying cause.In developing countries, iron deficiency anemia is nutritional, resulting from reduced intake of bioavailable iron , and often associated with infections causing hemorrhages, such as hookworm infestation . In Western societies, other than in individuals at risk, iron depletion results from chronic bleeding and/or reduced iron absorption, disorders that may be more relevant than anemia itself.The association between IDA and lymphocytopenia is poorly addressed in the literature. Objective: To assess the prevalence of lymphocytopenia in a large cohort with IDA and to study the effect of iron replacement on lymphocytes count. Materials and Methods We retrospectively reviewed the electronic medical records of patients attended haematology clinic with the diagnosis of IDA over 2 years in Hamad Medical Corporation, Qatar. Patients with other forms of anemia were excluded as those with chronic or systemic diseases. Complete blood count and iron parameters were collected and analysed. Lymphocytopenia was defined as lymphocyte count less than 1000/microlitre. Statistical analysis was done using mean and SD and paired t test to compare variables after versus before treatment. Results The mean age of our IDA patients was 37.95 years with a mean BMI = 31.82. Out of 1567 case of IDA, 20 had lymphocytopenia, (1.276%). The mean lymphocytes count mean increased from 0.73 +/- 0.15 x 10^9 before iron replacement, to 1.79 +/- 0.74 x 10^9 after iron treatment (p < 0.05) (iron dose of 1000 mg of IV iron saccharate or ferric carboxymaltose) . Four out of the 20 patients with lymphopenia had mild infections (2 upper respiratory tract infections, 1 urinary tract infection and one gastroenteritis) with no serious complications. These findings suggested that the lymphopenia associated with IDA is correctable and does not increase infection risk in these patients. Discussion Our study showed a possible negative impact of IDA on lymphocytes count in a small number of patients that was corrected with the correction of anemia with iron therapy. Animal studies showed that iron deficiency may lead to impaired T lymphoid differentiation and may negatively affect all cell lineage in haematopoiesis not only on erythroid line. A case control study by Das et al. found significantly lower levels of CD4+ T-cell counts and CD4:CD8 ratios in iron deficient children, however there was no significant effect on immunoglobulin levels. Conclusions: Lymphopenia may occur in a small percentage of patients with IDA. Significant increase in the lymphocyte count occur with iron therapy and correction of the anemia. Lymphopenia was not associated with serious infections. Disclosures No relevant conflicts of interest to declare.

INTRODUCTION Iron deficiency is the most prevalent nutritional deficiency worldwide. Iron deficiency anemia (IDA) is the most common type of anemia, its prevalence is 1 out of 5 of the population. IDA is a well-known cause of reactive thrombocytosis which is mostly asymptomatic. Only few observational studies and case reports have described thromboembolic events in the context of this reactive thrombocytosis in the absence of other hypercoagulable states OBJECTIVES To assess the frequency of thromboembolic events in Arab patients with reactive thrombocytosis secondary to iron deficiency anemia (IDA). METHODS We retrospectively reviewed thromboembolic events in iron-deficient patients with reactive thrombocytosis. Our study sample included female patients who received iron replacement for IDA between April 2018 and March 2020 at Hamad Medical Corporation, Doha, Qatar. We excluded pregnant, non-Arab patients and patients under 18 or over 65 years of age. Reactive thrombocytosis was defined as thrombocyte count of more than or equal to 450 x 109 /L in the presence of iron deficiency anemia and ferritin level less than 30µg/l. RESULTS Out of 1567 patients (mean age =50 +/- 8.66 years) with the diagnosis of IDA, 292 (18.63%) had thrombocytosis. They had a mean platelet count = 534 +/- 121 x 109 /L). None of them had any symptom or sign of thromboembolic events. Discussion Thrombocytosis can be categorized into primary causes such as primary bone marrow disorders and myeloproliferative neoplasms, and secondary causes including infection, inflammation or drug-induced. Iron deficiency anemia leads to reactive thrombocytosis in a mechanism that is yet to be fully understood. The clinical impact of increased platelet counts is not well recognized in literature, and it has not been studied in the Arab population. Although reactive thrombocytosis has been generally considered benign, few case reports described thromboembolic events in patients with IDA reactive thrombocytosis. Few cases in the literature described thromboembolic events in reactive thrombocytosis with IDA. H. Z. Batur Caglayan et al published a case report of a 41-year-old Turkish female patient who presented with transient ischemic attack (TIA) due to intraluminal carotid artery thrombus, which was attributed to IDA-associated thrombocytosis. Another case series by P T Akins et al described three women with severe IDA and thrombocytosis secondary to menorrhagia who developed carotid artery thrombi. The mechanism by which low iron can affect thrombocyte count is still unknown. One study in mice and humans demonstrated that iron deficiency caused reduced megakaryocyte proliferation but increased ploidy independent of thrombopoietin. However, another study failed to identify the exact mechanism by which iron deficiency leads to increased platelet count. CONCLUSION Our study did not find any thromboembolic incident in a large number of patients with reactive thrombocytosis secondary to IDA diagnosed over two years in our Arab population. Disclosures No relevant conflicts of interest to declare.